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Fall Y3 > Rheum Exam 1 > Flashcards

Rheum Exam 1 Flashcards

1
Q

What are the main inflammatory cytokines?

A

IL-1, IL-6, TNFa

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2
Q

What is not an immune response to food?
-IgA and TGFB
-IFNy and IgG
-IL-4, Il-5, IL-13, IgE
-IFNy and IgA

A

IFNy and IgA

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3
Q

Which gender is more likely to suffer with a viral infection; M, F, both, neither?

A

M

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4
Q

A 56 yo F was infected with SAR-CoV2 at her work. She goes home and wants to sleep. Which cytokine mediates this effect?

A

IL-1

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5
Q

Your pt was exposed to SARS-CoV2 for the first time on a plane three days ago. Which cells do you expect to be activated now, at 72 hours?

A

NK cells, macrophages, T cells

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6
Q

Which of the following cell types is already in the tissue when a pathogen invades?
-Neutrophils
-Macrophages
-B cells
-T cells

A

Macrophages

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7
Q

How do you start your production of inflammatory cytokines?

A

An inflammatory triggers ikappaB to let go of NFkappaB and NFkappaB translates to the nucleus

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8
Q

Which proteins are involved in resolving infection?

A

Protectins, maresins, resolvins

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9
Q

Which cytokine is associated with hostile and aggressive behavior?

A

TNFa

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10
Q

Which T cell is associated with candida infection?

A

Th17

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11
Q

A microbe binds to a TLR on a macrophage. If this is going to trigger an autoimmune response, what must be present on the macrophage to activate an autoreactive T cell?

A

CD86

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12
Q

Which cytokines are made in response to Th2?

A

IL-4, IL-5,IL-13

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13
Q

In a Th1 response, IFN gamma triggers B cells specific to the antigen to produce which type of immunoglobulin?

A

IgG

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14
Q

You have a pt with mononucleosis, which is caused by Epstein Barr Virus, and causes B cells to overgrow. Which protein would you expect to find elevated in the blood?

A

Antibodies

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15
Q

SARS-CoV2 virus is able to infect multiple tissues, why?

A

ACE2 receptors that the virus uses for entry are in multiple tissues

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16
Q

What response type occurs with bacteria + virus? What cytokines are present?

A

Th1

IFN gamma

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17
Q

What response type occurs with worms? What cytokines are present?

A

Th2

IL-4, IL-5, IL-13

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18
Q

What response type occurs with food? What cytokines are present?

A

Th3/Treg

TGFbeta

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19
Q

What response type occurs with asthma? What cytokines are present?

A

Th2

IL-4, IL-5, IL-13

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20
Q

What response type occurs with mold? What cytokines are present?

A

Th17

IL-17

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21
Q

What cells and cytokines changes occur with chronic inflammation?

A

↑ IL-1, IL-6, TNFa

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22
Q

What cells and cytokines changes occur with cancer?

A

↓ Th1 (↑ TGFB,Treg)

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23
Q

What cells and cytokines changes occur with autoimmunity?

A

↑ Th1 and Th17

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24
Q

What cells and cytokines changes occur with infections?

A

↑ Th1 (↓Th2)

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25
Q

What cells and cytokines changes occur with allergies?

A

↑ Th2 (↓TH1)

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26
Q

What vitamin is important in the production of defensins/antimicrobial peptides (AMP)?

A

Vit D > IL-22 > defensins

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27
Q

Difference between M1 and M2 macrophages

A

M1 > IL-12 > Th1
M2 > IL-4 > Th2

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28
Q

Common causes of chronic inflammation

A

Stress: cortisol
Food: hypersensitivity, obesity, inflammatory foods [sugar, omega 3/6]

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29
Q

Describe the antibody order

A

My Dog Goes Everywhere Always

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30
Q

What is the main function of T reg cells/TGFB?

