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Chemistry! > acid/base liver > Flashcards

acid/base liver Flashcards

1
Q

what is a buffer made of?

A

weak acid + salt conjugate base (resist changes in pH when adding acid or base)

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2
Q

what is the formula for carbonic acid and bicarb? and under what conditions are each made?

A

carbonic acid: H2CO3
- made when there’s additional H+ ions in the body that add to bicarb

bicarb: HCO3-
- made when a strong base is added: carbonic acid joins with OH- to make H2O and the subsequent weak conjugate base (bicarb) is made

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3
Q

what is the henderson-hasselback equation?

A

pH = pKa + log(A-/HA)

where pKa is assumed 6.1

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4
Q

What is the relationship between carbonic acid and partial pressure of CO2? (used in the HH equation)

A

H2CO3 = pCO2 x 0.03

so in the equation, pH = pKa + log[(bicarb/(pCO2 x 0.037)]

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5
Q

in the tissues, CO2 diffuses _____ of the tissues and _____ plasma and RBCs. What then diffuses out of the RBCs, and what goes into the RBCs?

A

CO2 out of tissue and into plasma and RBCs

then bicarb diffuses out of the RBCs and chloride diffuses into the RBCs

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6
Q

in the lungs, ____ diffuses from alveoli into blood where it binds to Hgb. What happens to bicarb? Then what?

A

in the lungs, oxygen diffuses from alveoli into blood where it binds to Hgb.

Bicarb binds with hydrogen ions to make carbonic acid

then carbonic acid dissociates into H2O and CO2 so then the CO2 can leave through alveoli/ventilation

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7
Q

what are the kidneys main role in the acid-base balance, and how does it do this?

A

its main role is to reabsorb bicarb from filtrate.

  1. bicarb is reabsorbed using Na+ in exchange for H+.
  2. increased pH limits Na+/H+ exchange, which limits bicarb reabsorption
  3. and decreased pH increases the Na+/H+ encage, leading to more bicarb reabsorption
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8
Q

acid-base disorder compensation is done by the _____ and ______. Which is associated with pCO2, and which is associated with HCO3-? The compensation is done by the organ ______ assisted with the primary process

A

kidneys: HCO3-
lungs: pCO2

compensation for a problem in the kidneys is done by the lungs, and vice versa

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9
Q

how fast are the lungs and kidneys when responding to an acid-base imbalance?

A

lungs: immediate compensate by retaining or expelling CO2 (short-term)

kidneys: take 2 -4 days to respond, but the affects are long-term and sustained

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10
Q

what are the four acid-base imbalances, and what is the primary defect of each?

A

repository acidosis: primary accumulation of pCO2
- with decreased pH

respiratory alkalosis: primary deficit of pCO2
- with increased pH

metabolic acidosis: primary deficit of HCO3-
- with decreased pH

metabolic alkalosis: primary accumulation of HCO3–
- with increased pH

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11
Q

what are causes for respiratory acidosis (increased pCO2)

A

ineffective removal of CO2 from blood
- Lung diseases: asthma, emphysema, bronchitis

airway obstruction
- COPD and intra/extra-pulmonary problems

depression of respiratory centers
- barbiturates, morphine, alcohol

decreased pulmonary circulation
- CHF and other circulatory disorders

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12
Q

how does the body compensate for respiratory acidosis?

A

kidneys retain bicarb to increase bicarb levels. Because this is an acidosis problem, kidneys will excrete H+ ions to help increase the pH
- this takes hours to days

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13
Q

what are causes for respiratory alkalosis (primary deficit of pCO2)?

A
  1. high altitudes decreased pCO2
    - leads to hyperventilation
  2. anxiety-induced hyperventilation
    - hysteria
  3. aspirin overdose
  4. pulmonary embolism/fibrosis
    - O2 exchange is impaired
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14
Q

how does the body compensate for respiratory alkalosis?

A

kidneys decrease bicarb level by excreting it into the urine and reclaiming H+ to the blood (which will increase pH)

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15
Q

what are causes for metabolic acidosis (primary deficit of HCO3-)?

