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FOOD INTOLERANCE AND ALLERGY Flashcards

1
Q

WHAT PERCENTAGE OF UK POPULATION SELF REPORT FOOD ALLERGY VS WHAT PERCENTAGE HAS BEEN REALLY DIAGNOSED?

A

20-30% vs 2%

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2
Q

FOOD INTOLERANCE MAINLY AFFECTS WHICH SYSTEM IN THE BODY?

A

GI

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3
Q

ROLE OF IMMUNE SYSTEM IN FOOD INTOLERANCE?

A

NONE

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4
Q

SYMPTOMS OF FOOD INTOLERANCE AND HOW DO THEY GO AWAY?

A

GAS, BLOATING, FLATULENCE, CRAMPING, DIARRHOEA..
SYMPTOMS USUALLY CORRELATED WITH THE INGESTED AMOUNT OF THE OFFENDING FOOD SO THEY GO AWAY ONCE THE FOOD LEAVES THE GI TRACT

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5
Q

WHAT IS THE MOST COMMON/FAMOUS CAUSE OF FOOD INTOLERANCES?

A

ENZYME DEFICIENCIES

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6
Q

APART FROM GI SYMPTOMS SIMILAR TO THOSE OF FOOD INTOLERANCE, WHICH OTHER SYMPTOMS ARE SPECIFIC FOR FOOD ALLERGIES?

A
  • HIVES, ITCHINESS, SWELLING OF THE SKIN

- RESPIRATORY SYMPTOMS

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7
Q

DO ALL FOOD ALLERGIES INCLUDE ANAPHYLAXIS?

A

NO

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8
Q

WHAT DOES THE IMMUNE SYSTEM DO IN FOOD ALLERGIES?

A

MISTAKENLY IDENTIFIES A FOOD COMPONENT AS AN INVASIVE THREAT

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9
Q

2 SUB TYPES OF ADVERSE FOOD REACTIONS?

A

IMMUNE MEDIATED AND NON-IMMUNE MEDIATED

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10
Q

4 CATEGORIES OF NON-IMMUNE MEDIATED ADVERSE FOOD REACTIONS + EXPLANATIONS + EXAMPLES?

A

METABOLIC; ENZYME DEFICIENCIES, MALABSORPTION ( LACTOSE INTOLERANCE..)
PHARMACOLOGIC; CHEMICAL SENSITIVITY (CAFFEINE, MONOSODIUM GLUTAMATE..)
TOXIC; (FISH TOXIN, BACTERIA ETC.)
OTHER/IDIOPATHIC/UNIDENTIFIED; ADVERSE REACTIONS TO ARTIFICIAL PRESERVATIVES (E.G. SULPHITES, BENZOATES..)

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11
Q

WHICH OF THE 4 CATEGORIES OF NON IMMUNE MEDIATED ADVERSE REACTIONS TO FOOD IS NOT RECOGNISED BY THE BRITISH NUTRITION FOUNDATION?

A

TOXIC CAUSES

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12
Q

WHICH FOODS CONTAIN MONOSODIUM GLUTAMATE (MSG)?

A

SOY SAUCE, MUSHROOMS, SOME CHEESE AND TOMATOES

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13
Q

WHICH TRANSPORTER MOVES MONOMERS GOTTEN FROM LACTOSE BREAKDOWN (GLUCOSE AND GALACTOSE) INTO THE ENTEROCYTES FROM THE INTESTINAL LUMEN?

A

SGLT1

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14
Q

OSMOTIC DIARRHOEA IS ASSOCIATED WITH WHICH CONDITION?

A

LACTOSE INTOLERANCE

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15
Q

WHAT ARE POSSIBLE CAUSES OF LACTOSE INTOLERANCE?

A

LACTASE DEFICIENCY

LACTASE NON-PERSITENCE

HYPOLACTASIA

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16
Q

WHAT HAPPENS IN THE GI TRACT IN LACTOSE INTOLERANCE AFTER INGESTING LACTOSE?