A

STOP SIGN:
> Th1 stop making IFNg
> Th2 stop making IL-4, IL-5, IL-13
> regulates Th1 and Th2
> shut down Th17 and inflammatory cytokines

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31
Q

What are the 5 different forms of IL-17? Which are pro-inflammatory and which are anti-inflammatory?

A

Pro-Inflammatory:
IL-17A, IL-17B

Anti-inflammatory:
IL-E, IL-F

IL-C, IL-D

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32
Q

How can you drive a Th1 response?

A

Hydrotherapy: alternation of temps stimulates heat shock proteins

Astragalus, berberine, goldenseal, oregon grape, mints (holy basil, oregano, lemon balm)

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33
Q

How can you drive a Th2 response?

A

Worms (3-6 worms prevented from dividing given; worm infection is hundreds to thousands); AI, severe allergies

Immune system is focused on worm instead of pollen, etc

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34
Q

How can you drive a Treg response?

A

Avoid sugar, high fructose corn syrup, no artificial sweeteners, no AGEPs, no charred foods; high fiber, psyllium husks*, 12hr+fasting (7pm-7am)

Prebiotics, probiotics, vit D, vit A, vit C, mushrooms; mold

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35
Q

What cytokines are associated with Th9 cells?

A

IL-8

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36
Q

What cytokines are associated with macrophages/DC?

A

IL-1, IL-6, TNF

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37
Q

What causes the class switch for IgG?

A

IFNgamma

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38
Q

What causes the class switch for IgE?

A

IL-5

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39
Q

What causes the class switch for secretory IgA?

A

TGFbeta

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40
Q

What causes the class switch for IgM?

A

IL-2

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41
Q

What is the age of onset for b cell disease?

A

6 months

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42
Q

What is the age of onset for T cell disease?

A

< 5 mon

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43
Q

What is the age of onset for combined T and B cell disease?

A

At birth

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44
Q

Which immunodeficiency presents with gingivitis and skin abscesses?

A

Phagocytic defects

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45
Q

Which immunodeficiency presents with URI/sinopulmonary infections?

A

B cells

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46
Q

Which immunodeficiency presents with meningitis?

A

Complement defect

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47
Q

Which vaccines do those with immunodeficiencies need to avoid?

A

Live attenuated vaccines
MMR, TB, chickenpox, and polo

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48
Q

Which organisms infect those with T cell defects?

A

Viral, fungal, mycobacterial, or opportunistic

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49
Q

Which organisms infect those with B cell defects?

A

Invasive encapsulated bacteria

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50
Q

Which organisms infect those with neutrophil abnormality?

A

Bacteria of low virulence

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51
Q

Which organisms infect those with terminal complement defects?

A

Nisseria

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52
Q

What is a granuloma?

A

Chronic inflammation/infection causes the body to wall off the area

An organism that the macrophages can’t get rid of they recruit more macrophages to the area and fuse which forms a giant cell in the center then T cells are attracted to the area and create a wall around the macrophages

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53
Q

Disease due to ___ abnormalities are termed primary immunodeficiencies. A secondary immunodeficiency is ____, rather than genetic

A

Genetic; acquired

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54
Q

Match the neutrophil disorder to its pathophysiology

Body unable to produce neutrophils

Neutrophils can not travel to site of infection due to lack of integrin production

Neutrophil is unable to fuse phagosome with lysosome or degranuate, leaving them unable to kill microbe

Neutrophil is unable to produce superoxide and can not kill catalase positive microbes

A

Severe congenital neutropenia

Leukocyte adhesion defect

Chediak-Higashi syndrome

Chronic granulomatous disease

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55
Q

Match the immunodeficient component to the type of infection

Staph aureus skin infections
Viral infections
Neisseria caused meningitis
Enterovirus

A

Phagocytes
T cells
Complement
B cells

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56
Q

A deficiency in the complement protein is associated with an increased risk of

Lupus
Type 2 diabetes
Cardiac defects
Neisseria infection

A

Lupus

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57
Q

What is the pathophysiology to lupus in relation to complement?

