Alcohol and its types, the tests associated with it and the clinical conditions arising from it along with the various types of diseases.

1. ALCOHOL
METABOLISM

2. CONTENTS
ETHANOL
• METABOLISM
• ACTIONS
• ABSTINANCE
• EFFECTS ON ORGANS
• TERATOGENICITY
METHANOL
ISOPROPANOL
ESTIMATION
• BLOOD ALCOHOL
• BREATH ALCOHOL
• SALIVARY ALCOHOL
• URINARY ALCOHOL
• POSTMORTEM ALCOHOL
ALCOHOLIC LIVER DISEASE

3. ETHANOL
• WEAKLY CHARGED MOLECULE
• MOVES EASILY THROUGH CELL MEMBRANES
• RAPIDLY EQUILIBRATING BETWEEN BLOOD AND TISSUES
IN BEVERAGES IN ADDITION TO ALCOHOL
• LOW MOLECULAR WT ALCOHOLS(METHANOL ,BUTANOL)
• ALDEHYDES
• ESTERS
• HISTAMINE

4. • PHENOLS
• TANNINS
• IRON,
• LEAD
• COBALT
• ADVERSE CONSEQUENCES WITH HEAVY DRINKING

5. ABSORPTION
RATE INCREASED BY
• RAPID GASTRIC EMPTYING
• ABSENCE OF PROTEINS
FATS AND CARBOHYDRATES
• ABSENCE OF CONGENERS
• CARBONATION(EG.
CHAMPAGNE)

6. EXCRETION
• LUNGS, URINE AND SWEAT (SMALL AMOUNTS)
• LIVER (GREATER PART)

7. ALCOHOL
• SUPPLIES CALORIES
• DEVOID OF MINERALS, PROTEINS AND VITAMINS
• INTERFERES WITH VITAMIN ABSORPTION FROM INTESTINE
• DECREASES THEIR STORAGE IN THE LIVER
• MODEST EFFECT ON FOLATE, VIT B6, THIAMINE, NIACIN AND VIT A

8. Mitochondrion
Ethanol
Acetaldehyde
Acetate
Cytosol
ER
ADH
NAD+
NADH
AlDH
NAD+
NADH
MEOS
NADP+
NADPH
O2
P450
Extra-hepatic tissue
Disulfiram
CELLULAR PROCESSING

12. Glc
Malate
MDH
NADHNADH
Malate
PEPCK
G6P
GK
F6P
F16BP
PFK
PEP
Pyr
PK
NADH
Malate
Suc
Fum
PDH
Acetyl CoA
Cit
ICit
Mitochondrion
Cytosol
NADHPC
OAA
MDH
NAD+
OAAMDH
NAD+
αKG
IDHNAD+
Lactate
LDH
NAD+
S CoA
αKGDH
NAD+
G6Pase
F16BPase
NADH
FA
β-Ox
NADH
PATHWAY PERTURBATIONS
NADH

13. HYPOGLYCEMIA AND ALCOHOL
INTOXICATION
VULNERABLE INDIVIDUALS
• FASTED
• PROLONGED STRENUOUS EXERCISE
• USING INSULIN-HYPOGLYCEMIA OCCURING MANY HOURS AFTER ALCOHOL
CONSUMPTION

14. ALCOHOL KETOACIDOSIS
• POOR DIET
• RECURRENT VOMITING
• MISDIAGNOSED AS DIABETIC KETOSIS
• INCREASE IN KETONES
• MILD INCREASE IN BLOOD GLUCOSE
• LARGE ANION GAP
• MILD TO MODERATE INCREASE IN SERUM LACTATE
• Β-HYDROXYBUTYRATE/LACTATE RATIO BETWEEN 2:1 AND 9:1 (NORMAL 1:1).

15. MEOS PATHWAY
• P450-DEPENDENT MICROSOMAL ETHANOL OXIDIZING SYSTEM
• INVOLVING NADPH AND O2
• INCREASES IN ACTIVITY IN CHRONIC ALCOHOLISM
• GENERATES ACETALDEHYDE AND SUBSEQUENTLY ACETATE
• WHILE OXIDIZING BIOSYNTHETIC REDUCING POWER, NADPH, TO NADP+.
• BECAUSE IT USES OXYGEN, THIS PATHWAY GENERATES FREE RADICALS THAT DAMAGE TISSUES.
• MOREOVER, BECAUSE THE SYSTEM CONSUMES NADPH, THE ANTIOXIDANT GLUTATHIONE CANNOT BE
REGENERATED EXACERBATING THE OXIDATIVE STRESS.

