Clinical Biochemistry part I Blood glucose and Diabetes Mellitus, Lipid metabolism disorders, Water and electrolytes disorders and therapeutic drug monitoring TDM

1. Clinical Biochemistry
AASER ABDELAZIM
Professor Medical Biochemistry and Molecular Biology
FAIMER fellow 2021 (Medical education)
Clinical Chemistry consultant
amabdalazim@ub.edu.sa
8/15/23 1
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

2. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
2
1. Clinical biochemical tests comprise over1/3 of all hospital
laboratory investigations
2. Most biochemical tests are now performed at the site of clinic
especially during major operations like transplantation not only
in clinical biochemistry labs.
3. Most laboratories are now computerized and use:
q The par-coding for specimens
q Automated methods in analysis
This leads to:
A. High degrees of productivity .
B. Improves the quality of service.
C. Allow direct access to the results by clinicians.
A. INTRODUCTION

3. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
3
History
Clinical examination
Diagnostic services
Imaging Physiological tests
ECG, EEG, lung functions
Lab services
Hematology Histopathology Immunology Microbiology
Clinical biochemistry
Core tests Emergency tests
Specialized tests
B. Place of clinical biochemistry in medicine

4. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
4
Core tests commonly
requested by physician
e.g., U, LFTs and Es (Urea,
liver function tests
electrolytes)
Core tests
1. Not all labs introduce
the service but it
restricted only to some
reference centers
2. Needed to diagnose
rare diseases
Specialized tests
1. Done immediately
2. Results taken on call
3. Need to work out of
normal hours of lab.
4. All labs should perform
theses tests.
Emergency tests
Core biochemical tests
Sodium, potassium, chloride, bicarbonates
Urea, creatinine
Calcium, phosphates
Total proteins, albumins
Bilirubin, alkaline phosphatase
ALT, AST
T4, TSH
ɣ-GT, CK
Blood gases
Amylase
Specialized tests Emergency tests
Hormones Urea and electrolytes
Special proteins Blood glucose
Trace elements Blood gases
Vitamins Paracetamol
Drugs Salicylates
Lipids and lipoproteins Calcium
DNA analysis Amylase

5. Clinical biochemical laboratory
qBiochemical tests are used for diagnosis, monitoring, treatment,
screening and for prognosis.
q core biochemical tests are performed in every biochemistry
laboratory.
qSpecialized biochemical tests are preferred to be performed in larger
departments.
q laboratory personnel should be able to select the perfect type of tests
and interpret the results based on his knowledge.
8/15/23 5
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

6. 8/15/23 6
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

7. 8/15/23 7
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
1
By
Aaser M. Abdelazim, PhD
Assistant professor of Biochemistry and Molecular biology

8. A tour in carbohydrates metabolism
Digestion Absorption Metabolism
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
8

9. Digestion of
carbohydrates
60% of our food [starch,
glycogen, sucrose, lactose, and
cellulose]
Salivary α-amylase (pH 6-7)
Mouth
stomach
Pancreas
Pancreatic α-amylase (pH 7.1)
Maltose /isomaltose/starch dextrins
Maltose /isomaltose
Small intestine
Lactase/sucrase/maltase/α-dextrinase
Cocktail of sugars
[monosacchrides]
We have not β-glucosidase so cellulose passes as such
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
9

10. Absorption of
carbohydrates
GLUCOSE – GALACTOSE-FRUCTOSE Jejunum
Portal vein
GLUCOSE
Active transport system
SGLT-1
Na-K pump
Faster than passive
Need ATP
From lumen to intestinal
cells
Passive transport system
GLUTs
No need ATP
From lumen to intestinal
cells
GLUT-5
Form intestinal /renal /liver
cells /β-cells to
circulation
GLUT-2
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
10

11. GLUCOSE – GALACTOSE-FRUCTOSE
Portal vein
GLUCOSE
Fate of absorbed sugars
OXIDATION
STORAGE
CONVERSION
Glycogen
Glycolysis-
Krebs
MAJOR PATHWAY
Uronic acid
Detoxification
NADPH
Ribose
HMP-shunt
Lactose
Glucosamine
Galactose amine
Fructose
Glycogenesis
Lipids
Lipogenesis
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
11

12. Blood glucose
Fasting (70-110mg/dl)
One hour (120-150 mg/dl)
Two hours(70-140 mg/dl)
Dietary carbohydrates
Liver glycogen
Amino acids and non
carbohydrate-substance
Absorption
Gluconeogenesis
Glycogenolysis
BLOOD
GLUCOSE
HORMONAL REGULATION
HEPATIC REGULATION
RENAL REGULATION
INSULIN
Glucagon
Growth
Glucocorticoids
Catecholamines
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
12

13. BLOOD
GLUCOSE
HORMONAL REGULATION
Glucagon
Growth H
Glucocorticoids
Catecholamines INSULIN
Glucose uptake
Glucose oxidation
Glycogenesis
+
+
+ Lipogenesis
+ Glycogenolysis
Gluconeogenesis
-
-
Glycogenolysis
Gluconeogenesis
+
+
GLUCAGON
Catecholamine Gluconeogenesis
+ Gluconeogenesis
Glucose uptake
+
-
Glucocorticoids
Insulin action at cell mem
Glucose uptake
-
-
Growth H
THYROID H Glycolysis / Gluconeogenesis
+ ?!
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
13