A
  • LACTOSE TRANSITS UNDIGESTED INTO THE LARGE INTESTINE
  • GUT BACTERIA METABOLISE LACTOSE AND THE RESULTING FERMENTATION PRODUCES GAS (CO2, HYDROGEN AND METHANE)
  • THE GAS PRODUCED LEADS TO FLATULENCE, BLOATING AND PAIN
  • THE UNABSORBED LACTOSE AND FERMENTATION PRODUCTS (E.G. SHORT CHAIN FATTY ACIDS) RAISE THE OSMOTIC PRESSURE IN THE COLON
  • THIS INCREASES FLOW OF WATER INTO THE COLON CAUSING OSMOTIC DIARRHOEA
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17
Q

PERCENTAGE OF WORLD POPULATION EXPERIENCING A DECREASE IN LACTATE ACTIVITY AFTER INFANCY?

A

65-70%

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18
Q

IN WHICH POPULATIONS ARE THERE THE HIGHEST LACTATE ACTIVITY LEVELS POST INFANCY?

A

NORTHERN EUROPEAN

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19
Q

PERCENTAGE OF PEOPLE IN THE UK SUFFERING FROM LACTOSE MALDIGESTION?

A

5%

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20
Q

PEOPLE OF WHICH DESCENT HAVE AMONG THE HIGHEST LACTOSE DEFICIENCY RATES?

A

ASIAN, AFRICAN, JEWISH, HISPANIC AND CARIBBEAN

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21
Q

WHICH GENE IS LACTASE ENCODED BY AND MUTATIONS IN WHICH GENE (AND THEN SUBSEQUENTLY ITS PROTEIN) HELP REGULATE THAT GENE (KEEP IT TURNED ON)

A

GENE ENCODING LACTASE: LCT

PROTEIN: MCM6

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21
Q

WHICH GENE IS LACTASE ENCODED BY AND MUTATIONS IN WHICH GENE (AND THEN SUBSEQUENTLY ITS PROTEIN) HELP REGULATE THAT GENE (KEEP IT TURNED ON)

A

GENE ENCODING LACTASE: LCT

PROTEIN: MCM6

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22
Q

OTHER NAME FOR CONGENITAL LACTASE DEFICIENCY?

A

ALACTASIA

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23
Q

PREVALENCE, CAUSE AND MANAGEMENT OF CONGENITAL ALACTASIA?