16. • BELOW 100 MG/DL (22 MMOL/L), THE MEOS SYSTEM, (HIGH KM FOR ALCOHOL), CONTRIBUTES LITTLE.
• WHEN LARGE AMOUNTS OF ETHANOL ARE CONSUMED, THE ADH SYSTEM BECOMES SATURATED OWING
TO DEPLETION OF NAD+.
• ABOVE 100 MG/DL, THERE IS INCREASED CONTRIBUTION FROM THE MEOS SYSTEM, WHICH DOES NOT RELY
UPON NAD+
• DURING CHRONIC ALCOHOL CONSUMPTION, MEOS ACTIVITY INCREASES.
• CHRONIC ALCOHOL CONSUMPTION RESULTS ALSO IN THE INCREASED CLEARANCE OF OTHER DRUGS
ELIMINATED BY THE MEOS SYSTEM.

17. • LIVER MITOCHONDRIA CAN CONVERT ACETATE INTO ACETYL COA IN A REACTION
REQUIRING ATP.
• ENZYME IS THE THIOKINASE THAT NORMALLY ACTIVATES SHORT-CHAIN FATTY ACIDS.
• HOWEVER, FURTHER PROCESSING OF THE ACETYL COA BY THE CITRIC ACID CYCLE IS
BLOCKED, BECAUSE NADH INHIBITS
• ISOCITRATE DEHYDROGENASE AND A-KETOGLUTARATE DEHYDROGENASE

18. CONSEQUENCES OF ACETYL COA
ACCUMULATION
• ↑KETONE BODIES FORMATION, EXACERBATING THE ACIDIC CONDITION ALREADY RESULTING FROM THE
HIGH LACTATE CONCENTRATION.
• THE PROCESSING OF THE ACETATE IN THE LIVER BECOMES INEFFICIENT, LEADING TO A BUILDUP OF
ACETALDEHYDE.
• THIS VERY REACTIVE COMPOUND FORMS COVALENT BONDS WITH MANY IMPORTANT FUNCTIONAL
GROUPS IN PROTEINS, IMPAIRING PROTEIN FUNCTION.
• IF ETHANOL IS CONSISTENTLY CONSUMED AT HIGH LEVELS, THE ACETALDEHYDE CAN SIGNIFICANTLY
DAMAGE THE LIVER, EVENTUALLY LEADING TO CELL DEATH

19. ↑NADH
• INHIBITS FATTY ACID OXIDATION
• ↑FATTY ACID SYNTHESIS
• INCREASED ESTERIFICATION OF FATTY ACIDS IN TRIACYLGLYCEROL
• INCREASED LIPOGENESIS
• ↑ CHOLESTEROL SYNTHESIS FROM ACETYL-COA,
• ↑ LIPID PEROXIDATION
• CITRIC ACID CYCLE IS BLOCKED
• INHIBITS ISOCITRATE DEHYDROGENASE AND A-KETOGLUTARATE DEHYDROGENASE
• HYPERLACTIC ACIDEMIA
• DECREASES EXCRETION
OF URIC ACID-GOUT

21. ETHANOL
• CNS ACTIONS OF ETHANOL PRONOUNCED DURING ABSORPTIVE PHASE THAN
ELIMINATION PHASE- PHENOMINON OF ACUTE TOLERANCE
• SYNERGISTIC ACTION WITH CNS DEPRESSIVE DRUGS
• DEATHS OCCURRED

22. MECHANISM OF CNS DEPRESSION
• ENHANCEMENT OF MAJOR INHIBITORY
NEURONS
• IMPAIRMENT OF EXCITATORY NEURONS
• INHIBITORY NEURONAL SYSTEM-GABA

23. GABA binds to post
synaptic receptor
subtype GABAA
This complex opens
Inward flux
of Cl-
Membrane
hyper
polarization
Decreased
electrical response

24. GABA MEDIATED INHIBITORY RESPONSE ENHANCED BY
• ETHANOL
• BARBITURATES
• BENZODIAZEPINES
• MOST GENERAL ANAESTHETIC AGENTS

25. • CNS EXCITATORY RESPONSE MEDIATED BY GLUTAMATE
• ETHANOL INHIBITS THE EXCITATORY RESPONSE MEDIATED BY CA ION GATED
GLUTAMATE RECEPTOR SUBTYPE N-METHYL D ASPARTATE(NMDA)RECEPTOR
• ↑ THE ACTIVITY OF PHENYLETHANOLAMINE N METHYLTRANSFERASE
NOREPENEPHRINE EPENEPHRINE
PNMT
• EPINEPHRINE IN TURN ACTIVATES PRESYNAPTIC Α2 RECEPTORS WHICH INHIBITS RELEASE
OF NOREPINEPHRINE

