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Biochemistry Flashcards

1
Q

Properties of vectors (2C)

A

Capable of replication inside the host cell
Contains at least 1 restriction site for 1 restriction endonuclease.

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2
Q

Types of vectors

A

Plasmids: Double stranded circular/small. Clone small DNA fragments up to 10 kb.

Phage: Virus, clones large DNA fragments 20 kb

Cosmid: responsible for packing DNA, up to 50 kb

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3
Q

Process of cloning consists of

A

Plasmids from bacteria/ foreign DNA are cut by restriction endonuclease

The cohesive ends of foreign DNA recombine with plasmid and joined by ligase to form recombinant DNA

Recombinant DNA is introduced into bacterial host cell. Uptake of DNA is called transformation

The transformed bacterial cell grow and divide and so does the recombinant plasma DNA

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4
Q

Requirements for PCR: TD TD B

A
  1. Two DNA primers.
  2. Deoxyribonucleoside triphosphate (dATP)
  3. Thermostable DNA polymerase (taq polymerase).
  4. DNA to be amplified.
  5. Buffer solution.
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5
Q

Polymerase chain reaction (PCR)

A

In vitro method for DNA amplification

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6
Q

PCR steps

A

a. Denaturation: Heating to 95° C.
b. Primer annealing: Cooling to 50° C.
c. Elongation: Heating 72 C allowing taq to elongate the primers. After 10 cycles DNA amplified 1000 times, after 30 cycles DNA amplified 10^9

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7
Q

Apparatus in PCR heating cooling heating is called

A

automated thermocycler

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8
Q

Advantages of PCR

A

Sensitive
Faster
Technically less difficult

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9
Q

Applications of PCR: 2S 2P FG

A
  1. Synthesis of DNA for sequencing and cloning.
  2. Synthesis of proteins: insulin - GH -Vaccines - monoclonal Ab.
  3. Diagnosis of genetic diseases as sickle cell anemia.
  4. Detection of bacterial and viral infection i.e., HIV and hepatitis B.
  5. Forensic medicine: amplification of DNA from hair or sperm.
  6. Gene therapy.
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10
Q

Hemoglobinopathies from Production of abnormal hemoglobin:

A

* Sickle cell anemia (HbS disease).
* HbC disease.
* HbM disease (Methemoglobinemia).

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11
Q

Hemoglobinopathies from Decreased Production of normal hemoglobin:

A

* alpha Thalassemia: Defect in production of the alpha chain.
* Beta Thalassemia: Defect in production of the beta chain.

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12
Q

Sickle cell anemia (HbS disease)

A

a type of Point mutation;

There are 2 genes for the B chain so, Patient may be:

* Homozygous for sickle cell anemia: Contains Hb S only.

* Heterozygous for sickle cell anemia (sickle cell trait): Contains Hb A and Hb S.

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13
Q

Thalassemia

A

Hereditary hemolytic diseases due to gene mutation or deletions.

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14
Q

alpha Thalassemia:

A

There are 4 a genes (2 on each chromosome 16).

a. Defect in 1 gene -> carrier for a thalassemia.
Symptoms: Completely normal (silent carrier).

b. Defect in 2 genes -> a thalassemia trait.
Symptoms: Mild anemia.

c. Defect in 3 genes -> a thalassemia major.
Symptoms: Severe anemia.

d. Defect in 4 genes -> Homozygous for a thalassemia.
Effects: - Dies intrauterine (Hydrops fetalis).

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15
Q

Beta thalassemia

A

There are 2 beta globin genes

Defect in 1 gene –> Beta thalassemia minor (trait)
Symptoms: mild anemia

Defect in 2 gene—–> Beta thalassemia major
Symptoms: severe anemia later on after birth

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16
Q

Patient with p thalassemia major appears normal at birth …. Explain why?

A

Due to presence of HbF

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17
Q

High levels of HbF and HbA2 in patient with p thalassemia………….Explain why?

A

To compensate the absence of HbA.