14. Condition Insulin Level
Insulin Level (SI
Units*)
Fasting < 25 mIU/L < 174 pmol/L
30 minutes after glucose administration 30-230 mIU/L 208-1597 pmol/L
1 hour after glucose administration 18-276 mIU/L 125-1917 pmol/L
2 hour after glucose administration 16-166 mIU/L 111-1153 pmol/L
≥3 hours after glucose administration < 25 mIU/L < 174 pmol/L
*SI unit: conversional units x 6.945
NORMAL INSULIN LEVELS
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
14

15. BLOOD
GLUCOSE
HEPATIC REGULATION
AFTER MEAL
FASTING
Glycogenolysis
Gluconeogenesis
+
+
Ketogenesis
+
BRAIN
Add sugar to blood
BRAIN
MUSCLES
ADIPOSE
LIVER
PORTAL
Lipids
Glucose-6-P
Glycogen
Lipogenesis
Glycogenesis
40% of glucose
Circulation
Insulin secretion
+
60% of glucose
LIVER
Glucokinase
+
HYPERGLYCEMIA
Glucose uptake
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
15

16. BLOOD
GLUCOSE
RENAL REGULATION
LOW RENAL THRESHOLD
HIGH RENAL THRESHOLD
URINE
RENAL THRESHOLD
180 mg/dl
100 mg/dl
Diabetes innocence
20% of pregnant
220 mg/dl
Elderly people
Diabetes associated renal
damage
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
16

17. Diabetes mellitus:
Is a family disorder characterized by hyperglycemia
Etiology:
Type Etiology
Type I 1. ᵦ- cell destruction lead to absolute insulin deficiency
2. Immune mediated
3. Idiopathic
Type II May range from predominantly insulin resistance with relative
insulin deficiency to a predominantly Secretory defect with
insulin resistance.
Gestational diabetes (GDM) Similar to type II; it is diabetes that diagnosed in pregnancy as
pregnancy is associated with increase tissue cells resistance
to insulin; the hyperglycemia of GDM diminishes after delivery
and other cases develop type II diabetes.
Other specific types 1. Genetic defect of beta cells functions
2. Genetic defect in insulin action
3. Diseases of exocrine pancreas (cystic fibrosis)
4. Endocrinopathies (cushing’s syndrome)
5. Drug – or – chemical induced (protease inhibitors or
glucocorticoids)
6. Infections
7. Uncommon forms of immune- mediated diabetes
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
17

18. DIABETES MELLITUS
Biochemical disturbances in Diabetes Mellitus
Syndrome Disease
LIPIDS
PROTEINS
HYPERGLYCEMIA
CARBOHYDRATES
DYSLIPIDEMIA
DYSPROTEINEMIA
Relative /absolute deficiency of INSULIN
Chronic metabolic disorder
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
18

19. Biochemical disturbances in Diabetes Mellitus
CARBOHYDRATES
GLUCNEOGENESIS GLYCOGENOLYSIS
Glucose uptake
Intracellular glucose
POLYPHAGIA
HYPERGLYCEMIA
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
19

20. Biochemical disturbances in Diabetes Mellitus
HYPERGLYCEMIA
Glucose >renal threshold Plasma osmolality
Dehydration
Intra cellular water
POLYDEPSIA
Brain dehydration
Hyperglycemic
hyperosmolar
coma
Loss of water
POLYUREA
Loss of water soluble vitamins and minerals
GLUCOSURIA
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
20

21. 8/15/23 21
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Glucose homeostasis

22. 8/15/23 22
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Action of insulin

23. 8/15/23 23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Development of diabetic ketoacidosis:

24. Blood Glucose (Blood sugar)
Normal level = 70 – 110 mg/dl
I- Hyperglycemia
•Diabetes mellitus
•Gestational diabetes GDM(24th- 28th week)
•Acromegaly
•Acute stress (response to trauma, heart attack, stroke)
•Chronic renal failure
•Cushing syndrome (excess glucocorticoids)
•Hyperthyroidism
•Pancreatitis
•Pancreatic tumors
•Excess food intake
•Drugs (corticosteroids, tricyclic antidepressants, diuretics,
epinephrine, estrogen, Lithium, phenytoin, Salicylates.)
8/15/23 24
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

25. II- Hypoglycemia
Hypoglycemia in Diabetic patients
1. Patients taking blood
glucose lowering
medications
q Excess dose of insulin
q High dose of
sulfonylurea
q Extra dose of
Meglitinides.
1. Increase the activity or
the exercise
2. Excess drinking of
alcohols.
Hypoglycemia in non Diabetic
patients
Reactive hypoglycemia
(postprandial, after meal)
Fasting
(post absorptive)
8/15/23 25
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

26. 1) Some people that were sensitive
to normal release of
epinephrine.
2) Deficiency in Glucagon
secretion.
3) Gastric surgery (rapid passage
of food to intestine).
Diagnosed from blood samples
lower than 50 mg/dl
1. Alcohols: especially binge
drinking(depletion of pyruvate
and Oxaloacetate)
2. Critical illness: (hepatocellular
damage, renal insufficiency ,
sepsis, starvation )
3. Hormonal deficiency:(cortisol,
GH, Glucagon, epinepherine )
4. Tumors :(insulinoma: tumor of B –
cells )
5. Drugs:(salicylates in large dose,
Pentamedines (pneuomenia
treatment),Quinine(malaria ttt) )
8/15/23 26
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Appears after 3-4 hrs after meals

27. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
27
1- Babies from diabetic mothers.
2- In born error of metabolism.
A. Glycogen storage diseases.
B. Galactosemia
Etiology:
New born with
risk of
hypoglycemia
12%
New born
without risk of
hypoglycemia
88%

28. The clinical effect of hypoglycemia
Catecholamin
es and
glucagon
starts to face
the problem
Starts to enter
in coma
Brian damage Coma
8/15/23 28
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

29. 8/15/23 29
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
(1) Oral glucose in conscious patients:
If patient can swallow, give sweet drink,
sweets, or glucose tablets
(2) Oral glucose in comatose patients:
If patient unable to swallow, jam or any
available glucose gel smeared on inside
the cheeks
(3) i.m Glucagon:
May be given to comatose patients
(4) i.v Glucose:
Treatment of choice in comatose patients

30. 1. Blood sugar
2. Urine sugar
3. Glycated HB
4. Glycated proteins
1- Venous blood
2- Capillary blood
RBCs level is less than plasma level due
to less water contents of RBCs G soluble
in water
1) Separated rapidly
2) Rapid transported to lab.
3) Cooling of samples
4) Add sod. Fluoride to inhibit glycolysis
1) Fasting
2) Random
3) Timed interval (glucose tolerance)
8/15/23 30
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Precautions
Samples
Types of Samples Monitoring

31. ORAL GLUCOSE TOLERANCE TEST
8/15/23 31
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
1) Mild or no DM symptoms
2) Glucose absorbance and utilization
3) Renal threshold (note next slide)
4) Persistent glycosuria
5) Pregnant woman with family history of diabetes
Indications
1) Let patient to be fasted for not more than 12 hours
2) Measure fasting blood glucose level (0) time and
register the results.
3) Give the patient 75 gm of sugar in about 400-500 ml
water orally.
4) Every hour take blood and urine samples for
determination of glucose
draw the oral glucose tolerance curve

32. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
32
Remarks on The curve:
1. Ascending limb: explains the glucose absorbance
2. Descending limb: explains glucose utilization and insulin response
3. Usually glucose does not appears in urine until it be over the threshold level
4. Diabetes diagnosed from FBG= >126 and at least one sample > 200 after the 1st 30 minutes
50
200
180
100
1 3
2
0
150
Blood
glucose
mg
/dl
Hours
Max level=120-150 mg /dl
Fasting level =
70-110 mg/dl
Renal threshold of glucose = 180 mg/dl
Hypoglycemic response/insulin overshoot
Usually max value (after one hour) = 1.5 time fasting value
Ascending limb
Descending limb
Return to fasting level
ORAL GLUCOSE TOLERANCE curve

33. Renal threshold of glucose
It is the blood glucose level above which glucose appear in urine
Average =180 mg/dl
1 mmol/L = 18 mg/dl
1. Persons of diabetes innocence
2. In 20% of pregnant females
1. Elderly people due to reduced GFR
2. Diabetes associated with renal damage
8/15/23 33
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Renal threshold of glucose
Low renal threshold High renal threshold
100 mg/dl 220 mg/dl

34. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
34
Types of oral glucose tolerance curves:
50
200
180
100
1 3
2
0
150
Blood
glucose
mg
/dl
Hours
300
400
500
(1) Severe diabetic curve:
Urine:
Time 0 1 2
Glucose + ++ +++
Ketones Trace Trace Trace
Renal threshold

35. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
35
50
200
180
100
1 3
2
0
150
Blood
glucose
mg
/dl
Hours
(2) Mild diabetic curve:
Urine:
Time 0 1 2
Glucose 0 0 0
Ketones 0 0 0
Renal threshold

36. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
36
50
200
180
100
1 3
2
0
150
Blood
glucose
mg
/dl
Hours
50
200
180
100
1 3
2
0
150
Blood
glucose
mg
/dl
Hours
(3) Hypoglycemic curve: (4)Flat curve: blood glucose fails to rise
normally after glucose load
Occurs in; malapsorption, myxodema,
hypopitutrism
Urine:
Time 0 1 2
Glucose 0 0 0
Ketones 0 0 0
Urine:
Time 0 1 2
Glucose 0 0 0
Ketones 0 0 0

37. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
37
50
200
180
100
1 3
2
0
150
Blood
glucose
mg
/dl
Hours
50
200
180
100
1 3
2
0
150
Blood
glucose
mg
/dl
Hours
(5) Renal glucosuria curve: it
resemble normal curve while we can find glucose
in urine.
Urine:
Time 0 1 2
Glucose 0 + ++
Ketones 0 0 0
Renal threshold
Renal threshold
(6)Lag storage curve: FBG level is normal,
after 30 minutes of glucose load the level be up renal
threshold , then the level falls sharply in less than 2
hours
Occurs in; after gasterectomy; due to rapid passage of
glucose to intestine, severe liver diseases when no
glucose is used in glycogenesis and all Glc goes directly
to blood, rare in thyrotoxicosis due to rapid absorption
of glucose.
Urine:
Time 0 1 2
Glucose 0 + 0
Ketones 0 0 0

38. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
38
Remarks on OGTT in children
Point Comments
Indications of the test
in children
üDiabetic child with equivocal fasting or random level.
üHypoglycemic child
üTo exclude excess Growth H.
üCystic fibrosis
üFor the following conditions [polycystic ovary, strong family history, obesity and fatty liver
disease]
Precautions qOnly when blood glucose level 5.6 to < 7.o mmol/L.
qDon’t performed in patients with thyroid dysfunctions, under physical stress e.g post
surgery, hypokalemic periodic paralysis.
Side effect Many child feel nauseated or vasovagal symptoms.
Preparation of patient qEnsure that the child has had an adequate carbohydrate diet for at least 5 days before
the test (150g/day).
qAvoid prolonged fasting of child (only for 4 hour night fast) allow him to drink water with
no sweet drinks.
qPhysical exercise is not allowed before or during the test.
qYou should perform the test at morning.
Protocol 1. Measure the fasting level.
2. Prepare glucose load as following
§ Liquid contains 0.66 g /mL of anhydrous glucose (the dose is 2.64 ml/Kg body weight
with maximum dose 113 ml.) you can add water up to 200 ml volume.
§ Anhydrous glucose (dose 1.75 g/kg body weight) maxium dose 75 g
§ Rapilose contains 75 g of glucose in 300 mL for child of weight less than 43 Kg .
3. Child should take the glucose load with in 5 minutes.
4. Take the second blood sample after 2 hours.

39. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
39

40. Biochemical disturbances in Diabetes Mellitus
PROTEINS
Depletion of glucose as source of energy
Breakdown of tissue proteins
Infection
Muscle wasting
Poor healing
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
40

41. Biochemical disturbances in Diabetes Mellitus
LIPIDS
Depletion of glucose as source of energy
Lipolysis
Hyperlipidemia
Loss of weight
Fatty acid oxidation
Acetyl CoA
Ketogenesis /ketosis
Ketotic coma
Hyperkalemia
8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
41

42. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
42
Diabetes mellitus:
Is a family disorder characterized by hyperglycemia
Etiology:
Type Etiology
Type I 1. ᵦ- cell destruction lead to absolute insulin deficiency
2. Immune mediated
3. Idiopathic
Type II May range from predominantly insulin resistance with relative
insulin deficiency to a predominantly Secretory defect with
insulin resistance.
Gestational diabetes (GDM) Similar to type II; it is diabetes that diagnosed in pregnancy as
pregnancy is associated with increase tissue cells resistance
to insulin; the hyperglycemia of GDM diminishes after delivery
and other cases develop type II diabetes.
Other specific types 1. Genetic defect of beta cells functions
2. Genetic defect in insulin action
3. Diseases of exocrine pancreas (cystic fibrosis)
4. Endocrinopathies (cushing’s syndrome)
5. Drug – or – chemical induced (protease inhibitors or
glucocorticoids)
6. Infections
7. Uncommon forms of immune- mediated diabetes

43. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
43
Insulin dependant diabetes mellitus (IDDM) versus non-insulin dependant diabetes
mellitus NIDDM
Main features IDDM NIDDM
Epidemiology:
1. Frequency in northern
Europe
2. Predominance
0.02-0.4 %
N. European Caucasian
1-3 %
World wide; lowest in rural
areas of developing countries
Clinical characteristics:
1. Age
2. Weight
3. Onset
4. Ketosis
5. Endogenous insulin
6. HLA associations
7. islets cells antibodies
< 30yrs
Low
Rapid
Common
Low / absent
Yes
Yes
>40yrs
Normal / increase
Slow
Under stress
normal / high
No
No
Pathophysiology:
1. Etiology
2. Genetic association
3. Environmental factors
Autoimmune destruction of ᵦ-
cells
Polygenic
Viruses and toxins are
implicated.
Unclear/ impaired insulin
secretion and insulin
resistance.
Strong
Obesity and physical inactivity

44. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
44
Criteria for diagnosis of diabetes mellitus:
Reference range for blood glucose level(mg/dl)
Normal Impaired
OGTT
Indication of
diabetes
Fasting blood glucose (mg/dl) 70-110 100-125 >126
Two- hours postprandial blood glucose (mg/dl) < 140 140-200 > 200
Criteria for diagnosis and monitoring of DM Notes
(1) Symptoms of diabetes + random plasma glucose
>200 (mg/dl or 11.1 mmol/l)
Random: means any time of day.
Symptoms: include polyuria,
polydipsia, polyphagia, unexplained
weight loss.
(2) Fasting plasma glucose (FPG) > 126 mg/dl (7
mmol/l)
Fasting: means no caloric intake for
at least 8 hours. Not more 12 hours.
(3) two-hours post load glucose >200 mg/dl (> 11.1
mmol/l)
During OGGT using 75 g anhydrous
glucose dissolved in water.
(4) Glycated hemoglobin (HBA1c) > 12% of normal
Hb and fructosamine and microalbuminuria (30-200
mg/l) index of early affection of kidney in diabetes
(diabetic nephropathy)
HBA1c: index over 2-3 months;
fructosamine index over 2-3 weeks;
microalbuminuria normally (20-30
mg/l urine)

