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CP Board Review - Chemistry > Acid/Base > Flashcards

Acid/Base Flashcards

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1
Q

Acid/Base Definitions

A

 Acid - compound donating H+

 Base - compound accepting H+

 pH - negative log of [H+]

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2
Q

Acid/Base Formula

A

pH = 6.1 + log HCO3/H2CO3

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3
Q

BUFFERS

A
  •  Systems that resist change in pH when acid, base added
  •  Usually composed of weak acid, conjugate base
  •  Work best when near equal amounts of each present (within ± 1 pH unit of pKa of weak acid)
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4
Q

ACIDOSIS vs  ACIDEMIA

A
  • Acidosis - increase in amount of acid present relative to base
  • Acidemia - increase in [H+]
  • All persons who are acidemic have an acidosis; not all persons with acidosis have acidemia!!!
  • Compensation, mixed acid base disorders may minimize acidemia in presence of acidosis
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5
Q

ANION GAP

A
  • Difference between measured cation (Na+), anions (Cl-, HCO3 -), ~ 6-12 mmol/L
  • Measure of relative amounts of other anions (esp. albumin, acid anions), cations (Ca, Mg, immunoglobulins)
  • High anion gap = acid anions
  • Low anion gap: low albumin +/or high Ig’s (myeloma, AIDS, cirrhosis)
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6
Q

LABORATORY TESTS OF ACIDBASE STATUS

A

Blood Gases

Electrolytes

Osmotic Gap

Lactate, Ketones

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7
Q

Blood Gases

A
  • Critical for evaluating respiratory component (as pCO2)
  • Also allows evaluation of oxygenation
  • Measures pH, pCO2, calculates bicarbonate, O2 saturation
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8
Q

ELECTROLYTES

A
  • Total CO2 content = bicarbonate + carbonic acid + carbamino compounds; usually 1-2 mmol/L higher than true bicarbonate
  • Also used to calculate anion, osmotic gap
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9
Q

OSMOTIC GAP

A
  • Difference between measured, calculated (2 * Na + BUN/3 + glucose/20) osmolality
  • Normal may be up to 10 mmol/L
  • Increase indicates uncharged substances; usually alcohols (volatiles), glycols
  • Osmotic gap = concentration (in mmol/L) 
  • Use freezing point depression; vapor pressure osmometers don’t detect volatiles
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10
Q

LACTATE, KETONES

A
  • Product of anaerobic glycolysis; prevent in vitro glycolysis with NaF
  • Ketones come from fatty acid metabolism
  • Normally, -OH butyrate dominant, not measured in “ketone” assay; as metabolized, “ketones” rise
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11
Q

Acid/Base Disorders
General Concepts

A
  • For board purposes, acid-base disorders occur singly; if compensated, pH near normal but always on proper side (slightly low in acidosis, slightly high in alkalosis)
  • Combined disorders always same direction (e.g., metabolic and respiratory acidosis)
  • In real life, these rules don’t apply!!
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12
Q

Acid/Base Disorders
General Concepts 2

A
  • In metabolic disorders, pH, pCO2, HCO3 all change in same direction; in respiratory disorders, pCO2, HCO3 change in one direction, pH in opposite
  • Anion gap high ONLY with metabolic acidosis (but there are also non-anion gap metabolic acidoses)
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13
Q

Acid/Base Disorders
General Concepts 2

A

see image

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14
Q

COMPENSATION

A
  • An adaptive response to return pH towards normal by restoring normal ratio of pCO2 to HCO3
  • With respiratory disorders, alters renal excretion of HCO3
  • With metabolic disorders, alters respiratory rate to change pCO2
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15
Q

METABOLIC ACIDOSIS

A

Increased anion gap usually due to overproduction; renal failure rare cause, acute renal failure (rise 1-2/d), end stage chronic renal failure (SCr > 10 mg/dL)