A
  1. acid addition:
    - aspirin, ethanol, methanol, ethylene glycol
    - diabetic keto acidosis / lactic acidosis (creation of acid)
  2. base subtraction:
    - renal failure (tubular necrosis)
    - diarrhea (excessive tubular bicarbonate ion loss)
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16
Q

how does the body compensate for metabolic acidosis (primary deficit of HCO3-)?

A

Hyperventilation: the lungs will begin to excrete pCO2 in order to decrease the pH, and then eventually the kidneys will retain that missing bicarb and excrete H+ to decrease the pH

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17
Q

what are causes of metabolic alkalosis (primary accumulation of HCO3-)?

A
  1. increased acid subtraction
    - loss of stomach acid via vomiting or nasogastric suction
    - prolonged use of diuretics (increased acidic urine and alkaline blood)
  2. increased base addition
    - ingested NaHCO3- or antacid
  3. potassium depletion (hypokalemia)
    - Cushing’s, adrenal tumors, steroid therapy
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18
Q

how does the body compensate for metabolic alkalosis (primary accumulation of HCO3-)?

A

Hypoventilation: the lungs will begin to retain pCO2 in order to decrease pH

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19
Q

what is used to measure pO2 and pCO2 and pH?

A

pO2: amperometry
- reduction of oxygen produces a current that is proportional to the amount of oxygen present

pCO2 and pH: potentiometry
- electric potential between two electrodes (change in voltage indicates the [analyte])

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20
Q

what is the normal range for the following:
- pH
- pCO2
- pO2
- Bicarb (HCO3-)
- O2 saturation

A

pH: 7.35 - 7.45
pCO2: 35 - 44 mmHg
pO2: 80 - 100 mmHg
HCO3-: 23 - 29 mmol/L
Saturated O2: > 95%

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21
Q

What are the blood gas sample parameters?

A
  • arterial draw
  • mix tube asap to prevent clots
  • run within 30 minutes of collection (if not, pH decreased and pCO2 will increase; also false K+ increase)
  • can use ice but not for long
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22
Q

the liver functions to metabolize what four things? What other 3 functions does it do?

A
  1. metabolizes: carbs, lipids, proteins, and bilirubin
  2. detoxes harmful substances
  3. stores essential compounds
  4. cleans waste products into bile or blood for excretion
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23
Q

what two places does the liver receive blood? Where do supplies merge? And where does blood flow before leaving the liver?

A

liver receives blood in the
- hepatic artery
- portal vein: digestive tract to liver (main source)

supplies merge in the sinusoid (that is lined with hepatocytes that removes toxins)

blood flows to the central canal of each lobe before it leaves the liver

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24
Q

what are the two types of cells of the liver, and what are their functions?

A

hepatocytes: the major kind of liver cell that regenerate the liver

kupffer cells: macrophages that line the sinusoids and act as phagocytes (engulf bacteria, debris, toxins, ect)

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25
Q

Bilirubin is the ______ product of ____ cells. It’s basically ______ waste.

A

bilirubin: breakdown product of RBCs. Heme waste after hemoglobin is broken down

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26
Q

Bilirubin is first bound to _____ and transported to the ______. This kind of bilirubin is called what? Is this form soluble in water?

A

It’s bound to albumin and transported to the liver. This is unconjugated, or indirect bilirubin.

It is NOT water soluble

27
Q

Once in the liver, unconjugated bilirubin is _______ by ________ by the addition of ______ acid to the side chains of bilirubin. Now it is ____-soluble.

A

in the liver, unconjugated bilirubin is conjugated by glucuronyl transferase by the addition of glucuronic acid. Now this is conjugated (or direct) bilirubin that is water-soluble

28
Q

After becoming conjugated in the liver, conjugated/indirect bilirubin goes through the ______ _____ _____ to the _________ where _____ convert it to _______ (colorless)

A

after liver conjugation, conj/direct bilirubin goes through the common bile duct to the intestines where bacteria turn it into urobilinogen (colorless).

29
Q

most urobilinogen is oxidized into _______ (urobilin) which is what color and excreted where? The other 10% of this urobilinogen goes where?