26. PHYSICAL ABSTINANCE SYNDROME
• ABRUBT WITHDRAWL-PHYSICAL ABSTINANCE SYNDROME
• CNS EXCITATION
• ANXIETY, IRRITABILITY
• INSOMNIA
• MUSCLE TREMOR AND CRAMPS
• SEIZURES
• HALLUCINATIONS
• ↑TEMPERATURE, BP, HEART RATE

27. DELIRIUM TREMENS
• INTENSE ACUTE WITHDRAWL
• DELIRIUM- MENTAL CONFUSION, AGITATION AND FLUCTUATING LEVELS OF
CONSCIOUSNESS
• TREMENS- ↑ PULSE, BP AND RESPIRATION
• CONCOMITANT MEDICAL DISORDERS

29. EFFECTS OF ETHANOL ON ORGAN SYSTEMS
NERVOUS SYSTEM
• BLACKOUT, AN EPISODE OF TEMPORARY ANTEROGRADE AMNESIA
• DISTURBED SLEEP
• DISTURBING DREAMS
• SNORING
• EXACERBATES SLEEP APNOEA
• IMPAIRED JUDGEMENT AND COORDINATION

30. CHRONIC ALCOHOLISM
• PERIPHERAL NEUROPATHY
• CEREBELLAR DEGENERATION OR ATROPHY-PROGRESSIVE UNSTEADY STANCE AND GAIT OFTEN
ACCOMPANIED BY MILD NYSTAGMUS
WERNICKE’S (OPHTHALMOPARESIS, ATAXIA, AND ENCEPHALOPATHY)
KORSAKOFF ’S (RETROGRADE AND ANTEROGRADE AMNESIA)
• THIAMINE DEFICIENCY
• TRANSKETOLASE DEFICIENCY

31. PSYCHIATRIC PROBLEMS
• IMPULSIVITY AND DISINHIBITION
• PREEXISTING SCHIZOPHRENIA OR MANIC DEPRESSIVE DISEASE
• ANXIETY DISORDERS SUCH AS PANIC DISORDER.
• INTENSE SADNESS LASTING FOR DAYS TO WEEKS IN THE MIDST OF HEAVY DRINKING
• AUDITORY HALLUCINATIONS

32. GASTROINTESTINAL SYSTEM
ESOPHAGUS AND STOMACH
• EPIGASTRIC DISTRESS AND GASTROINTESTINAL BLEEDING
• MALLORY-WEISS LESION
PANCREAS AND LIVER
• ACUTE PANCREATITIS
• ALCOHOL-INDUCED HEPATITIS, PERIVENULAR SCLEROSIS, AND CIRRHOSIS

33. • (A) ABDOMINAL X RAY OF A PATIENT WITH ALCOHOLIC PANCREATITIS. NOTE
THE SPECKLED CALCIFICATION (I.E., CALCIUM DEPOSITS) WITHIN THE
PANCREAS (MARKED BY ARROWS).
• (B) ABDOMINAL X RAY FROM A SUBJECT WITHOUT PANCREATITIS.

34. CANCER
• BREAST CANCER
• ORAL AND ESOPHAGEAL CANCERS
• RECTAL CANCERS
HAEMATOPOETIC SYSTEM
• INCREASE IN (MCV)
• ACCOMPANIED BY FOLIC ACID DEFICIENCY-HYPERSEGMENTED NEUTROPHILS, RETICULOCYTOPENIA
• MILD THROMBOCYTOPENIA
• CHRONIC HEAVY DRINKING-DECREASED PRODUCTION OF WBCS

35. CARDIOVASCULAR SYSTEM
• MILD TO MODERATE HTN
• CORONARY ARTERY DISEASE
• CARDIOMYOPATHY
• UNEXPLAINED ARRHYTHMIAS TO HEART FAILURE
“HOLIDAY HEART.”
• ATRIAL OR VENTRICULAR ARRHYTHMIAS, ESPECIALLY PAROXYSMAL TACHYCARDIA, CAN ALSO OCCUR
AFTER A DRINKING BINGE IN INDIVIDUALS SHOWING NO OTHER EVIDENCE OF HEART
• OBSERVED TRANSIENTLY IN THE MAJORITY OF ALCOHOLICS ENTERING TREATMENT.