Non-anion gap due to base loss from GI tract (diarrhea, vilous adenoma), kidneys (renal tubular acidosis) – K low in all of these except high in type IV RTA

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16
Q

ACID OVERPRODUCTION

A

Diabetic ketoacidosis

 Uremia

 Methanol

 Paraldehyde

 Salicylates

 Alcoholic ketoacidosis

 Lactic acidosis

 Ethylene Glycol

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17
Q

METABOLIC ALKALOSIS

A
  • High HCO3-, high pH, low K+
  • Most commonly due to vomiting, dehydration (urine Cl low)
  • Rarely due to excess mineralocorticoids (Cushing’s, hyperaldosteronism)
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18
Q

RESPIRATORY ACIDOSIS

A
  • Increased pCO2, low pH
  • Due to decreased alveolar ventilation
  • Usually chronic (COPD)
  • Acute due to worsening of COPD, respiratory depression, pneumonia, ARDS, chest injury
19
Q

RESPIRATORY ALKALOSIS

A
  • Decreased pCO2, high pH
  • Due to increased alveolar ventilation
  • Usually acute, due to anxiety, pain,
  • Chronic due to chronic hypoxia, stimulating respiratory center - shunting, interstitial lung disease
20
Q

OXYGEN AND HEMOGLOBIN

A

Factors affecting pO2 include ventilation, capillary exchange, and hemoglobin binding

High oxygen affinity (left shift), less tissue delivery: low 2,3 DPG, T, pCO2, H+

Low affinity (right shift) increases oxygen delivery: high 2,3 DPG, T, pCO2, H+

21
Q

Oxyhemoglobin Saturation

A

see image

22
Q

BODY COMPARTMENTS

A
  • Total body is ~ 60% water
  • Intracellular fluid - 60% of H2O - high in K, PO4, protein
  • Extracellular fluid – 40% - high in Na, Cl
    • Interstitial fluid - 30% - low in protein
    • Intravascular plasma - 10% - higher in protein
23
Q

FLUID BALANCE

A
  • Water lost daily; urine losses average 1.5 L, minimum about 0.5 L
  • “Insensible” losses in sweat, breath about 1 L/d
  • Thirst most important defense mechanism; AVP (ADH), aldosterone also important
  • Natriuretic peptides only active hormones for water/Na+ loss
24
Q

SERUM TESTS of Fluid and Electrolytes

A
  • Na, K measured in serum, regulated in water phase of serum; when H2O < 93% of plasma ( protein, lipids), serum Na falsely low (indirect ISE, flame)
  • Na activity (related to Na in H2O) not affected by change in plasma water (direct ISE: Vitros, whole blood)
  • Osmolality (discussed earlier); BUN/creat. evaluate plasma volume (high when V , low when V )
25
Q

URINE TESTS

A

Urine Na best evaluated by FENa; maximal reabsorption = FENa << 1%

Urine osm: maximum dilution < 100, maximum concentration > 500

26
Q

HYPERNATREMIA

A
  • Almost always due to dehydration (loss of low sodium fluid) without water replacement
  • Common in those without access to water (infants, bed-bound) or with impaired thirst receptors (dementia, neurologic disorders)
  • Rarely due to diabetes insipidus, hypertonic solutions
27
Q

HYPONATREMIA

A

Usually due to one of five mechanisms:

  • Pseudohyponatremia (very rare)
  • Osmotic water shifts (rare)
  • Na wasting (renal, extrarenal)
  • Excess water (SIADH, polydipsia)
  • Edematous states (cirrhosis, CHF, nephrotic syndrome)
28
Q

Laboratory Findings in Hyponatremia

A

see pic

29
Q

HYPERKALEMIA (exclude artifactual)

A

Must first exclude artifactual hyperkalemia:

  •  Hemolysis
  •  Delayed separation (especially if refrigerated)
  •  EDTA contamination
  •  Fist clenchinng/relaxing during draw
  •  Thrombocytosis (serum only)
  •  Lymphocytosis (plasma only)
30
Q