A

Self cells are apoptosed and can’t get cleared from the body so B cells make antibodies against components of self cells
Lack of complement makes it harder to clear cells

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58
Q

A deficiency in complement proteins 5-9 are associated with

Neisseria infections
Autoimmune disease
Vasculitis
Infections with staph and strep

A

Neisseria infections

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59
Q

A deficiency of complement C1 inhibitor can lead to an overstimulation of the complement cascade creating excess and unregulated C3a. This C3a binds to macrophages, which in turn release histamine leading to life threatening

Hereditary angioedema
Neisseria infections
Respiratory paralysis
Fungal infections

A

Hereditary angioedema

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60
Q

Primary immunodeficiencies

Are frequent in low income countries
Affect only the adaptive immune system
Can be cause by infections with HIV
Are the result of a single gene defects in immune function

A

Are the result of a single gene defects in immune function

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61
Q

Common opportunistic infections in patients with reduced antibody responses are due to

Influenza
Intestinal helminths
Encapsulated bacteria
Atypical mycobacteria

A

Encapsulated bacteria

62
Q

X-linked agammaglobulinemia results from a mutation in

IFNg receptor
The CIITA promoter protein
An HLA gene
A tyrosine kinase gene

A

A tyrosine kinase gene

63
Q

what types of organisms are pts with wiscott aldrich susceptible to

A

encapsulated bacteria s/a neisseria meningitidis, haemophilus influenzae, strep pneumoniae

viruses: molluscum contagiosum, varicella zoster

fungus: pneumocystitis jiroveci, candida albicans

64
Q

what types of organisms are pts with SCID susceptible to

A

Fungal, viral, opportunistic or mycobacteria pathogens

65
Q

what types of organisms are pts with b cell disorders susceptible to

A

Encapsulated bacteria
Enteroviruses
Sinopulmonary

66
Q

what types of organisms are pts with CGD susceptible to

A

catalase pos bacteria and fungi

Staph aureus, B cepacia, aspergillus, other organisms

67
Q

what types of organisms are pts with leukocyte adhesion def susceptible to

A

pyogenic bacterial infection

68
Q

what types of organisms are pts with chediak higashi susceptible to

A

bacteria

69
Q

name the B cell/humoral immunodeficiencies

A

agammaglobulinemia
selectiva IgA def
hyper IgM syndrome
CVID

70
Q

name the T cell (cellular)/combined immunodeficiencies

A

SCID
digeorge
wiscott aldrich

71
Q

name the complement immunodeficiencies

A

hereditary angioedema (HAE)

terminal complement defect

72
Q

name the neutrophil/phagocytic immunodeficiencies

A

CGD
chediak-higashi
leukocyte adhesion deficiency

73
Q

what types of organisms are pts with complement immunodeficincies susceptible to

A

neisseria meningitis

74
Q

Which one of the following is true concerning common variable immune deficiency disorders?

Patients always present before the age of 10 years

Is due to a single gene defect on the x chromosome

Patients are treated by replacement immunoglobulin, intravenously or subcutaneously

Most patients die from complication of malignancy

A

Patients are treated by replacement immunoglobulin, intravenously or subcutaneously

75
Q

For which of the following immunodeficiency disorders is the conjugate vaccine for H. influenzae type B contraindicated?

B cell
T cell
Complement
None of these

A

None of these

76
Q

Pt w/ primary immunodeficiencies are at higher risk of developing

Infections
Autoimmune disease
Cancer

A

ALL

77
Q

Which of the following is not a condition associated with secondary immunodeficiency?