45. WHO Criteria for diagnosis of diabetes mellitus and impaired
glucose tolerance (IGT) :
RANDOM GLUCOSE SAMPLE (MMOL/L)
Diabetes unlikely Diabetes uncertain Diabetes likely
Venous plasma < 5.5 5.5 -less 11 11
Venous blood < 4.4 4.4 -less 10 10
Capillary plasma < 5.5 5.5 - less 12.2 12.2
Capillary blood < 4.4 4.4 – less 11.1 11.1
likely= confirmed
Uncertain = unconfirmed
unlikely-= discarded
1 mmol/L = 18 mg/dl
STANDARDIZED OGGT (MMOL/L)
Diabetes IGT
Venous plasma Fasting >7.8 < 7.8
2 hrs >11.1 7.8 - < 11.1
Venous blood Fasting >6.7 < 6.7
2 hrs >10.0 6.7 - < 10.0
Capillary plasma Fasting >7.8 < 7.8
2 hrs >12.2 7.8 - < 12.2
Capillary blood Fasting > 6.7 < 6.7
2 hrs > 11.1 6.7 - < 11.1
8/15/23 45
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

46. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
46

47. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
47

48. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
48

49. 8/15/23 49
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Case study 1

50. 8/15/23 50
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Answer of Case study 1

51. 8/15/23 51
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Case study 2

52. Answer of Case study 2
Requests Explanation
(1) The most likely diagnosis Diabetic ketoacidosis – infection can accelerate the
appearance of such condition.
(2) Bedside tests help in
confirmed diagnosis
1. Blood glucose level will help in the treatment.
2. Urine samples for ketone bodies.
(3) Laboratory tests requested 1. Urea and electrolytes can help us to check renal
conditions.
2. Serum sodium and potassium levels for checking
of hyperkalemia.
3. Acid base balance tests for detection the
severity of acidosis.
4. Sputum sample for microbiology to confirm
presence of infection.
8/15/23 52
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

53. 8/15/23 53
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Case study 3

54. 8/15/23 54
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Answer of Case study 3

55. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
55
2
Aaser Abdelazim, PhD
Assistant professor of Medical Biochemistry and Molecular Biology
amabdalazim@ub.edu.sa

56. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
56
1. Sequelae of lipid determination
2. Major points during sampling for
lipid profile.
3. Plasma appearance

57. A. Sequelae of lipids determinations
1. Coronary heart diseases(CHD)
2. Acute pancreatitis
3. Failure to grow and weakness
4. Cataract
8/15/23 57
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Diagnose
Major points for sampling for blood lipid profile:-
1) Patient should be fasted at least12 hours before sampling
2) Test should not performed during acute illness
3) Test should not performed on hospitalized patients until 2-3 months of illness
4) Blood lipids affected by body posture, drugs, smoking and alcohol
5) Samples should not heparinized
6) Plasma or serum Samples should be separated as soon as possible
7) Body weight should be remain constant at least for 2-3 weeks
8) Abnormal results should be confirmed before change the type of therapy

58. (1) Plasma appearance
8/15/23 58
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Clear Turbid Cloudy to opaque Creamy layer
appeared on the
surface of the plasma
within 4 hours
TG <200 mg/dl
TG~300 mg/dl
TG >600 mg/dl CM present

59. Lipid profile
8/15/23 59
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

60. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
60
(1) Serum Total Cholesterol (N= 130-220 mg/dl)
1. Used to monitoring the CHD
2. Monitoring other lipoprotein disorders
1. Idiopathic hypercholesterolemia
2. Hyperlipoproteinemia
3. Chronic renal failure
4. Smoking
5. Hypothyroidism
6. Obstructive liver diseases
7. Pregnancy
8. Pancreatic diseases include DM
1. Hyperthyroidism
2. Malnutrition
3. Severe liver cell damage
4. Chronic anemia
LOW CHOLESTEROL

61. (2) Serum HDL-Cholesterol (N=30-75 mg/dl )
(levels >60 mg/dl good indication
–ve CHD)
1.Vigorous exercise
2.Some familial lipoproteins
disorders
3.Mild alcohol intake
4.Estrogen treatment
5.Insulin treatment
6.Increase clearance of TG
1. Nephrosis
2. Chronic liver diseases
3. Stress
4. Obesity
5. Smoking
6. Lack of exercise
7. Hyperthyroidism
8. DM
9. Familial LCAT deficiency
8/15/23 61
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
High HDL-CH low HDL-CH

62. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
62
Risk factor for CHD =
Every 1 mg/dl decrease in HDL increases the risk of CHD by
2-3%
Risk factor
Low :3.3-4.4 Average: 4.4-7.1 Moderate: 7.1-11 High:>11
Interpretation for Risk factor
Total cholesterol
HDL-cholesterol
NOTE: Now there are many applications on
mobile stores can calculate this risk factor

63. 1. Idiopathic hypercholesterolemia
2. Hyperlipoproteinemia
3. Chronic renal failure
4. Smoking
5. Hypothyroidism
6. Obstructive liver diseases
7. Pregnancy
8. Pancreatic diseases include DM
9. Diet reach in cholesterol, saturated FA
10. antihypertensive B blocker drugs
1. Oral estrogen
2. Sever illness
3. A betalipoproteinemia
8/15/23 63
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
High
(3) Serum LDL-Cholesterol (N=65-175mg/dl)
low

64. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
64
Determination of LDL-cholesterol level
1. Total Cholesterol= HDL+VLDL+LDL (in lab we can measure TC,HDL,TG but
neither LDL nor VLDL )
2. Major amount of TG present in VLDL= 5 times the amount of CL so we can
calculate the amount of CL in VLDL by TG/5
Friedwald formula: LDL=(HDL+TG/5)-Total CL