A

90% of urobilinogen is oxidized into stercobilin that is orange and excreted in the feces

the other 10% of urobilinogen is reabsorbed and filtered into the kidneys into the urine

30
Q

what does the liver do with carbohydrate metabolism?

A
  1. liver uses glucose for energy
  2. circulation of glucose for tissues to use
  3. stores glucose for later use
31
Q

what does the liver do with lipid metabolism?

A

production of acetyl-CoA
- makes triglycerides, phospholipids, and cholesterol

32
Q

what does the liver do with protein metabolism?

A

synthesizes positive and negative phase reactants and coagulation proteins

also stores amino acids

33
Q

How does the liver act as the gatekeeper between substances absorbed in the GI and those released into circulation?

A
  1. bind the material reversibly to inactivate the compound
  2. chemically modify the compound to be excreted

(also detoxes drugs)

34
Q

jaundice is the retention of _______. Prehapatic jaundice happens prior to _____ metabolism. Increased amounts of bilirubin leads to what two things?

A

jaundice: retention of bilirubin

prehepatic jaundice: prior to liver metabolism

increased bilirubin: acute and chronic hemolytic anemia, and also increase in unconj/indirect bilirubin

35
Q

Gilbert’s syndrome is a genetic mutation of _______ ______ leading to what kind of bilirubin?

A

mutation of glucuronyl transferase, so there’s an increase in unconjugated bilirubin (intermittent)

36
Q

what is the defect in Crigler-Najjar syndrome? Is it more or less serious that Gilbert’s syndrome?

A

This is also a defect in glucuronyl transferase, like Gilbert’s, but it’s inherited and more serious than Gilbert’s. It leads to chronic increase unconjugated bilirubin

37
Q

Dublin-Johnson syndrome is a problem with what that leads to increased _________ bilirubin

A

problem of the liver: it cannot remove bilirubin from liver cells. (transportation issue)

leads to increased conjugated bilirubin

38
Q

What is the defect in Rotor syndrome, and this leads to an increase in what kind of bilirubin?

A

proteins are shorter than normal, so bilirubin is less efficiently taken up by the liver

increased conjugated bilirubin

39
Q

Physiologic jaundice of the newborn is caused by what? What condition can this lead to in newborns?

A

caused by deficiency of glucuronyl transferase, one of the last function active in prenatal life

can lead to kernicterus: increased unconj bilirubin in the brain. Treated with UV light to break down the indirect bilirubin

40
Q

post-hepatic jaundice is another way of saying ______ ________

A

biliary obstruction
- gallstones, tumors, (ect) that prevent the flow of conj bili into the bile canaliculi (leads to the common bile duct)

leads to improper excretion (leads to normal stool pigment lost)

41
Q

What takes place with tissue when cirrhosis happens?

A
  1. scar tissue replaces normal tissue
    - nodes, firbosis
  2. scar tissue takes over
    - blockage of blood flow through liver
  3. liver function deteriorates
    - fatigue/nausea, jaundice, GI tract bleeding, legs/abdomen swelling
42
Q

what are some causes of cirrhosis?

A

chronic alcoholism, hepatitis, autoimmune conditions, Wilson’s disease, hemochromatosis, blocked bile ducts, and nutritional deficiencies

43
Q

how to test for cirrhosis?

A

liver enzymes AST/ALT increased (ratio over 2) with markedly increased total bilirubin

increased ammonia levels

decreased albumin

beta-gamma bridge

44
Q

what kind of hepatitis is most common, and what are causes of hepatitis?

A

viral hepatitis most common

causes: viruses, bacteria, parasites, radiation, acute/chronic autoimmune hepatitis

45
Q

what is the testing for hepatitis?

A

indirect immunofluorescence with anti-SM antibody and hypergammaglobulinemia

46
Q

what are symptoms of viral hepatitis?

A

jaundice, dark urine, fatigue, nausea, vomiting, and abdominal pain

47
Q

how are the following usually contracted?
- HAV
- HBV
- HCV
- HDV
- HEV

A
  • HAV: fecal/oral, or contaminated food/water
  • HBV: serum hepatitis/long incubation hepatitis. Can be acute or chronic. Parental, perinatal, or sexual
  • HCV: parental or blood transfusion. Most cases become chronic, leading to cirrhosis, ESLD, and/or death
  • HDV: as a result from HBV
  • HEV: fecal/oral and mild
48
Q

how to test for HAV, HCV, and HBV?