HIV
Measles
Cancer
Type 2 diabetes
Malnutrition
Genetic mutation

A

Genetic mutation

78
Q

This pathogen typically causes immune deficiency and increases the risk of secondary infections
Measles
Toxoplasma
Candida albicans
Rabies virus

A

Measles

79
Q

X linked hyper IgM syndromes is primarily due to

Lack of B cell help from NK cells

A low B cell count due to inadequate development in the bone marrow due to inadequate development in the bone marrow

A lack of T cell help via CD40 ligands

A lack of follicular dendritic cells needed for b cell maturation in the germinal center

A

A lack of T cell help via CD40 ligands

80
Q

Deletions in the T-cell CD40L gene produce

hyper-IgM syndrome
Congenital x-linked agammaglobulinemia
IgA deficiency
Wiskott-aldrich syndrome
Deficiency in cytotoxic t-cell activity

A

hyper-IgM syndrome

81
Q

Which one of the following is true concerning transient hypogammaglobulinemia of infancy:

Occurs at 3 months of age
Is due to placental absorption of IgG

Is linked with autoimmune disease in later life

Involves only the IgA immunoglobulin class

Is due to waning maternal antibodies in infant circulation

A

Is due to waning maternal antibodies in infant circulation

82
Q

Which one of the following statements concerning XLA is correct?

XLA present immediately after birth

It is a disease found in equal numbers of boys and girls

Patients with XLA present with recurrent severe bacterial and fungal infections

Patients usually have panhypogammaglobulinemia i.e. very low serum levels of IgG, IgA, and IgM all of which are < 10% of normal for age

Patient have normal numbers of plasma cells in the gut

A

Patients usually have panhypogammaglobulinemia i.e. very low serum levels of IgG, IgA, and IgM all of which are < 10% of normal for age

83
Q

Which one of the following is true concerning the replacement therapy for hypogammaglobulinemia

Consist mainly of IgM
Consist mainly of IgG
Consist mainly of IgD
Consist mainly of IgE
Consist mainly of IgA

A

Consist mainly of IgG

84
Q

Which of the following is not associated with a state of B cell immunodeficiency?

IgA deficiency

Leukocyte adhesion deficiency

Transient hypogammaglobulinemia

Common variable immunodeficiency

A

Leukocyte adhesion deficiency

85
Q

Which one of the following is true concerning individuals with selective IgA deficiency?

All individuals can be considered to be normal w/o risk of infections

They are more likely to develop heart disease than those with normal IgA

Will always have a high risk of HIV infection

They have a high risk of recurrent serious bacterial infection

They have higher risk of developing an organ specific autoimmune disease than the general populations

A

They have higher risk of developing an organ specific autoimmune disease than the general populations

86
Q

Which of the following organisms is someone with a T cell immunodeficiency more prone to infection?

Haemophilus influenzae
Candida albicans
Neisseria
Staph aureus

A

Candida albicans

87
Q

Di George syndrome results from a defect in

Purine nucleoside phosphorylase
WASP
Thymic development
DNA repair

A

Thymic development

88
Q

Which one of the following findings is the most common indicator in an infant with severe combined immune deficiency?

Lymphopenia
Severe asthma
Dry skin
Pneumonia
Staphylococcal abscess

A

Lymphopenia

89
Q

Which combined immunodeficiency is most likely to be fatal under the age of two if left untreated?

SCID
Wiskott-aldrich syndrome
DiGeorge syndrome
Hyper IgM syndrome

A

SCID

90
Q

SCID primarily affects

Macrophages, mast cells, t cells
T cells only
T cells and dendritic cells
T cell, B cells, and in some cases NK cells

A

T cell, B cells, and in some cases NK cells

91
Q

Which one of the following statements about Wiskott-aldrich syndrome is true?

Platelet size is large

It is a combined primary immune deficiency due to abnormal cell motility

It is always a severe disease

It is common in girls
Staphylococcal abscesses

A

It is a combined primary immune deficiency due to abnormal cell motility

92
Q

Which of the following would you suspect the presence of a primary immunodeficiency disease consisting of a problem with neutrophil function?

Recurrent ear, sinus, and lung infection

Recurrent thrush

Recurrent skin abscesses or poor wound healing

Recurrent warts

A

Recurrent skin abscesses or poor wound healing

93
Q

Which one of the following is the primary defect in chronic granulomatous disease?

