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Rheumatolgy > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q
  • Affect who more? 4
  • m/c disability in US?
  • 66% of those diagnosed with arthritis are?
  • More common over age of?
A
  • Affects women more than men
  • Leading cause of disability among persons age 65 and older in the US
  • 66% of those diagnosed with arthritis are overweight or obese
  • More common over age 65 (49.5%)
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2
Q

The most famous transmembrane PRRs are called?

A

toll-like receptors (TLRs) – they play a huge roll in autoimmune diseases

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3
Q

Common molecules that trigger innate immunity: 2

A
  • Pathogen-associated molecular patterns (PAMPs) – microbial molecules “Intestinal dysbiosis” (turn it on or off)
  • Damage-associated molecular patterns (DAMPs) – molecules from damaged or necrotic host cells (Cell destruction)
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4
Q

•Activated complement does the following: 3

A
  1. Coats microbes
  2. Stimulates phagocytosis
  3. Chemotaxis of leukocytes
  4. Stimulates inflammation
  5. Cause direct cell lysis
  • Coats microbes and stimulates phagocytosis by the innate immune system
  • Promotes chemotaxis of leukocytes and stimulates inflammation
  • Forms a complex that can cause direct cell lysis
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5
Q

•C3 and C4 can be measured in the blood: 2

A
  • Increased values: cancer, infection, UC

* Decreased values: liver disease, autoimmune disease (lupus), kidney disease.

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6
Q

B Cell Lymphocytes do what?: 2

A
  1. Present
  2. Recognise antigens
  • B-cells present antigens to T-helper cells through MHC peptides
  • Antibodies are responsible for recognizing antigens – they can stimulate the complement cascade, activate phagocytes or stimulate activation of T-cells.
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7
Q

T cell Lymphocytes do what?: 3

A
  1. stimulate further immune response
  2. (MHC) bind to T-cells (at TCRs) and stimulate activation.
  3. MHC in humans = known as (HLAs) - human leukocyte antigens -> highly polymorphic
  • Their biggest function is to interact with other cells to stimulate further immune response (phagocytes/B cells) or kill infected cells.
  • Major histocompatibility complexes (MHC) on antigen presenting cells will bind to T-cells (at TCRs) most often and stimulate activation.
  • MHC proteins in humans are known as human leukocyte antigens (HLAs) – they are highly polymorphic in humans.
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8
Q

Types of T-Cells: 3 (MEN)

A
  • Th1 – produce IFN-gamma – associated with macrophages, autoimmunity and chronic inflammation
  • Th2 – produce IL-4, IL-5, IL-13 – associated with eosinophils and allergy
  • Th17 – produce IL-17, IL-22 – associated with neutrophils and autoimmunity

MEN- macrophages Th1, eosinophils Th2, neutrophils Th3

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9
Q

Immunogenic Determinants: 7

A
  • Foreignness (“self” vs “non-self”)
  • Molecular size (The bigger the protein, the more immunogenic it tends to be)
  • Chemical-structural complexity
  • Antigenic determinants (epitopes) (Different epitopes can elicit different immune responses)
  • Dosage, route and timing of antigen administration
  • Genetic constitution of the host (HLA genes)
  • Adjuvants – or immune system enhancers
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10
Q

The Development of Autoimmunity: 4 (SIP-R)

•Onset of autoimmune response and development of clinical symptoms are generally separated in time.

  • Susceptibility phase
  • Initiation phase
  • Propagation phase
  • Regulation/resolution phase
A
  • Susceptibility phase – several preconditions for disease are satisfied (Environment)
  • Initiation phase – autoimmune response present but no clinical disease
  • Propagation phase – clinical disease begins
  • Regulation/resolution phase – immunoregulatory pathways activated; may result in resolution but this is rare.
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11
Q

Autoimmunity Pathogenesis: 2
Environmental triggers for autoimmunity: 6

  • Susceptible genes + environmental triggers are needed to trigger autoimmunity.
  • Many autoimmune diseases are linked to HLA (MHC) alleles.
A

•Environmental triggers for autoimmunity:

  1. Hormone production (Reproductive & Cortisol)
  2. Infections
  3. Microbial flora (skin, GI, vaginal…etc)
  4. UV radiation
  5. Toxic exposure (heavy metals, pharmaceuticals…etc)
  6. Diet and lifestyle (obesity, food allergies…etc)
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12
Q

Laboratory Assessment:

*Common Basic Laboratory Testing: 8

A
  • CBC
  • Chem Panel
  • CRP/ESR
  • Serum Ferritin
  • Thyroid Panel
  • 25-Hydroxy Vitamin D
  • Specific antibody testing
  • Serum uric acid
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13
Q