A

HAV: anti-HAV IgM in serum
HCV: anti-HCV IgM in serum

HBV:
- surface antigen, core protein, envelope antigen, ect.

49
Q

biliary obstruction is secondary to _____ _____. What liver enzymes are increases with biliary obstruction?

A

secondary to biliary cirrhosis

increased
- ALP
- GGT
- 5’Nucleotidase
- AST > ALT

50
Q

Wilson’s disease has total body copper deposited in what three sites? What is the key testing for this disease?

A
  1. liver
  2. basal ganglia
  3. lens
    - kaiser fleisher rings

decreased alpha-1 ceruloplasmin is key testing, with increased copper in urine (and decreased serum copper)

51
Q

what are risk factors for hepatocellular carcinoma? (malignant liver tumors)

A

hepatitis, heavy alcohol consumption, toxin consumption, tobacco, and nonalcoholic fatty liver disease

52
Q

Reye’s syndrome (causes swelling in the brain and liver damage) is caused by what three things? It’s preceded by what?

A

caused by:
- infectious disease
- metabolic disease
- toxic/drug-induced disease

preceded by:
- varicella
-gastroenteritis
- URT infection

53
Q

what happens in Reye’s syndrome?

A

noninflammatory encephalopathy and fatty degeneration of the liver
- profuse vomiting/neurologic impairment
- mild increase in bilirubin
- huge increase in ammonia and AST/ALT ratio

54
Q

drug/alcohol related disorders are ___ of all reported cases of liver failure. What causes alcoholic cirrhosis?

A

1/3

heavy, prolonged consumption of ethanol causes alcoholic cirrhosis

55
Q

what are the three stages of drug / alcohol related liver disorders?

A
  1. fatty liver
    - benign alcoholic stage
    - slight increase of AST/ALT and GGT
  2. alcoholic hepatitis
    - AST 2x the upper limit
    - ALT lower than AST (ratio greater than 2)
    - decreased albumin with increased PT
  3. alcoholic cirrhosis
    - GI bleeding, ascites, weight loss, hepatosplenomegaly
    - liver biopsy needed to make definite diagnosis
56
Q

hemochromatosis is due to? And it leads to what?

A

due to recessive inherited disorder (mutated hepcidin/HAMP gene) that leads to increased absorption of iron from GI tract
- iron overload in tissue
- iron accumulates in liver, heart, pancreas
- diabetes mellitus / bronzing of skin

57
Q

what are the four bilirubin analysis methods?

A

diazo reaction, Evelyn Malloy, jendrassik-grof, DMSO

58
Q

what happens in the diazo reaction?

A

bilirubin + diazotized sulfanilic acid solution to make purple color
- conj bilirubin gives immediate reaction
- unconj bilirubin is bonded to albumin; bind must be broken by methanol

59
Q

what happens in the Evelyn Malloy reaction, and also what happens in the jendrassik-grof reaction?

A

Evelyn-Malloy: bilirubin + diazo reagent = azobilirubin

jendrassik-grof: sodium acetate + caffeine + benzoate + diazo
- ascorbic acid as stop reagent
-alkaline tartare to change pH

60
Q

in the DMSO reaction, total bilirubin reagent consists of what there things? What does DMSO do to unconjugated bilirubin?

A

consists of sulfanilic acid, sodium nitrite, and DMSO

DMSO solubilizes unconj. bilirubin

61
Q

urobilinogen is the _______ end product of ________ metabolism. Increased urinary urobilinogen levels are found in what two diseases?

A

colorless, bilirubin

found in hemolytic disease and defective liver cell function (hepatitis)

62
Q

absence of urobilinogen in urine and stool is seen in with what?

A

complete biliary obstruction

63
Q

liver enzymes are used to differentiate _________ from ________ liver disease

A

hepatocellular (functional) from obstructive (mechanical) liver disease

Chemistry! (9 decks)

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