Neutrophil production in the bone marrow

Neutrophil chemotaxis

Neutrophil intracellular killing of organism

Opsonization

Cytotoxic T cell activity

A

Neutrophil intracellular killing of organism

94
Q

Defects in neutrophil NADPH oxidase system produce

Chronic granulomatous disease

chediak-Higashi disease

Leukocyte adhesion deficiency

Hashimoto’s disease
Streptococcal infection

A

Chronic granulomatous disease

95
Q

The most frequently diagnosed form of specific primary immunodeficiency is

Severe combined immunodeficiency

X-linked agammaglobulinemia

Chronic granulomatous disease

SelectiveIgA deficiency

DiGeorge anomaly

A

SelectiveIgA deficiency

96
Q

Poor skin tests to a range of microbial antigens such as tuberculin and mumps indicate a deficiency of

NK cell
B cells
T cell
Complement
Phagocytes

A

T cell

97
Q

Primary immunodeficiency producing susceptibility to infection by viruses and fungi is due to

B cell deficiency
T cell deficiency
Complement deficiency
Eosinophil deficiency
Phagocyte deficiency

A

T cell deficiency

98
Q

Primary immunodeficiencies are due to

Genetic mutations
Viruses
Medications
Chemical exposures

A

Genetic mutations

99
Q

T or F.

Patients with selective IgA deficiency are at increased risk for developing many autoimmune diseases as well as atopy. The safest and most effective approach to treatment is early administration of IgA antibodies to correct the deficiency

A

False

100
Q

What cytokines and immunoglobulin are made in a Th2 response?
IL-4, IL-5, IL-13; IgE
IL-1, IL-6, TNF-alpha; IgG
IL-12, IL-6, IL-1; IgG
IL-4, IL-5, IL-1; IgE

A

IL-4, IL-5, IL-13; IgE

101
Q

What does peroxidase cause?

  • Cause histamine release
  • Breaks down collagen
  • Increased local blood flow
  • Breaks down tissue
A

Causes histamine release

102
Q

What does histamine cause?
* Increased local blood flow
* Increases vessel permeability
* Causes edema
* All of the above

A

All of the above

103
Q

What do mast cell granules contain?
* Histamine
* Chymase
* Tryptase
* Serine esterase
* TNF-alpha
* All of the above

A

All of the above

104
Q

What does serine esterase?
* Activates metalloproteinases
* Break down tissue
* Neurotoxin
* Breaks down collagen

A

Activates metalloproteinases

105
Q

Which of the following is NOT an encapsulated bacteria?
* neisseria meningitidis
* haemophilus influenzae
* strep pneumoniae
* mycobacteria

A

mycobacteria

106
Q

Which of the following is a test that can be done for allergic asthma?

  • Fractional excretion of nitric oxide
  • Total serum IgE and specific IgE
  • Complete blood cell count with an elevated absolute eosinophil count
  • All of these are true
A

All of these are true

107
Q

Which cytokine in the gut helps people develop and remain tolerant to food?

  • TGF beta
  • IFN gamma
  • IL-2
  • IL-7
A

TGFb

108
Q

Your pt gets diarrhea when he eats eggplant. You run a food hypersensitivity test. Which ab do you expect to show up positive?

IgA
IgE
IgG
IgM

A

IgG

109
Q

Exposure to secondhand smoke in kids under 4 is highly associated with respiratory allergies in older adults. From this, what ab would you suspect is higher in kids of smoking adults?

A

IgE

110
Q

Your pt got a new gold plated fit-bit. She notices she’s developing a rash on the back of her wrist. Which type of hypersensitivity is likely?

A

Type IV

111
Q

One of the therapies for COVID19 is convalescent plasma. This is similar to giving immunoglobulin to people with immunodeficiency. What is the danger?

Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity

A

Type III

112
Q

Your patient discovers that local honey makes her allergies better. Which of the following explains why?