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18
Q

Respiratory (Volatile) acids

A

as carbonic acid H2CO3, excreted by lungs

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19
Q

Metabolic (Fixed) acids:

A

Not excreted by the lungs as:
Sulfuric acid/ phosphoric acid
Uric acid and nucleic acid
lactic acid

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20
Q

Mechanisms of regulation of pH:

A
  1. Buffers:
    - 1st line of defense
    - Acts in a fraction of a second (immediate response)
  2. Respiration (Ventilation):
    - By increase/decrease CO2 excretion so regulates the amount of H2CO3 in the body
  3. Kidneys:
    - 2nd line of defense
    - Slow process (takes several days to reach maximum capacity)
    - By excretion of excess acids (H+) or bases (HCO3)
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21
Q

Buffers can be

A

A weak acid and its salt with strong base
H2CO3/ Na bicarbonate (NAHCO3)
Acetic acid/ Na acetate (CH3COOH/CH3COO)

A weak base and its salt with strong acid
Ammonium hydroxide/ ammonium chloride

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22
Q

Physiological Buffers types

A
  1. Bicarbonate buffer system: mainly in Extracellular fluid
  2. Phosphate buffer system: in all types of cells
  3. Protein buffer system: in cells and plasma
  4. Hemoglobin buffer system: in RBCs and Specific for buffering CO2 Produced by oxidation in tissues
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23
Q

Bicarbonate buffer system:

A

BHCO3/H2CO3, ratio 20:1, main buffer system in lungs

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24
Q

Advantages of Bicarbonate buffer system:

A
  1. Present in higher concentrations than other buffers
  2. Easily formed at the tissues from CO2 by Carbonic Anhydrase enzyme
  3. Easily corrected by respiration; CO2 is excreted with expired air at Lungs
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25
Q

Phosphate buffer system:

A

Structure: B2HPO4/ BH2PO4 (Alkaline phosphate/ Acid phosphate)
Ratio: 4 : 1
Characters: Strictly related to the kidneys (healthy kidneys are needed for proper
function)

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26
Q

. Protein buffer system:

A

Structure: H-proteinate / B-proteinate (Acid protein / proteinate salt)
Characters: include hemoglobin in RBCs and plasma proteins of the blood

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27
Q

Normal levels of blood

A

■ Bicarbonate: 22- 26 mEq/L
■ PCO2: 35-45 mmHg
■ pH: 7.35-7.45
■ PO2: 80-100%

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28
Q

Acidosis

A
  • 4, BHCO3 / H2CO3 Less than 20/1
  • PH Less than 7. 4
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29
Q

Alkalosis

A
  • BHCO3 / H2CO3 More than 20/1
  • PH More than 7. 4
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30
Q

Causes of respiratory acidosis

A
  1. Failure of Lungs to excrete CO2 -> ‘b H2CO3
    • Extensive Lung disease : A BEP
    ► Asphyxia
    ► Bronchia Asthma
    ► Emphysema
    ► Pneumonia
  2. Morphine or barbiturate Poisoning -> 4, of respiratory center
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31
Q

Causes of respiratory alkalosis

A
  • Hyperventilation -increase Loss of CO2 decrease H2CO3
    HFHAM
    • High altitudes
    • Fever
    • Hysterical
    • Aspirin overdose
    • Meningitis & encephalitis
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32
Q

Compensation of Respiratory Acidosis :

A
  • ↑ excretion of acids ( H ),
  • ↑ reabsorption of (HCO3-) by the kidneys.
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33
Q

Compensation of Respiratory Alkalosis

A
  • ↑ Excretion of HCO3.
  • ↓ Excretion of H+ by the kidneys.
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34
Q

Causes of metabolic acidosis :

( decrease of HCO3- )

A
  • High protein diet & severe muscular exercise.
  • Renal failure & Diarrhea.
  • Ketosis (severe uncontrolled diabetes mellitus , starvation and carbohydrate deficiency).
  • vomiting
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35
Q

Compensation of metabolic Alkalosis :

A
  • Depression of the respiratory center →↓ rate
    of respiration.
  • ↓ Excretion of co2 by the lungs.
  • Renal compensation .
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36
Q

ELECTROPHORESIS
Definition:

A

 Migration of a charged molecule in an electric field.