65. (4) Serum Triglycerides (N=40-160 mg/dl)
1. Idiopathic hypercholesterolemia
2. Hyperlipoproteinemia
3. Chronic renal failure
4. Smoking
5. Hypothyroidism
6. Obstructive liver diseases
7. Pregnancy
8. Pancreatic diseases include DM
1. TG should be measured after 12 hours
2. fasting serum levels are 5% higher than
plasma
3. While HDL is the same at fasting and
after meal
4. TGs are not strong predictors for
atherosclerosis and CHD
Precautions
8/15/23 65
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
mg/dl=88.4 mmol/L
High triglycerides

66. Lipid Desirable Borderline High risk
Total Cholesterol <200 200-239 240
HDL- Cholesterol 60 35-45 <35
LDL- Cholesterol 60-130 130-159 160-189
Triglycerides <150 150-199 200-499
Lipid profile interpretation
All data in the table measured by mg/dl
8/15/23 66
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

67. 8/15/23 67
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
LIPOPROTEINS METABOLISM DISORDERS
[A]: Introduction to lipoprotein structure

68. Apolipoprotein Molecular weight Site of synthesis Functions
A-I 28,000 Intestines, liver Activates LCAT
A-II 17,000 Intestines, liver
B100 549,000 Liver 1. Triglycerides
and cholesterol
transport.
2. Binds to LDL
receptors.
B48 264,000 Intestines Triglycerides
transport.
C-I 6600 Liver Activates LCAT
C-II 8850 Liver Activates LPL
C-III 8800 Liver Inhibits LPL
E 34,000 Intestines, liver and
macrophage
Binds to LDL
receptors and
other liver
receptors.
[b]: Properties of human apolipoproteins
8/15/23 68
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

69. Lipoprotein Apolipoproteins Properties Functions
Chylomicrons B48, A-I, C-II and E
qLargest lipoprotein.
qSynthesized in gut
after meal.
qNot present in
normal fasting
plasma.
It is the main carrier of
dietary triglycerides.
VLDL B100, C-II and E Synthesized in liver
Main carrier of
endogenous triglycerides.
LDL B100
Generated from
VLDL in circulation.
The main carrier of
cholesterol.
HDL A-I and A-II The smallest type
It has a protective
function.
It takes cholesterol from
extra hepatic tissues to
liver for excretion.
[c]: Properties of human apolipoproteins
8/15/23 69
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

70. [d]: Composition of blood lipoproteins
Components Chylomicro
ns
VLDL IDL LDL HDL
Triglycerides 85% 55% 26% 10% 8%
Proteins 2% 9% 11% 20% 45%
Apolipoproteins B, C, E B, C, E B,E B A, C, E
Cholesterol 1% 7% 8% 10% 5%
Cholesterol
ester
2% 10% 30% 35% 15%
Phospholipids 8% 20% 23% 20% 25%
8/15/23 70
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
NOTE: The highest cholesterol concentration is present in LDL, highest triglycerides is
present in chylomicrons, highest protein concentration is present in HDL, highest
phospholipids concentration is present in HDL.

71. 8/15/23 71
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
[e]: lipoproteins metabolism

72. 8/15/23 72
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
[f]: LDL and its receptors

73. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
73
[g]: clinical disorders of lipid metabolism (dyslipidemias)
Genetic causes Secondary causes
Disorder Genetic defect Fredrickson Risk
(1) Lipoprotein lipase
deficiency
Reduced the activity of LPL I Pancreatitis
(2) Apo C-II deficiency
Inability to synthesis Apo C-II the
cofactor for LPL
I Pancreatitis
(3) Familial
hypercholesterolemia
Reduced the number of
functional LDL receptors
IIa or IIb CHD
(4) Familial
hypertriglyceridemia
Single gene defect IV or V
(5) Familial combined
hyperlipidemia
Single gene defect
IIa, IIb, IV or V CHD
(6) A
betalipoproteinemia
Inability to synthesize ApoB Normal
Deficiency of fat
soluble vitamins
and neurological
defects
(7) An
alphalipoproteinemia
(Tangier disease)
Inability to synthesize ApoA Normal
Storage of
cholesteryl ester in
abnormal places
and neurological
defects
A. Genetic causes of dyslipidemias

74. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
74
A. Secondary causes of dyslipidemias
Disorder Dominant lipid that affected
(1) Diabetes mellitus
Triglyceride
(2) Excess alcohol intake
(3) Chronic renal failure
(4) Drugs as (thiazide diuretics, nonselective
B-blockers )
(5) Hypothyroidism
Cholesterol
(6) A betalipoproteinemia
(7) Nephrotic syndrome

75. 8/15/23 75
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
[h]: Frederickson (WHO) classification of dyslipidemias
NOTE: Fredrickson classification of dyslipidemias based on the appearance of fasting plasma
samples after standing for 12 hrs at 4 ºC then determination of its cholesterol and triglycerides
content.