Honey has sugar crystals that stabilizes mast cells so they dont degranulate
Honey can coat pollen and prevent TLR binding
Honey can trigger a class switch from IGE specific for pollen to IgA
All of these are true

A

Honey can trigger a class switch from IGE specific for pollen to IgA

113
Q

Why does a Type II Penicillin hypersensitivity result in hemolytic anemia?

Penicillin creates antigen-antibody complexes in the blood vessels
Penicillin interferes with the clotting cascade in sensitive individuals
Antigen (penicillin) sticks to the RBCs and is cleared by macrophage and NKs
Penicillin changes the shape of RBCs and the spleen eats it

A

Antigen (penicillin) sticks to the RBCs and is cleared by macrophage and NKs

114
Q

What cell types does IgE activate?

A

Eosinophils
Mast cells

115
Q

What are the granules in eosinophils?

A

Peroxidase
Collagenase
Major basic protein
Cationic protein

116
Q

What does peroxidase do?

A

Breaks down H2O2 > H2O
Causes histamine release

117
Q

What does major basic protein do?

A

Toxic, causes histamine release
Brain fog

118
Q

What does cationic protein do?

A

Neurotoxin
Brain fog

119
Q

What does histamine do?

A

Inc local blood flow (red nose)
Inc vessel permeability
Causes edema

120
Q

What do chymase and tryptase do?

A

Break down tissue

121
Q

What does serine esterase do?

A

Activates metalloproteinases

122
Q

What does TNFa do when released from mast cells?

A

Brings more lymphocytes, macrophages, eosinophils
Breaks down tissue

123
Q

Why is a second allergy response faster and more intense?

A

Once you have memory B cells for pollen, B cell started as IgM now already class switched to IgE so at second exposure no need for T cell rxn or macrophage carrying pollen

IgE can already be bound to mast cells and eosinophils > so they can degranulate more quickly (almost immediately after exposure to antigen)

124
Q

What is the basis of oral allergy syndrome?

A

Antigens that cross react because proteins share similar sequences (molecular mimicry)

Ex: 50-75% ppl allergic to birch tree pollen can develop itchy throat or mouth when eating apple or celery

125
Q

What types of responses occur with a type I hypersensitivity rxn?

A

Allergy
IgE
Th2

126
Q

What types of responses occur with a type II hypersensitivity rxn?

A

IgG to surface antigen
Penicillin hypersensitivity

127
Q

What types of responses occur with a type III hypersensitivity rxn?

A

IgG to soluble antigen
Immune response to inhaled mold
Streptokinase (rx for MI)
Lymphoglobulin (ab for immunodeficiency)

128
Q

What types of responses occur with a type IV hypersensitivity rxn?

A

Delayed type; DTH response
TB test
Allergic dermatitis
Food hypersensitivity

129
Q

Explain the mechanism of Type I hypersensitivity rxn

A

Pollen contacts macrophage > mo eat pollen through TLR > carries to nearest lymph node > presents pollen ag on iMHC molecule and mo produces IL-4

> pollen specific CD4 T cells binds to MHC molecule on mo
CD86 binds CD28 and activates CD4 T cell
IL-4 binds to IL-4 receptor and tells T cell to become a Th2 T cell

All within about 24 hours..

Once CD4 T cell is producing IL-4, IL-5, and IL-13 > triggers B cells to make IgE to pollen > IgE binds to pollen to try to “sop up” pollen

B cell secretes IgE which binds to FcE receptor on eosinophil > when we cross link FcE receptors with two IgE molecules bound to same antigen on both eosinophils and mast cells > causes degranulation

130
Q

Explain the mechanism of Type II hypersensitivity rxn

A

Immune system mistakes own cells with pathogens and activates the complement

IgG and IgM bind to target cells and causing complement activation

B&T cells create auto-antibodies against self antigens which damages cells and tissues

Autoantibodies target body own cells and disrupt normal function

131
Q

Explain the mechanism of Type III hypersensitivity rxn

A

Antigen-antibody complexes deposit activating the complement system → neutrophils → degranulate causing damage to area