 Used for separating amino acids , proteins , peptides and nucleic acids .

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37
Q

Unit of electrophoresis consist of

A

1-Electrodes :
 Cathode (-ve).
 anode (+ ve) .
Best types of electrodes are made of platinum

2-Buffer reservoirs (tanks or chambers ) .

3-A support for the electrophoretic medium.

4-A transparent insulating cover to minimize evaporation of buffer.

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38
Q

Importance of buffer in electrophoresis

A

1- Transmit electric current.

2-Adjust the pH: determine the electric charge on the solute to be separated .

3- Facilitate migration of the substance to be separated .

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39
Q

High ionic strength buffers

A

give sharp bands,↓ rate of migration.

↑ Current & heat production → denature
proteins

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40
Q

Low ionic strength buffers

A

Bands become more diffuse and wider,
↑ rate of migration
↓current & hence heat production

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41
Q

Types of supporting media in electrophesis

A

1 Paper (old fashioned)
2 Cellulose acetate membrane
3 Agar
4 Agarose gel (common in use)
5 Polyacrylamide gel (common use)

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42
Q

Paper Electrophoresis :

A

Not in common use as it is not inert (charges on paper may interfere with
electrophoresis).

  • It is time consuming (16-18 hr).
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43
Q

Agarose Gel Electrophoresis: advantages

A
  1. Inert→ no adsorption & very little interference with migration of charged samples.

2 Small amount of sample applied (0.6-3 / µ) .

3 Short electrophoretic time (30-90 minutes).

  1. clarity which permits excellent densitometric scanning .
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44
Q

Atherosclerosis is promoted by high level of______ (bad cholesterol) without
adequate removal of cholesterol by functional _________(good or protective
cholesterol) .

A

LDL, HDL

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45
Q

Mechanism of LDL:HDL ratio

A
  1. Hyperglycemia (as in diabetes mellitus) →↑ Plasma LDL level → modified
    into oxidized & glycated LDL by oxidants (ROS).
  2. LDL is taken up by macrophage and arterial smooth muscle by:
    - Scavenger receptors. - or non - receptor pinocytosis .
  3. Macrophages become overloaded with cholesterol → foam cells .
  4. Accumulated foam cell in arterial wall stimulate :
    o Release of growth factors.
    o Proliferation of smooth muscle.
    o Formation of plaque (atheroma) .
    o Narrowing of blood vessels → predispose to thrombosis .
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46
Q

Total plasma cholesterol normal level is ______, high risk is ______

A

< 200 mg/dL , >240 mg/dL

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47
Q

is an excellent indicator for early
acute myocardial infarction .

A

An isoform ratio of 1.5 or greater

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48
Q

______Are released into blood stream with myocardial injury. _______ accurate than CK-MB but _______diagnose reinfarction

A

Troponin I and T. More accurate. cannot

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49
Q

Myoglobin is a sensitive indicator to _________. It is not specific to _______muscles

A

muscle injury, cardiac

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50
Q

Because the ______(level) the myoglobin, the larger the size of infraction, a negative myoglobin rise can rule out _________

A

higher, myocardial infarction

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51
Q

Plasma AST

A

returns to normal about 5th day

52
Q

Plasmas LDH

A

returns to normal after a week

53
Q

Risk factors of myocardial infarction

A

Hypertension. hypercholesterolemia, obesity, diabetes, smoking, stress, sedentary life style and family history

54
Q

Symptoms of Myocardial infarction

A

Anxiety, nausea, chest pain, shortness of breath, rapid irregular heart beat

55
Q

Jaundice

A

↑↑ serum bilirubin above 2 mg/dL → yellowish discoloration of the skin, sclera and mucous membranes.