36. GENITOURINARY SYSTEM CHANGES AND SEXUAL
FUNCTIONING
MEN
• MODEST DOSES-INCREASE SEXUAL DRIVE
CHRONIC ALCOHOLISM-
• IRREVERSIBLE TESTICULAR ATROPHY
• SHRINKAGE OF THE SEMINIFEROUS TUBULES,
• DECREASES IN EJACULATE VOLUME,
• LOWER SPERM COUNT

37. WOMEN
• AMENORRHEA, A DECREASE IN OVARIAN SIZE,
• ABSENCE OF CORPORA LUTEA WITH ASSOCIATED INFERTILITY,
• INCREASED RISK OF SPONTANEOUS ABORTION.

38. BONE
• CHANGES IN CALCIUM METABOLISM
• LOWER BONE DENSITY
• DECREASED GROWTH IN THE EPIPHYSIS
• ↑RISK OF FRACTURES
• OSTEONECROSIS OF FEMORAL HEAD

39. OTHER EFFECTS
• ALCOHOLIC MYOPATHY
• ↑CORTISOL
• ↑ VASOPRESSIN AT RISING BLOOD ALCOHOL CONC
• ↓ VASOPRESSIN AT FALLING BLOOD ALCOHOL CONC
• MODEST ↓ IN T4
• MARKED ↓ IN T3

40. FETAL ALCOHOL SYNDROME
• HEAVY DRINKING DURING PREGNANCY
• PLACENTAL TRANSFER OF ETHANOL AND ACETYLDEHYDE

42. ACUTE ALCOHOL INTOXICATION
• CORTISOL RELEASE
• ↑PLASMA CATECHOLAMINES
• SHARP REDUCTION IN PLASMA TESTOSTERONE
• ↑ PLASMA LH

43. CHRONIC ALCOHOLISM
• ↑GGT
• CARBOHYDRATE DEFICIENT TRANSFERRIN
• ABNORMAL PITUITORY, ADRENOCORTICAL AND
MEDULLARY FUNCTION
• DESIALYLATION OF PROTEINS
• ↑MCV

44. METHANOL
• CONSTITUENT OF ANTIFREEZE AND WINDOW CLEANING FLUIDS AND CANNED FUEL
• INTENSIONAL CONSUMPTION-ETHANOL SUBSTITUTE
• ACCIDENTALLY-ILLEGAL WHISKY
• ACCIDENTAL –CHILDREN
• CNS EFFECTS LESS SEVERE
THAN ETHANOL
• LIVER ADH

45. FORMIC ACID
• SERIOUS ACIDOSIS
• OPTIC NEUROPATHY
• BLINDNESS
• DEATH
• FORMATE IS TOXIC BECAUSE IT INHIBITS MITOCHONDRIAL CYTOCHROME C OXIDASE, CAUSING THE
SYMPTOMS OF HYPOXIA AT THE CELLULAR LEVEL, AND ALSO CAUSING METABOLIC ACIDOSIS
• SERUM FORMATE CORRELATE WITH ACIDOSIS AND SEVERITY OF CNS AND OCULAR TOXICITY THAN DO
SERUM METHNOL CONC
• ETHANOL IS SOMETIMES DENATURED (ADULTERATED), AND THUS MADE UNDRINKABLE, BY THE ADDITION
OF METHANOL. THE RESULT IS KNOWN AS METHYLATED SPIRIT

46. TREATMENT OF METHANOL INTOXICATION
• ETHANOL
• FOMEPIZOLE TO INHIBIT METHANOL METABOLISM
• SODIUM BICARBONATE THERAPY FOR METABOLIC ACIDOSIS
• FOLATE-ENHANCE FOLATE MEDIATED METABOLISM OF FORMATE
• HAEMODIALYSIS- CLEARANCE OF METHANOL AND FORMATE

47. ANALYSIS
• HEAD SPACE GAS CHROMATOGRAPHY-METHOD OF CHOICE FOR METHANOL
ESTIMATION
• ENZYMATIC ASSAY
• BASED ON FORMATE DEHYDROGENASE

48. ISOPROPANOL
• 70% AQUEOUS SOLUTION- RUBBING ALCOHOL
• TWICE THE CNS DEPRESSANT ACTION AS ETHANOL
• NOT AS TOXIC AS METHANOL
• SHORT HALF LIFE-6HOURS
• RAPIDLY METABOLISED BY ADH TO ACETONE WHICH IS ELIMINATED MORE SLOWLY(T1/2 17 TO27 HRS)
• ALVEOLAR AIR AND URINE
• ACETONE CONC EXCEEDS ISOPROPANOL IN ELIMINATION PHASE