132
Q

Explain the mechanism of Type IV hypersensitivity rxn

A

Antigen presented on MHC II of dendritic cell → CD4 T cell binds via T cell receptor and CD4 receptor → it will express CD28 which will bind to B7 on surface of dendritic cell → dendritic cell releases IL-12 → T cell differentiates into Th1 → release IL-2 and IFN-gamma → ↑ T cell differentiation and macrophage activation → IL-1, IL-6, TNF, lysosomal enzymes, complement, ROS species → inflammation

CD8 target antigens presented on MHC 1 and bind → perforin forms pores and granzymes induce apoptosis

133
Q

Allergies are characterized by what type of response? What do the cells produce?

A

Th2
T cells > IL-4, IL-5, IL-13 (mucus)
B cells > IgE (bc of IL-4 production)
Mast and eosinophil degranulation (IL-4, IL-5)

134
Q

What is the suspected cause of atopic allergies?

A

Cytokine imbalance, too many IL, IgE, eosinophils, etc
Hygiene hypothesis

135
Q

What are random allergies attributed to?

A

MHC related; run in families
Normal cytokine and eosinophil levels

136
Q

What is the most common EDS?

Hypermobile
Vascular
Classic
Classical-like

A

Hypermobile

137
Q

What are common sx for hEDS?

Joint pain
Fatigue
Easy bruising or poor skin healing
All of the above

A

All of the above

138
Q

What is the name of the criteria for generalized joint hypermobility?

Beighton score
Alvarado score
Amsel score
Centor score

A

Beighton score

139
Q

How is hEDS diagnosed?

Clinical
Labs
Imaging
Genetic testing

A

Clinical

140
Q

What are common complications of hEDS?

Aortic root dilation
Aortic dissection
Mitral valve prolapse
All of the above

A

All of the above

141
Q

What area doesn’t cause pain in patients with hEDS?

Joint pain
Muscle pain
Nerve pain
GI pain
Headaches
Eye pain

A

Eye pain

142
Q

What is the possible connection between MCAS and EDS?

Disordered connective tissue/collagen influences mast cell behavior
There is no connection
They are caused by the same thing
EDS causes MCAS

A

Disordered connective tissue/collagen influences mast cell behavior

143
Q

What foods contain histamine?

A

Tofu
Cheese
Yeast products
Smoked fish
Processed meats
Nuts or seeds
Foods with vinegar
Sweetened beverages
Over ripe fruit
Sauerkraut
Fermented drinks
Chocolate
Mushrooms
Leftovers in the fridge

144
Q

What is the significance of tryptase levels in MCAS and mastocytosis?

A

Tryptase levels are normal in MCAS but high in mastocytosis

Run in pts with suspected MCAS still to rule out mastocytosis

145
Q

What are the names of the two criteria for dx MCAS and what is the major difference?

A

Valent (requires lab findings; created by those who think MCAS is rare)

Molderings (clinical dx; created by those who think MCAS is common)

146
Q

What is the approach for treatment of MCAS?

A

Stepwise; add 1 supplement of med at a time and wait 2-4 weeks before adjustments or additions

147
Q

What are common comorbidities with MCAS?

SIBO
Crohn’s
GERD
All of the above
A + C

A

A + C

148
Q

What are some botanicals for MCAS?

A

Nettle
Curcumin
Butterbur
CBD

149
Q

What types of medications are indicated in MCAS tx?

A

H1 and H2 receptor blockers

150
Q

Dx criteria of POTS in adults says an increase or at least ___ bpm from supine to standing within 10 mins OR HR exceeding ____ bpm within 10 minutes.

Children: HR increases at least ____ bpm from supine to standing within 10 minutes.

A

30
120

Children: 40

151
Q

What are the two types of POTS? Which is more common?

A

Neuropathic (most common)
Hyperadrenergic

Fall Y3 (10 decks)

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