56
Q

Unconjugated hyperbilirubinemia types

A

Hemolytic jaundice
Physiological neonatal jaundice
Crigler-Najjar Syndrome type 1
Crigler-Najjar Syndrome type 2
Gilbert syndrome

57
Q

Conjugated Hyperbilirubinemia types

A

Obstructive Jaundice
Dubin-Johnson And Rotor Syndrome

58
Q

Difference between Conjugated and unconjugated hyperbilirubinemia

A

Liver to can’t conjugate bilirubin → unconjugated hyperbilirubinemia.

Liver cells swell → blocking the biliary canaliculi → conjugated hyperbilirubinemia.

59
Q

In both conjugated and unconjugated hyperbilirubinemia

A

↓ Stereobilin in the feces (faint stool).

 Both urobilinogen and bilirubin appear in the urine → dark brown in color.

 Serum levels of the enzymes ALT and AST and γ-GT are elevated Due to liver cell damage.

60
Q

Hemolytic jaundice

A

 ↑ Stercobilin in feces → dark brown stool.

 ↑ Urobilinogen in urine.

61
Q

Causes of hemolytic jaundice

A

Abnormal hemoglobin

Abnormal cell membrane

Red cell enzyme deficiency (G6PD and pyruvate kinase)

Red cell antibodies

Infections; malaria

62
Q

Physiologic neonatal jaundice

A

↑ hemolysis & immature UDP-glucuronyltransferase Enzyme.

63
Q

Physiologic neonatal jaundice treatment

A

Exposure to blue fluorescent light (phototherapy)
Phenobarbital

64
Q

Crigler-Najjar Syndrome, type I

A

Total deficiency of UDP-glucuronyltransferase

Serum unconjugated bilirubin exceeds 20 mg/dL → kernicterus.

fatal within one year as phenobarbital therapy doesn’t work

65
Q

Crigler-Najjar Syndrome, type II

A

 Partial deficiency of UDP-glucuronyltransferase.

 Serum unconjugated bilirubin does not exceed 20 mg/dL.

Patients respond to large doses of phenobarbital therapy

66
Q

Gilbert Syndrome:

A

Benign condition caused by a defect in the uptake of unconjugated bilirubin by the liver.

67
Q

Obstructive Jaundice causes

A

obstruction of the biliary passages: gallstones, pancreatic cancer or inflammation of pancreas

↑ Serum bilirubin, mainly conjugated bilirubin.
feces clay colored
Dark brown urine with bile salts

68
Q

Dubin-Johnson and Rotor Syndrome

A

Cause: defect in the ability of hepatocytes to secrete conjugated bilirubin into bile.

Hepatic lobules contain dark pigment

69
Q

Normal fasting glucose blood levels are:
2 h post prandial are

A

70-100 mg/dL
less than 140 mg/dL

70
Q

Sources of blood glucose:

A

During fasting: glycogenolysis and gluconeogenesis

During feeding: carboydrates

71
Q

GIT (Gastrointestinal tract): prevents sudden ↑ in blood glucose through

A

Slow rate of evacuation: Allows good time for gradual absorption

Secretion of gastric inhibitory peptide

72
Q

Liver: Main glucose homoeostat during hyperglycemia and hypoglycemia?

A

During hyperglycemia “↑insulin”: Liver ↓ blood glucose by:
↑ Uptake of glucose (GLUT2)
↑ Utilization of glucose (oxidation and storage)

During hyperglycemia “↓insulin” (fasting):
Liver ↑ blood glucose by:
↑ glycogenolysis & gluconeogenesis

73
Q

Kidney regulation of insulin

A

During hyperglycemia: Glycogenesis & excretion of glucose (if exceeds 180mg/dl) .