49. ISOPROPANOL
• ACETONE-CNS DEPRESSANT ACTIVITY SAME LIKE ETHANOL
• LONGER HALF LIFE-PROLONGS THE CNS EFFECTS
SEVERE INTOXICATION-
• COMA OR DEATH
• TREATMENT- HAEMODIALYSIS
• ETHANOL NOT INDICATED

50. ISOPROPANOL -ESTIMATION
• HEAD SPACE GAS CHROMATOGRAPHY
• NMR SPECTROMETRY

51. BLOOD ALCOHOL
• SERUM, PLASMA OR WHOLE BLOOD
• SITE CLEANSED WITH ALCOHOL FREE DISINFECTANT LIKE BENZALKONIUM CHLORIDE
• SERUM: WHOLE BLOOD ETHANOL RATIO IS 1.14
• SPECIMENS WELL CAPPED
• BLOOD PROPERLY SEALED-14 DAYS AT ROOM TEMP
• 4 DEG WITH OR WITHOUT PRESERVATIVE
• LONGER STORAGE-SODIUM FLUORIDE PRESERVATIVE
• NON STERILE POST MORTEM SPECIMENS-SODIUM FLUORIDE

52. ESTIMATION
• ENZYMATIC ANALYSIS USING ALCOHOL DEHYDROGENASE
• ETHANOL TO ACETALDEHYDE
• AMOUNT OF NADH FORMED AT 340NM
• ADH RELATIVELY SPECIFIC TO ETHANOL
• INTERFERENCE 7% -ISOPROPANOL, 3 % METHANOL AND 4 % ETHYLENE GLYCOL
• SPECTROPHOTOMETERS OR AUTOMATED ANALYSERS
• SERUM COMMONLY
• URINE OR SALIVA
• WHOLE BLOOD-PRECIPITATION STEP- AVOID HAEMOGLOBIN INTERFERENCE

53. BREATH ALCOHOL
• POINT OF CARE
• PRINCIPLE-ALCOHOL IN CAPILLARY ALVEOLAR BLOOD RAPIDLY EQUILIBRATES WITH
ALVEOLAR AIR IN A RATIO 2100:1(BLOOD:BREATH)
• BREATH ALCOHOL G/210L=G/DL IN WHOLE BLOOD
• BLOOD:BREATH=2100:1
• WAITING PERIOD-15 MIN
• VERY RECENT DRINKING, ALCOHOL CONTAINING MOUTHWASH OR VOMITING ALCOHOL
RICH GASTRIC JUICE

54. BREATH ALCOHOL
• ACTIVE ALCOHOL ABSORPTION-30-120 MIN
• ARTERIAL BLOOD ALCOHOL>PERIPHERAL VENOUS BLOOD
• BREATH ALCOHOL>VENOUS BLOOD BECAUSE END EXPIRATORY AIR EQUILLIBRATES
WITH PULMONARY ARTERIAL BLOOD

55. US DEPARTMENT OF TRANSPORTATION
• BREATH ALCOHOL
• 0.02-0.04G/210L-NO DUTIES FOR 8HRS
• 0.04G/210L-SUSPENDED FROM DUTY UNTIL EVALUATION BY SUBSTANCE ABUSE
PROFESSIONALS

56. BREATH ALCOHOL MEASUREMENT
• INFRA RED ABSORPTION SPECTROMETRY(MOST COMMON)
• DICHROMATE SULFURIC ACID OXIDATION REDUCTION
• GC(FLAME IONIZATIONOR THERMAL CONDUCTIVITY DETECTION
• ELECTROCHEMICAL OXIDATION
• METAL OXIDE SEMICONDUCTOR SENSORS

57. SALIVA ALCOHOL
• EASY
• NONINVASIVE
• ETHANOL DISTRIBUTION BETWEEN BLOOD AND SALIVA BY PASSIVE DIFFUSION
• 9%HIGHER THAN WHOLE BLOOD
• SIMILAR TO SERUM ALCOHOL
• CONCENTRATION TIMES SAME IN BLOOD, BREATH AND SALIVA

58. QED SALIVA ALCOHOL TEST
• ETHANOL IN SALIVA
• ADH REACTION COUPLED WITH DIAPHORASE MEDIATED COLOUR INDICATOR REACTION
• RESULTS IN AGREEMENT WITH VENOUS BLOOD OR BLOOD
• ON SITE USE
• EMERGENCY DEPT, WORKPLACE, ROADSIDE
• APPROVED BY DOT FOR ALCOHOL SCREENING
• DESIGNED FOR SALIVA
• ACCURATE MEASUREMENT OF SERUM ETHANOL AS WELL