76. 8/15/23 76
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Conversion factors
1. Cholesterol = x38.66
2. Glucose_____ x18.016
3. Triglycerides _____ x 87.5
4. BUN_____x2.808
5. Urea___-x6.006
6. Uric acid _____x 59.48
Case study 1

77. 8/15/23 77
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Answer of Case study 1

78. 8/15/23 78
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology

79. 8/15/23 79
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Case study 2

80. 8/15/23 80
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
Answer of Case study 2

81. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
81
3

82. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology 82
Body fluid compartments:
1. An average person weighting
70 kg; contains 42 liters of
water.
2. ECF can be classified into
plasma fluid and interstitial
fluids.
3. Inlet; oral or I/V injection fluids.
4. Outlet; through urine or
respiration or evaporation from
skin.
Inlet
Extracellular fluids
Intracellular fluids
Outlet
Normal

83. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
83
Fluid loss consequences
Intracellular loss Extracellular loss
Cellular dysfunctions, coma 1) Circulatory collapse
2) Renal failure
3) Shock
Normal Normal
Over hydration
Dehydration

84. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
84
Points Dehydration Over hydration
Pulse Increase Normal
BP Decrease Normal / increase
Skin trugor Decrease Increase
Eyeball Soft/sunken Normal
Mucous membrane Dry Normal
Urine output Decrease Normal/decrease
Consciousness Decrease Decrease
Clinical disorders of severe hydration disorders:

85. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
85
Electrolytes:
Na+
qNa is the main extracellular cation.
qHighest solute concentration in plasma so it
mainly used to determine plasma osmolality
qConcentration of Na may be changed due to
the change in Na conc. Itself or due to the
change in water conc.
K+
Proteins/ phosphates Cl-/ HCO3-
Osmolality:
Movement of water between body
compartments keeps osmolality the same
Osmol.
qOsmolality of a solution = mmol of solutes/kg solvents (water).
qNormal osmolality of serum and other body fluids except urine
= 285 mmol/kg.
qSerum osmolality (mmol/kg)= 2x serum conc. (mmol/l); this
formula use only if the serum urea and glucose are within the
reference range or the highest values should be added to correct
the calculated osmolality.
qOsmaolal gap: is the difference between calculated and
measured osmolality.
Osmol.

86. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
86
Water and sodium balance:
Unregulated
Other ways of water loss
are:
qFistulae
qDiarrhea
qVomiting
Regulated by AVP
Water intake
(0.5-5 liters/day)
Depends on the daily
habits
Body distribution
(42 liters)

87. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
87
0.5 ml/min
(decrease water
excretion)
AVP (ADH)
(Arginine vasopressin)
Posterior pituitary
Hypothalamus
15 ml/min
(increase water
excretion)
H2O
Solute conc. Low
(Low osmolality )
Solute conc. High
(High osmolality )
Regulation of water balance by AVP:

88. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
88
Sodium balance:
Sodium intake
100-300 mmol/day
In health total body level do not changed if
the intake between 5-750 mmol/dy
Body distribution
(3700 mmol)
for 70 kg man
Na losses in diarrhea
are usually fatal in
infants

89. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
89
Adrenal cortex
Renin
Angiotensinogen
Angiotensin II
Angiotensin I
Aldosterone
Angiotensin II
Angiotensin I
Angiotensinogen
Renin
Aldosterone
Aldosterone reduces sodium loss at the expense of K&H in
response to low blood pressure
Sodium regulation by Aldosterone:
Atrial natriuretic peptide increase Na loss by
increase urinary sodium loss.
Na retention in response of falling of BP Na loss in response to increase BP

90. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
90
Regulation of volume:
H2O
Na/Cl
Are mainly present in ECF
They held water outside the cell
qSo the amount of Na determine
the volume of the compartment
(ECF).
qAldosterone and AVP mainly
interacts to keep ECF.
H2O
Patients with loss of fluids due to
vomiting or diarrhea in GIT infections
without intake of Na or water
become fluid depleted.
So Aldosterone secretion is increase to retain any salts
during fluid therapy in the same time AVP ensures
water retain too. This rises ECF osmolality.
ECF loss

91. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
91
HYPERNATREMIA
Definition: increase serum sodium above 135-145 mmol/l
Before analyzing a patient sample for serum sodium many
considerations should be taken:
1.Is this patient lost fluids?
2.Is the volume of ECF reduced?
3.If there is a fluids loss is this loss water or water with sodium?
4.Is the patient has given the appreciate fluid therapy or ingested
sodium slats?
When these questions have been answered the type of hypernatremia
can be addressed and the treatment become easy.

92. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
92
Assessing the cause of hypernatremia:
A patient become hypernatremic because of:
1.Water depletion
2.Water and sodium depletion
3.Excess sodium intake or retention in ECF
4.Very rare in cases of renal failure when kidneys unable to secretes Na.
[Na+]
[Na+]
(a) ECF and ICF are reduced (b) ECF slightly expanded and ICF is
normal

93. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
93
HYPERNATREMIA
Na content normal&
H2O decreased
Na content decreased&
H2O very decreased
Na content increased&
H2O normal
Decrease H2O intake
Renal water loss
(diabetes insipidus)
Excessive sweating or
diarrhea in children
Osmotic diuresis
(diabetes mellitus)
Conn’s syndrome
Cushing’s syndrome
Na+
administration
Urine maximally
concentrated
& reduce urine volume
Urine not be concentrated
Normal or increased volume

94. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
94
HYPONATREMIA
DEFINITION: Is a significant fall in serum sodium concentration below the range 135-145
mmol/l.
CAUSES:
1. Water retention: more water in the ECF lead to dilute Na.
2. Loss of Sodium: for ECF e.g. (vomiting, fistulae).
[Na]

95. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
95
HYPONATRAEMIA WITH WATER RETINTION
Oedematous Non-oedematous
Water excretion
water intake
e.g. Nephrotic syndrome
e.g. Inappropriate I/V saline
Water excretion
water intake
e.g. Renal failure, So-called
syndrome of inappropriate
antiduresis (SIAD)
e.g. Compulsive water drinking

96. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
96
4

97. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
97
qDrug effect is assessed by observing
patients clinical state.
qTherapeutic drug monitoring (TDM) is :
measurement of drug concentration in
plasma, or saliva as a mean for calculation
of drug dosage adequacy.
qThe curve will give information about:
1) Half life of the drug.
2)Volume of drug distribution which estimate
the correct dose once or several times
doses.
THERAPEUTIC DRUG MONITORING
(TDM):
Figure (1): Concentration of drug in plasma

98. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
98
Sampling for TDM
Before taking the samples for TDM important things should be taken in mind like:
1)Ask the patient about the compliance (is the prescribed drug accurate for the compliance
?).
2)Check for drug interaction.
3)Note the doses and time of last dose.
4)Take the sample at appropriate time (the best time to take the sample is just before the dose
this known as trough concentration).
INTERPERTATION OF DRUG LEVELS
qHigher or lower levels than the expected depend on the
compliance and changes occurring with other drug or in
kidneys and liver.
qCumulative reports are very useful for the comparison
between levels.
qEach drug has a population reference range with minimal
toxicity and maximal therapeutic effect and the therapeutic
dose for a patient may be toxic to the other.

99. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
99
Drugs for which TDM is appropriate
Although many drugs are prescribed in the specialists units only small groups of them need to be
measured and need TDM most of them have a low therapeutic index means that toxic dose not
far from therapeutic dose (table 1 show them)
Drug
Reason for TDM
Notes
Toxicity Interactions Compliance
Phenytoin √ √ √ Has saturable kinetics
Digoxin
√ √ √
Highly depend on renal functions
Theophylline
√ √ √ Has low therapeutic index (common
toxicity)
Methotrexate
√ If slowly excreted patients need
folate
Cyclosporin
√ Nephrotoxic (need to measure
Creatinine )
Carbamazapine √ √ √
Risk of a plastic anemia and fetal
anomalies like
Primidone √
Metabolized to phenobarbitone and
both should be measured
Phenobarbitone √
Can cause depression of CNS and
PNS
Gentamycin and
other √
Both peak and trough concentration
should be measured

100. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
100
Drug Medical use
Phenytoin Is an anti-seizure medication. It is useful for the prevention of tonic-clonic seizures, partial
seizures, but not absence seizures.
Digoxin Digoxin is occasionally used in the treatment of various heart conditions, namely atrial
fibrillation, atrial flutter and sometimes heart failure that cannot be controlled by other
medication.
Theophylline known as 1,3-dimethylxanthine, is a methylxanthine drug used in therapy for respiratory
diseases such as chronic obstructive pulmonary disease (COPD) and asthma under a
variety of brand names.
Methotrexate It is used in treatment of cancer, autoimmune diseases, ectopic pregnancy, and for the
induction of medical abortions. It acts by inhibiting the metabolism of folic acid via
dihydrofolate reductase.
Cyclosporin Is an immunosuppressant drug widely used in organ transplantation to prevent rejection. It
reduces the activity of the immune system by interfering with the activity and growth of T
cells.
Carbamazapine used in the treatment of epilepsy and neuropathic pain. It may be used in schizophrenia
along with other medications and as a second line agent in bipolar disorder.
Primidone Is an anticonvulsant of the barbiturate class.
Phenobarbitone is a medication recommended by the World Health Organization for the treatment of
certain types of epilepsy.
Gentamycin and
other
aminoglycosides
It is an antibiotic used to treat several types of bacterial infections, This include bone
infections, endocarditis, pelvic inflammatory disease, meningitis, pneumonia, urinary tract
infections, and sepsis.

101. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
101
Common causes of sub-therapeutic or toxic levels
Sub-therapeutic levels Toxic levels
1. Non compliance
2. Dose too low
3. Malabsorption
4. Rapid metabolism
1. Overdose
2. Dose too high
3. Dose too frequent
4. Impaired renal function
5. Reduced hepatic metabolism

102. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
102
DRUG INTERACTIONS
qInterference of one drug with the metabolism and excretion of the other; on the other hand
addition of one drug will alter the plasma concentration of the another.
qIn these circumstances it is useful to lower the dose or discontinue the drug for a time.
EXAMPLE:
Patients with chronic asthma controlled on THEOPHYLLINE usually develop a sever chest
infection, the patients in this case were prescribed ERYTHROMYCIN which will interfere with
theophylline inducing tachycardia and dizziness. So we enforced to stop theophylline for two
days and once the infection was clear; the original dose of theophylline will restart.
Absorption Distribution
Metabolism Excretion
Affected
drug
Interacting drug (s)
Increase
decrease
Interacting drug (s)
Increase plasma level of affected
drug
decrease plasma level of affected
drug

103. 8/15/23
Aaser Abdelazim ---- Professor of Medical Biochemistry and
Molecular Biology
103
Answer of Case study 1
Case study 1