During fasting: ↑ gluconeogenesis

74
Q

Skeletal muscles regulation of glucose

A

During hyperglycemia: ↑ Uptake by Glut 4 ↑ storage (Glycogen)

During hypoglycemia:↓ Uptake & ↑ catabolism of muscle & release of amino acids

75
Q

Adipose tissues regulation of blood sugar

A

During hyperglycemia:-↑ Uptake by Glut 4 (insulin dependent)& ↑storage (Lipogenesis)

During hypoglycemia: ↓ Uptake& ↓catabolism of adipose tissue & release of FA → FA oxidation

76
Q

Insulin, where its from and what it does?

A

Secreted by the β - cells of pancreatic islets in response to hyperglycemia.

↑ Glucose uptake by GLUT- 4, by (heart, skeletal muscles & adipose tissues)

↑ utilization of glucose: Storage and oxidation

↓ glycogenolysis & gluconeogenesis

77
Q

Anti-insulins and what they do

A

Glucagon: ↑ Glycogenolysis & gluconeogenesis & ↓ Glycolysis, glycogenesis

Adrenaline: ↑ Glycogenolysis, gluconeogenesis, lipolysis & ↓Glycolysis, glycogenesis

Glucocorticoids: ↑Gluconeogenesis, lipolysis&↓ uptake, glycolysis

GH: ↑ Gluconeogenesis, lipolysis&↓ uptake, glycolysis

78
Q

Hypoglycemia defined as

A

↓ Blood glucose less than 70 mg/dl
Blood glucose below 45 is fatal

79
Q

Symptoms of hypoglycemia

A

Early signs and symptoms of mild hypoglycemia usually include:

Hunger , tremors , sweating , accelerated heart rate and tingling lips

Late signs and symptoms when more severe hypoglycemia:

Concentration problems , confusion and loss of consciousness .

80
Q

Causes of fasting hypoglycemia (more than 6 hours)

A

Insulin overdose

Decrease anti-insulins

Renal failure

Alcohol abuse

anorexia nervosa

genetic diseases

81
Q

. Hyperglycemic glucosuria: causes

A

Diabetes mellitus: The commonest cause

adrenaline glucosuria

82
Q

Normoglycemic glucosuria causes

A

renal glucosuria

Renal failure

Pregnancy

83
Q

Importance of ketone bodies

A

Main source of energy during starvation

KB can be oxidized easier than FA during fasting

Ketogenesis represents a preparatory step performed by liver,

84
Q

Causes of ketosis

A

Starvation, low carbohydrates and high fat in diet

Severe uncontrolled diabetes mellitus

Prolonged use of anti-insulin

Sever muscular exercise

85
Q

Effects of ketosis

A

↑ Production of acetoacetate & β-hydroxybutyrate → ketoacidosis → loss of buffer cations → electrolyte imbalance

86
Q

Ketogenic substances

A

FA, ketogenic AA, Anti-insulin

87
Q

Anti-ketogenic substances

A

Carbohydrates, glycerol, insulin and glucogenic AA.

88
Q

Management of ketosis

A

Hospitalization to Management of the cause

IV glucose and insulin

Bicarbonate to correct acidosis

IV K+

Fluids/electrolytes

89
Q

Where is insulin made and store?

A

Beta cells of the islets of Langerhans

90
Q

Beta cells release insulin in _____phases

A

two

91
Q

First phase of release is in response to

A

high blood glucose

92
Q

Second phase is a

A

sustained slow release of insulin

93
Q

Substances that stimulate release of insulin

A

Arginine and leucine, acetylcholine

94
Q

Measurement of which of the following is a good index of insulin secretion

A

C-peptide

95
Q

Insulin half life is

A

3-5 minutes

96
Q

Insulin catabolized through two systems

A

Hepatic glutathione

Insulin specific protease

97
Q

Action of insulin is terminated by

A

 de-phosphorylation of the receptor.
 followed by internalization of insulin and its receptor.
 Degradation in lysosomes

98
Q

Reason of Diabetes type 2 mellitus

A

resistance of insulin

99
Q

Tissues affected in insulin resistance

A

 In fat cells : ↑ lipolysis → release of free fatty acids in the blood .

 In muscle cells : ↓ glucose uptake →↓local glycogen.