59. QED TEST
USING THE COTTON SWAB INCLUDED, ACTIVELY SWAB
AROUND THE CHEEKS, GUMS, AND TONGUE FOR 30-60
SECONDS OR UNTIL THE COTTON SWAB IS COMPLETELY
SATURATED WITH SALIVA
PLACE THE TEST DEVICE ON A FLAT SURFACE. GENTLY TWIST THE
SWAB WITH THE COLLECTED SALIVA SAMPLE INTO THE ENTRY PORT
AND APPLY STEADY PRESSURE TO ACTIVATE THE CAPILLARY ACTION
UNTIL THE PINK FLUID PASSES THE QA SPOT™ LOCATED AT THE
TOP OF THE TEST DEVICE.
READ THE TEST RESULTS. ALLOW THE TEST DEVICE TO DEVELOP FOR
TWO MINUTES. A DISTINCT PURPLE BAR WILL FORM WITHIN THE
MARKED SCALE REGION. THE HIGHEST POINT OF THE PURPLE BAR
REPRESENTS THE LEVEL OF ALCOHOL EXPRESSED AS EITHER A
PERCENTAGE (.0X%) OR MILLIGRAMS (ML/DL) CONCENTRATION.

60. • U.S. DEPARTMENT OF TRANSPORTATION (DOT)
• ALCOHOL TESTING FORM
• (THE INSTRUCTIONS FOR COMPLETING THIS FORM ARE ON THE BACK OF COPY 3)
• STEP 1: TO BE COMPLETED BY ALCOHOL TECHNICIAN
• A: EMPLOYEE NAME______________________________________________________________________________________
• (PRINT) (FIRST, M.I., LAST)
• B: SSN OR EMPLOYEE ID NO. _____________________________________________________________________________
• C: EMPLOYER NAME _____________________________________________________________________________
• STREET CITY, ST ZIP _____________________________________________________________________________
• DER NAME AND
• TELEPHONE NO. ___________________________________________________(_____)____________________
• DER NAME DER PHONE NUMBER
• D: REASON FOR TEST: . RANDOM . REASONABLE SUSP . POST-ACCIDENT .RETURN TO DUTY . FOLLOW-UP . PRE-EMPLOYMENT
• STEP 2: TO BE COMPLETED BY EMPLOYEE
• I CERTIFY THAT I AM ABOUT TO SUBMIT TO ALCOHOL TESTING REQUIRED BY US DEPARTMENT OF TRANSPORTATION REGULATIONS AND THAT THE
• IDENTIFYING INFORMATION PROVIDED ON THE FORM IS TRUE AND CORRECT.
• ___________________________________________________________________ _____________/____/_____
• SIGNATURE OF EMPLOYEE DATE MONTH DAY YEAR
• STEP 3: TO BE COMPLETED BY ALCOHOL TECHNICIAN
• (IF THE TECHNICIAN CONDUCTING THE SCREENING TEST IS NOT THE SAME TECHNICIAN WHO WILL BE CONDUCTING THE CONFIRMATION TEST,
• EACH TECHNICIAN MUST COMPLETE THEIR OWN FORM.) I CERTIFY THAT I HAVE CONDUCTED ALCOHOL TESTING ON THE ABOVE NAMED
• INDIVIDUAL IN ACCORDANCE WITH THE PROCEDURES ESTABLISHED IN THE US DEPARTMENT OF TRANSPORTATION REGULATION, 49 CFR PART

61. • TEST # TESTING DEVICE NAME DEVICE SERIAL # OR LOT # & EXP DATE ACTIVATION TIME READING TIME RESULT
• CONFIRMATION TEST: RESULTS MUST BE AFFIXED TO EACH COPY OF THIS FORM OR PRINTED DIRECTLY ONTO THE
FORM.
• REMARKS:
• __________________________________________________________________________________________
• ALCOHOL TECHNICIAN’S COMPANY COMPANY STREET ADDRESS
• _______________________________________________
_______________________________(_____)_________________
• (PRINT) ALCOHOL TECHNICIAN’S NAME (FIRST, M.I., LAST) COMPANY CITY, STATE, ZIP PHONE NUMBER
• _______________________________________________ __________/____/________
• SIGNATURE OF ALCOHOL TECHNICIAN DATE MONTH DAY YEAR
• STEP 4: TO BE COMPLETED BY EMPLOYEE IF TEST RESULT IS 0.02 OR HIGHER
• I CERTIFY THAT I HAVE SUBMITTED TO THE ALCOHOL TEST, THE RESULTS OF WHICH ARE ACCURATELY RECORDED ON
THIS FORM. I UNDERSTAND
• THAT I MUST NOT DRIVE, PERFORM SAFETY-SENSITIVE DUTIES, OR OPERATE HEAVY EQUIPMENT BECAUSE THE
RESULTS ARE 0.02 OR GREATER.
• ______________________________________________________________________
_____________/_____/____
• SIGNATURE OF EMPLOYEE DATE MONTH DAY YEAR
• OMB NO. 2105-0529