A
  • EXTREMELY RARE
  • AUTOSOMAL RECESSIVE MUTATION ON LCT GENE CAUSING COMPLETE LACK OF LACTASE FROM BIRTH
  • INFANTS CANNOT BE BREASTFED OR GIVEN MILK AND THEY ARE FED WITH SOYBEAN-DERIVED FORMULAS
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24
MOST COMMON CAUSE/TYPE OF LACTOSE INTOLERANCE?
PRIMARY
25
WHAT IS PRIMARY LACTOSE INT.?
PRIMARY LACTASE DEFICIENCY AKA LACTASE NON-PERSISTENCE; GENETICALLY INHERITED, ABSENCE OF LACTASE PERSISTANCE ALLELE LEADING TO AGE RELATED DECREASE IN LACTASE ACTIVITY
26
PRIMARY LACTOSE INTOLERANCE USUALLY PRESENTS ITSELF IN WHICH STAGE OF LIFE?
ADULTHOOD (POSSIBLE IN CHILDHOOD BUT NOT USUAL)
27
SECONDARY LACTASE DEFICIENCY CAUSE?
DAMAGE OF THE LINING OF THE INTESTINE WHERE LACTASE IS FORMED, CAN BE CAUSED BY VARIOUS CONDITIONS LIKE GASTROENTERITIS, COELIAC, IBS, PARASITES, MEDS...
28
SECONDARY LACTOSE INTOLERANCE AFFECTS CHILDREN OR ADULTS MORE?
ADULTS
29
CAN SECONDARY LACTOSE INTOLERANCE BE REVERSED?
YES, BY THE RECOVERY OF THE INTESTINAL WALL
30
ARE LACTOSE INTOLERANCE TESTS ROUTINELY PERFORMED AND WHY?
NO BECAUSE AROUND 65% OF POPULATION IS AFFECTED
31
WHAT IS DONE IF SOMEONE HAS SYMPTOMS OF LACTOSE INTOLERANCE?
THEY ARE FIRST ENCOURAGED TO REMOVE LACTOSE FROM DIET FOR 2 WEEKS TESTS MAY BE PERFORMED TO DISTINGUISH BETWEEN PRIMARY AND SECONDARY
32
EXAMPLE OF LACTOSE INTOLERANCE TESTS AND EXPLANATION?
HYDROGEN BREATH TEST; PATIENT GIVEN 25-50g OF LIQUID GLUCOSE AFTER AN OVERNIGHT FAST, BREATH SAMPLES TAKEN EVERY 15-30 MINS FOR UP TO 3 HRS; A RISE IN BREAST HYDROGEN SUGGESTS LACTOSE WASN'T DIGESTED LACTOSE TOLERANCE TEST; MEASURES PRODUCTION OF GLUCOSE THAT WOULD NEED TO OCCUR IF LACTOSE WAS FULLY DIGESTED AFTER AN IVERNIGHT FAST STOOL SAMPLE FOR INFANTS AND CHILDREN BECAUSE THE PREVIOUS 2 TESTS INDUCE DIARRHEA, SEE IF STOOL HAS HIGH LEVELS OF ACIDITY AND SHORT CHAIN FATTY ACIDS SMALL BOWEL BIOPSY IF UNDERLYING CONDITION IS SUSPECTED
33
HYDROGEN BREATH TEST GIVES A FALSE NEGATIVE IN WHAT PERCENTAGE OF PATIENTS?
25% (VERY SPECIFIC)
34
PATIENTS WITH LACTOSE INTOLERANCE USUALLY TOLERATE UP TO HOW MANY GRAMS OF LACTOSE?
12g (250mL OF MILK)
35
MANAGEMENT OF LACTOSE INTOLERANCE?
LOW LACTOSE AND FODMAP DIET (FERMENTABLE CARBS), PREBIOTICS, LACTASE SUPPLEMENTATION..
36
LACTOSE INTOLERANCE; IMPACT ON QUALITY OF LIFE:
- LOWER QOL - ANXIETY OF INTOLERANCE GENERALIZED TO OTHER FOODS WHICH MAY LEAD TO VERY RESTRICTIVE DIETS - CAN LEAD TO AVOIDANT/RESTRICTIVE FOOD INTAKE DISORDER
37
WHICH EATING DISORDER IS SOMETIMES ASSOCIATED WITH LACTOSE INTOLERANCE?
AVOIDANT/RESTRICTIVE FOOD INTAKE DISORDER
38
CATEGORIES OF IMMUNE MEDIATED ADVERSE FOOD REACTIONS: (I.E. THE 4 TYPES OF ALLERGIC REACTIONS/HYPERSENSITIVITIES)
IgE MEDIATED NON IgE MEDIATED MIXED IgE AND NON IgE CELL MEDIATED