 In liver cells : ↓ glycogen synthesis & ↑ glucose production by gluconeogenesis .

100
Q

Causes of insulin resistance

A

Obesity: main cause

Anti-insulin antibodies

Hereditary mutations to receptors

Acquired causes: diet, aging, physical inactivity

101
Q

IF fasting insulinto glucose ratio greater than 4.5, you have

A

insulin resistance

102
Q

Type 1 diabetes

A

10% incidence, usually for under 20 years of age, some blood insulin left

103
Q

Type 2 diabetes

A

90% incidence, Above 40, absent insulin (due to insulin resistance), treatment is diet control, exercise oral hypoglycemic drugs.

104
Q

Roles of vitamin D

A

Increases pancreatic insulin release which reduces insulin resistance

105
Q

Gestational Diabetes mellitus

A

Placenta causes low sensitivity to insulin, can go away after 4 weeks but usually turns into diabetes 2

106
Q

Specific types of diabetes mellitus

A

Over production of anti-insulin

Surgical excision of pancreas

Hemochromatosis

Drug induced diabetes

107
Q

Metabolic changes of carbs in diabetes mellitus

A

decrease glucose uptakes

causes polydepsia

108
Q

Polydepsia

A

extreme thirst

109
Q

lipid metabolism changes due to diabetes mellitus

A

decrease lipogenesis which causes weight loss

Increase uptake of FA

110
Q

Changes in protein metabolism due to diabetes

A

decrease protein synthesis

Increase sensitivity to infection and slow healing time

111
Q

Changes in mineral metabolism diabetes mellitus

A

Polyuria

112
Q

Polyuria

A

pissing more than usual

113
Q

Macro vascular and microvascular diseases form Diabetes mellitus complications

A

Macro: stroke and coronary artery disease

Micro: Damage to retina

114
Q

Hyperglycemic coma types

A

Diabetic ketoacidosis

Hyperosmaolar hyperglycemic non-ketotic coma

115
Q

Diabetic ketoacidosis

A

more common in type 1 diabetes, cause of coma is ketoacidosis

116
Q

Manifestation of Diabetic ketoacidosis

A

Acetone smell on breath, deep rapid respirations, rapid pulse and low blood pressure

117
Q

Treatment of Diabetic ketone acidosis

A

IV infusion of K and HCOs

IV infusion of glucose and insulin

118
Q

Hyperosmolar Hyperglycemic Non - Ketotic Coma:

A

Occurs in elderly patients with uncontrolled type two diabetes, can be caused from kidney failure

119
Q

Symptoms of Hyperosmolar Hyperglycemic Non - Ketotic Coma:

A

Severe dehydration

Severe hyperglycemia

Decreased concuisness and seizures

120
Q

Treatment of Hyperosmolar Hyperglycemic Non - Ketotic Coma:

A

IV infusion of K, fluids, glucose and insulin

121
Q

Hypoglycemia coma

A

occurs in any type of diabetes, caused by overtreatment of diabetes. Coma from low blood glucose

122
Q

Hypoglycemia coma symptoms and treatment

A

Symptoms: headache, poor concntration, tremors of hand, sweating, strong rapid pulse

Treatment; give glucose

123
Q

Diabetes mellitus symptoms

A

Polyuria , polydipsia , polyphagia , prolonged time of wound healing , and weight loss .

124
Q

Diabetes mellitus diagnostic tests

A

Fasting and 2 hour post glucose plasma glucose levels

Oral glucose tolerance test

Measurement of Glycated-Hb (HbA1c)

Measurement of plasma fructosamine

Test for microalbuminuria

125
Q

Normal, impaired glucose tolerance and diabetes level

A

FPG (mg/dL) normal<100 IGT 100-125 Diabetes > 126

2hour PG Normal <140, IGT 140-200 Diabetes >200

126
Q

OGIT test steps

A

After 8 hours of fasting blood and urine samples taken

Patient takes oral 75g of glucose in water

4 samples are obtained at each half hour)

Practical (13 decks)

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