62. ONSITE ALCOHOL TEST CARD DEVICE
• SALIVA OR URINE
• SAME REACTION
• POSITIVE RESPONSE FOR ETHANOL CONCENTRATION GREATER THAN 0.02G/DL
• ALSO APPROVED BY DOT

63. THIRD DEVICE
• PLASTIC TEST STRIP
• DOT APPROVED
• ADH DIAPHORASE COUPLED INDICATOR COLOUR BAR
• IF 0.02G/DL OR GREATER

65. COLLECTION DIFFICULT
• FLOW OF SALIVA UNDER CONTROL OF PARASYMPATHETIC NERVOUS SYSTEM
• ANTICHOLINERGIC SYMPTOMS
• DRY MOUTH ASS WITH TCA OVERDOSE
• SALIVARY FLOW MAY BE IMPAIRED IN SOME ALCOHOLICS

66. URINE ALCOHOL
• ALTERNATIVE TO SALIVA
• LESS INVASIVE THAN BLOOD
• POST ABSORPTIVE PHASE-CONCENTRATION 1.3 TIMES BLOOD
• DISCOURAGED BY SOME AS THIS RATIO IS HIGHLY VARIABLE
• REPRESENTS AN AVERAGE OF BLOOD ALCOHOL
• EMPTYING THE BLADDER, COLLECTING URINE AFTER 20 TO 30 MIN
• PREVIOUS 8 HRS
• NOT APPROVED BY DOT

67. POSTMORTEM ALCOHOL
• POSTMORTEM BLOOD
• VITREOUS HUMOR
• MUSCLE

68. ALCOHOLIC LIVER DISEASE
RISK FACTORS
1.DURATION AND MAGNITUDE OF ETHANOL INGESTION
• THRESHOLD 40G/DAY IN MEN AND 10G/DAY IN WOMEN
• RISK DOSE-80G/DAY(200ML OF WHISKY OR EQUIVALENT)
• DAILY DRINKING RISKIER

69. 2. GENDER-WOMEN
• GREATER LIKELYHOOD OF PROGRESSION TO CIRRHOSIS
• WOMEN HAVE REDUCED ACTIVITIES OF ADH
3. HEPATITIS B OR C
• INCREASE THE SEVERITY IN PATIENTS WHO DRINK HEAVILY
4.GENETIC FACTORS
• INHERITED PREDISPOSITION TO ALCOHOLISM

70. 5. NUTRITIONAL STATUS
• PROTEIN CALORIE MALNUTRITION
• POOR INTAKE
• ABNORMAL NUTRIENT METABOLISM
• OBESITY MAY BE A RISK FACTOR

71. PATHOLOGY
• IMMUNOLOGICAL COMPONENT
• MODIFICATION OF LIVER PROTEINS BY ETHANOL METABOLITES

72. LIVER DAMAGE FROM EXCESSIVE ETHANOL CONSUMPTION OCCURS IN
THREE STAGES.
1. FATTY LIVER.
1. GOOD PROGNOSIS
2. STEATOSIS DISAPPEARS AFTER 3 MONTHS OF ABSTINANCE
2. ALCOHOLIC HEPATITIS
WORSE PROGNOSIS
3. CIRRHOSIS
• THE CIRRHOTIC LIVER IS UNABLE TO CONVERT AMMONIA INTO UREA,
• AMMONIA IS TOXIC TO THE NERVOUS SYSTEM AND CAN CAUSE COMA AND
DEATH.

73. ACUTE ALCOHOLIC HEPATITIS
• ACUTE FEBRILE ILLNESS
• LEUCOCYTOSIS
• ↑ACUTE PHASE PROTEINS
• AST>2 TIMES ALT
• CHOLESTATIC FORM WITH ↑ ALP>3 TIMES MAY BE SEEN-HIGHER MORTALITY
• ↑BILIRUBIN, ↓ALBUMIN AND PT-POOR PROGNOSIS