39
WHICH ANTIBODIES ARE INVOLVED IN NON IgE MEDIATED AKA TYPE II HYPERSENSITIVITY:
IgG AND IgM
40
WHAT ARE THE MEDIATORS IN TYPE IV HYPERSENSITIVITY?
CYTOTOXIC T CELLS AND MACROPHAGES
41
WHAT IS AN ALLERGEN?
AN ANTIGEN THAT PRODUCES AN ABNORMAL IMMUNE RESPONSE RESULTING IN ANTIBODY PRODUCTION
42
WHAT ARE THE USUAL ALLERGENS IN FOOD ON A CHEMICAL LEVEL?
PROTEINS, LIPOPROTEINS AND GLYCOPROTEINS
43
IMMUNOGLOBINS ARE A TYPE OF:
ANTIBODIES
44
HOW MANY TYPE OF IMMUNOGLOBINS ARE THERE?
5
45
WHAT IS THE MOST ABUNDANT AND WHAT IS THE LEAST ABUNDANT Ig?
MOST: IgG LEAST: IgE
46
WHAT IS THE FRAGMENT CRYSTALLIZABLE (Fc) REGION OF ANTIBODIES?
FORMED BY 2 HEAVY CHAINS COMING TOGETHER USUALLY LINKED BY DISULFIDE BONDS MANY IMMUNE CELLS HAVE RECEPTORS FOR IT
47
TYPE OF BONDS IN Fc REGION OF ANTIBODIES?
DISULFIDE BONDS
48
ANTIBODY BASIC STRUCTURE:
GLYCOPROTEIN CONSISTING OF 2 TYPES OF POLYPEPTIDE CHAINS (HEAVY AND LIGHT) WHICH ALSO CONTAIN CARBOHYDRATES
49
IgE ASSOCIATED (TYPE I) HYPER SENSITIVITIES AFFECT WHAT PERCENTAGE OF ADULTS AND WHAT PERCENTAGE OF CHILDREN?
3-8% OF CHILDREN | 1-3% OF ADULTS
50
COMMON INDUCERS OF IgE ALLERGIES:
MILK, EGGS, WHEAT, PEANUTS, SESAME, FISH, FRUIT AND VEG
51
ALLERGIES TO WHICH PRODUCTS ARE OFTEN OUTGROWN AND WHICH PERSIST:
OUTGROWN: MILK, EGG, WHEAT PERSIST: FISH, PEANUTS, TREE NUTS
52
HOW IS THE PREVALENCE OF TYPE I ALLERGIES CHANGING AND WHY?
IT IS INCREASING ACCORDING TO THE HYGIENE HYPOTHESIS THE REASON IS DECREASED FAMILY SIZE AND IMPROVED FAMILY HYGIENE, EATING LESS ORGANIC FOOD AND USING MORE ANTIBIOTICS AND VACCINES
53
EXPLAIN ALLERGIC SENSITIZATION AND SECONDARY IMMUNE RESPONSE IN TYPE I HYPERSENSITIVITY:
REGARDLESS OF THE ALLERGEN, FIRST EXPOSURE TO THE ALLERGEN ACTIVATES A PRIMARY IgE ANTIBODY RESPONSE (SO THERE ARE IgE ANTIBODIES PRODUCED BUT THERE IS NO ALLERGIC SYMPTOMS, THE INDIVIDUAL IS JUST SENZITIZED TO AN ALLERGIC REACTION UPON SUBSEQUENT EXPOSURE UPON SUBSEQUENT EXPOSURE, THE PRIMED IMMUNE SYSTEM REACTS WITHIN MINUTES (SECONDARY IMMUNE RESPONSE) LEADING TO A SYMPTOMATIC ALLERGIC REACTION
54
2 ROUTES OF ALLERGIC SENSITIZATION:
CLASS I FOOD ALLERGENS (MILK, EGG, PEANUT); ORAL ALLERGENS CAUSING SENSITIZATION THROUGH THE GI TRACT CLASS II FOOD ALLERGENS (E.G. BIRCH POLLEN); AEROALLERGENS THAT CAUSE SENSITIZATION VIA THE RESPIRATORY TRACT
55
HOW MANY IgE MOLECULES CAN AN INDIVIDUAL MAST CELL BIND?
500 000
56
HOW MANY ALLERGEN-SPECIFIC BINDING SITES DOES EACH IgE MOLECULE CONTAIN?
2
57
WHAT ARE MAST CELLS?
A mast cell is a resident cell of connective tissue that contains many granules rich in histamine and heparin. Specifically, it is a type of granulocyte that is a part of the immune and neuroimmune systems.