HYPERKALEMIA

A

True hyperkalemia usually due to:

  •  Decreased excretion (renal failure, low aldosterone) most common (also type IV RTA)
  •  Shift of potassium out of cells (low insulin, acidosis, cell lysis)
  •  Increased intake
31
Q

HYPOKALEMIA

A

True hypokalemia usually due to:

  •  Increased excretion (diuretics, hyperaldo, RTA, low Mg), GI losses (vomiting, diarrhea, villous adenoma)
  •  Decreased intake
  •  Shift of potassium into cells (correction of insulin deficiency, refeeding, alkalosis)
32
Q

TUMOR MARKERS - General Features

A

Either produced by or components of tumor cells

  •  Used to diagnose, monitor cancer
  •  Ideally, specific to tumor, tissue of origin; detect tumor at early stage; levels related to stage, useful for prognosis; can follow course of disease
  •  Most tumor markers not ideal
33
Q

Categories of Tumor Markers

A
  • Normal cell products (PSA, Tg, IgG)
  • Oncofetal antigens (CEA, AFP, HCG)
  • Surface proteins (CA 19-9, 125, 15-3)
  • Hormone receptors (ER/PR, EGFR, HER-2/neu)
  • Genetic markers
34
Q

CEA

A
  • Family of surface glycoproteins
  • Shed by cell injury, cleared by liver
  • Produced by variety of cancers (GI tract, pancreas, lung, uterus, breast)
  • In colon CA, increased in 25% of localized, 70-90% of metastatic
35
Q

AFP

A
  • Made by fetal hepatocytes, yolk sac (peak 2nd trimester 106 times adult levels)
  • Re-expressed by hepatocyte regeneration
  • When > 100x increased, fairly specific for HCC (50% sensitive), yolk sac tumor
  • L3 variant more specific for HCC, associated with more aggressive tumors
36
Q

PSA

A
  • Enzyme (human kallikrein 3)
  • Circulates bound to protease inhibitors; inactive (free) form higher in BPH
  • Relatively specific to prostate, not Ca
  • Rapid rises (> 0.75 ng/mL/yr), high values in small prostate more specific
  • Should be undetectable after surgery, within ref. range after XRT
37
Q

CA 15-3/27-29

A
  • Different assays for overlapping regions of same antigen
  • Originally found in breast cancer cells, also in lung, pancreas, colon, ovary
  • Like CEA, also high in 25% localized, 70% advanced; also high with liver disease
38
Q

CA 19-9

A
  • Related to Le blood antigen (not made in Le negative)
  • Found in pancreas, bile duct, GI tract, lung, breast CA
  • In pancreatic CA, high in 40% with small tumors, 80-90% with advanced
  • May be markedly increased by cholestasis/cholangitis, falls with stenting
39
Q

CA-125

A
  • Ovarian surface glycoprotein; also endometrial, pancreas, GI, lung, breast
  • High in ovarian surface tumors (not mucinous), 30-40% stage I, 80-90% stage IV tumors
  • Also increased by pregnancy, endometriosis, cirrhosis, ascites
40
Q

ER/PR

A
  • Found in hormonally responsive cells, not in circulation
  • In breast CA, indicates better prognosis, response to estrogen deprivation, tamoxifen, aromatase inhibitors
41
Q

EGFR

A
  • Epidermal growth factor receptor (I)
  • Prognostic in colon, lung, H&N, esophageal CA when overexpressed
  • Antagonists available for treatment of tumors expressing receptor
  • Those with mutated ras gene do not respond to antagonists
42
Q

HER-2/neu

A
  • Member of EGFR family
  • Overexpression in breast Ca indicates poor prognosis; can be treated with antagonist (Herceptin)
  • Gene can be detected by FISH, receptor by IHC in cells; excess protein can be detected in circulation (correlation not exact)
43
Q
A

CP Board Review - Chemistry (9 decks)

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