74. GENETIC COMPONENT
• BOTH ALCOHOLISM AND SUSCEPTIBILITY TO THE DEVELOPMENT OF CIRRHOSIS
• VARIATION IN ALCOHOL INTAKE-GENETIC
• GENETIC POLYMORPHISM OF THE (MEOS) MICROSOMAL ETHANOL OXIDISING SYSTEM AND ADH
• 50% ASIANS HAVE ABSENT ADH-FLUSH REACTION TO ALCOHOL THAT INHIBITS DRINKING
• HETEROZYGOTES OF ACETALDEHYDE DEHYDROGENASE(AADH)-IMPAIRED CLEARANCE OF
ACETALDEHYDE-PUTATIVE TOXIN-LIVER INJURY

75. FATTY LIVER
• ACCUMULATION OF FATTY ACIDS IN THE LIVER
• ENDOGENOUS SYNTHESIS
• NO IMPAIRMENT OF HEPATIC SYNTHESIS OF PROTEIN AFTER ETHANOL INGESTION

77. FATTY LIVER
• ↑ACETYL COA- ↑ FATTY ACID SYNTHESIS
• ACETALDEHYDE-PRIMARY TOXIN
• CAUSES GENERATION OF FREE RADICALS
• DEPLETION OF ANTI-OXIDANTS, LIKE GLUTATHIONE
• INJURY TO LIVER CELLS
• INDUCTION OF COLLAGEN SYNTHESIS- FIBROSIS AND CIRRHOSIS

78. 78
Alcohol and the Liver
Normal Liver Fatty Liver Cirrhotic Liver

79. BIOCHEMICAL MARKERS
AMINO TRANSFERASES
• AMINO TRANSFERASE ACTIVITIES RARELY EXCEED 300U/L-ACUTE ALCOHOLIC
HEPATITIS
• MUCH LOWER IN CHRONIC LIVER DISEASE
• ALCOHOL DEPLETES THE VIT B6 DEPENDENT PYRIDOXAL 5 PHOSPHATE-PRECURSOR
OF AMINO TRANSFERASE
• AST:ALT>2

80. BIOCHEMICAL MARKERS
• ↑APPEARANCE OF MITOCHONDRIAL AST(MAST)
• NOT SOLE CAUSE
• DAMAGE TO OTHER TISSUES WHICH RELEASE AST BUT NOT ALT, CONFINED TO LIVER
ALP ELEVATED 2 TO 4 FOLD
GGT
• GGT-SCREENING TEST
• GGT-INDUCIBLE ENZYME ELEVATED BY MANY DRUGS AND DISEASES

81. BIOCHEMICAL MARKERS
• CLINICAL SENSITIVITY FOR ALCOHOL CONSUMPTION SATISFACTORY
• NOT SPECIFIC FOR CHRONIC ALCOHOL ABUSE
ETHYL ESTERS OF FATTY ACIDS
COVALENT PROTEIN ADDUCTS-
• ETHANOL METABOLISM AND LIPID PEROXIDATION

82. BIOCHEMICAL MARKERS
• ALCOHOL INTERFERES WITH GLYCOCONJUGATION REACTIONS -ACETALDEHYDE
INHIBITION OF GLYCOTRANSFERASES
ISOFORMS OF TRANSFERRIN
• CHRONIC ABUSE-CARBOHYDRATE DEFICIENT(CDT) ISOFORMS(HYPOSIALYL AND
ASIALYLTRANSFERRIN)
• CDT AND GGT-INCREASES THE ACCURACY OF DETECTING PROLEM DRINKERS

83. ↑MEAN ERYTHROCYTE CORPUSCULAR VOLUME
• DYSFUNCTIONAL PRODUCTION OF RED CELLS
• MORE SPECIFIC THAN GGT
• PT PROLONGED
• DECREASED ALBUMIN
SERUM LEVELS OF PROCOLLAGEN TYPE III
• CORRELATE WITH COLLAGEN SYSTHESIS
• DISEASE SEVERITY

84. NON SPECIFIC LAB ABNORMALITIES
• HYPERURICEMIA
• HYPERLACTICACIDEMIA
• HYPERTRYGLYCERIDEMIA
• HYPOGLYCEMIA
• HYPERGLYCEMIA
• HYPOPHOSPHATEMIA
• HYPOMAGNESEMIA
• MACROCYTOSIS
Liver biopsy
•Disease severity
•Prognosis
•Rule out
treatable diseases
like chronic
hepatitis and
hemochromatosis

85. ACUTE ALCOHOLIC HEPATITIS
DISCRIMIANT FUNCTION
• [4.6X(PT-CONTROLPT)]+PLASMA BILIRUBIN(MG/DL)] VALUE >32
• HIGH MORTALITY RATE
MODEL FOR END STAGE LIVER DISEASE(MELD)SCORE>11
• SIMILAR SENSITIVITY
• BETTER SPECIFICITY

86. 86

87. 87