58
HOW ARE MAST CELLS ACTIVATED IN SECONDARY IMMUNE RESPONSE?
ALLERGENS BIND TO MULTIPLE IgE MOLECULES ON MAST CELLS AND CROSS LINK THEM WHICH ACTIVATES THE MAST CELLS AND TRIGGERS DEGRANUALTION AND THE RELEASE OF THE CONTENT OF THE GRANULES IN THE EXTRACELLULAR ENVIRONMENT
59
WHICH COMPONENTS ARE RELEASED FROM GRANULES OF THE MAST CELLS UPON ALLERGEN BINDING TO IgE ON THE MAST CELLS AND WHAT DO THEY DO?
HISTAMINE, SEROTONIN, BRADYKININ, LIPID MEDIATORS, CYTOKINES; ALL COLLECTIVELY CAUSE INFLAMMATION ON SYMPTOMS OF TYPE I HYPERSENSITIVITY
60
WHAT ARE SOME OF EXTERNAL FACTORS THAT CAN FACILITATE SENSITIZATION IN TYPE I HYPERSENSITIVITY?
ALCOHOL, STRESS, ANTI-INFLAMMATORY DRUGS, PATHOGENS..
61
WHEN IN LIFE DOES PRIMARY ALLERGIC SENSITIZATION OCCUR AND WHAT IS THE RESULT OF IT?
EARLY IN LIFE (CHILDHOOD) | LEADS TO T-CELL AND IgE MEMORY WHICH CAN BE BOOSTED UPON FURTHER ALLERGEN CONTACT
62
WHICH ANTIBOIDES ARE PRODUCED BY NON ALLERGIC INDIVIDUALS IN RESPONSE TO PRIMARY FOOD ALLERGENS?
IgG AND IgA
63
WHAT AFCTORS CONTRIBUTE TO THE TYPE AND SEVERITY OF ALLERGIC REACTION?
- AMOUNT OF INGESTED ALLERGEN - THE STABILITY OF ALLERGEN AGAINST DIGESTION - THE PERMEABILITY OF THE EPITHELIAL LAYER
64
EFFECTS OF HISTAMINE RELEASED FROM GRANULES OF MAST CELLS UPON SECOND EXPOSURE TO AN ALLERGEN IN TYPE I HYPERSENSITIVITIES?
- STIMULATES MUCUS SECRETION IN NASAL PASSAGES - STIMULATES TEAR FORMATION - WHEN IT INTERACTS WITH NERVE ENDINGS CAUSES ITCHING AND SNEEZING - TOGETHER WITH SEROTONIN IT CAN STIMULATE VOMITING CENTERS IN THE CEREBELLUM - RELAXATION IF INTESTINAL SMOOTH MUSCLES AND DIARRHEA
65
WHAT IS ANGIOEDEMA?
SWELLING AFFECTING LIPS, THROAT AND TONGUE
66
WHAT IS CYANOSIS?
BLUISH COLOR TO THE SKIN DUE TO LACK OF OXYGEN
67
WHAT IS DYSPNEA?
DIFFICULTY BREATHING
68
WHEN DO LATE-PHASE ALLERGIC REACTIONS DEVELOP?
4-12HRS AFTER THE EARLY/IMMEDIATE PHASE
69
IMMEDIATE ALLERGY REACTION IN TYPE I HYPERSENSITIVITY IS MEDIATED BY IgE AND THE LATE PHASE RESPONSE BY?
EOSINOPHILS, NEUTROPHILS AND LYMPHOCYTES
70
WHAT ARE MARKER ALLERGENS?
FOOD CONSTITUENTS THAT CAN BE USED TO CONFIRM SENSITIZATION TO A TYPE OF FOOD
71
ALLERGENIC FOODS USUALLY CONTAIN INDIVIDUAL OR MULTIPLE ALLERGENIC PROTEINS?
MULTIPLE
72
EGG ALLERGY PREVALENCE THROUGHOUT LIFE?
- ONE OF THE MOST PREVALENT IN CHILDHOOD (1.6-2.3% OF CHILDREN) - AFFECTS ONLY 0.2% OF ADULT POPULATION ( OUTGROWING RATE RELATIVELY HIGH)
73
CROSS REACTIVITY IN ALLERGIES?
OCCURS WHEN PROTEINS IN ONE FOOD SHARE PROPERTIES WITH THOSE IN ANOTHER FOOD AND CAN CAUSE AN ALLERGIC REACTION EVEN IF THEY THEMSELVES AREN'T THE ACTUAL ALLERGEN
74
COELIAC DISEASE IS AN EXAMPLE OF WHAT TYPE OF ALLERGY?
NON IgE MEDIATED

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