Pharmacologic Treatment:
•NSAIDs- CV event-just helps w/pain

Action & MOA- 3

A
  • Actions: analgesic, anti-inflammatory, antipyretic
  • MOA: inhibit cyclooxygenase (COX) activity
  • NSAIDs DO NOT stop progression of tissue injury
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14
Q

Pharmacologic Treatment:

NSAIDs Adverse effects: 3

A
  • Increased risk of MI, stroke and death
  • Gastrointestinal bleeding, hemorrhage and perforation
  • Acute renal failure
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15
Q

Pharmacologic Treatment:

•Glucocorticoids-Tapered/topical injections to jts- 4

A
  • Used to modify disease progression in acute flares
  • Actions: reduce activation, proliferation and differentiation of immune cells
  • Glucocorticoids are often not used in OA, Scleroderma and Sjögren’s
  • Glucocorticoids HAVE to be tapered down
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16
Q

Pharmacologic Treatment:

Glucocorticoids Adverse effects: 3

A

*Osteoporosis
•Fluid retention, hypertension, arrhythmias, MI
•Impaired wound healing

17
Q

Pharmacologic Treatment:
•DMARDs- immuno-suppressants- NEEDS to be Tapered

Action & MOA-4

A
  • Actions: anti-inflammatory, immunomodulatory
  • MOA: many different actions, usually down-regulating the immune system
  • DMARDs should NOT be discontinued after remission without careful consideration – this could lead to more flares in the future
  • Patient compliance with DMARDs is generally low due to adverse side effects or cost
18
Q

Pharmacologic Treatment:

DMARDS Adverse Effects and Toxicities-3

A
  • A CBC needs to be monitored on a regular basis (every 1-3 months) initially for every DMARD.
  • Myelosuppression can occur with use of methotrexate, sulfasalazine, azathioprine, cyclophosphamide.
  • Liver enzymes need to be monitored on a regular basis for methotrexate, azathioprine, leflunomide.
19
Q

Pharmacologic Treatment:
Methotrexate (MTX)- M/c DMARD (1st line->usually MonoTherapy)

•Side effects??? (10)

A

•Nausea, vomiting
•Skin rashes, photosensitivity
•Anemia, leukopenia
•Hepatotoxicity
•Thrombocytopenia
•Folic acid (1mg/day) should be given conjunctively (Folic acid analog inhibits cell division and
growth- lowers immune system)
•Liver Enzymes need to be monitored every 8-12 weeks
•Patients with MTHFR defects will have more severe adverse reactions
•SEVERAL block box warnings for this medication
•Pregnancy Category X (NEVER TO PREGNANT WOMEN)

20
Q

Pharmacologic Treatment:

Azathioprine (Imuran): 4

A
  • Black box warning for increased risk of lymphomas.
  • Liver enzymes need to be monitored every 1-2 months.
  • CBC needs to be monitored weekly for the first month,2x a month for months 2-3 then monthly.
  • Absolutely contraindicated in pregnancy – Category D
21
Q

Pharmacologic Treatment:

Leflunomide (Arava): 3

A
  • Absolutely contraindicated in pregnancy – Pregnancy Category X
  • Liver Enzymes need to be monitored every 8-12 weeks
  • Avoid use of this medication when possible
22
Q

Pharmacologic Treatment:

Sulfasalazine (Enteropathic arthritis – ulcerative colitis)-3

A
  • Monitor CBC with Diff and LFTs initially, then every other week for the first 3 months, then every month for second 3 months, then once every 3 months or as needed.
  • Avoid in those with allergies to sulfa drugs or salicylates
  • Pregnancy category B – can be used but with caution; supplement folic acid
23
Q

Pharmacologic Treatment:
Hydroxychloroquine (Plaquenil)-> Most used for Lupus/alopecia/

4- pregnancy?

A
  • Doses should not exceed 6.5mg/kg in chronic therapy to minimize the risk of retinal toxicity
  • Patient is REQUIRED to receive an initial and yearly eye exam while on this medication
  • Run CBC initially and then every 3 months for the first year.
  • Safe in pregnancy TQ
24
Q

Pharmacologic Treatment:

Cyclophosphamide (Last ditch efford in case of death-> anti-Cancer med): 3

A
  • Anti-neoplastic alkylating agents that crosslinks DNA which leads to cell death
  • CBC and LFT initially and then every other week for 3 months then every month for the next 3 months then every 3 months.
  • Urinalysis periodically for hematuria
25
Q

Pharmacologic Treatment:

Biological DMARDs: 4

A

*These are only to be used after the failure of non-biologic DMARD therapy
•MOA: inhibit TNF-alpha and IL-1 (key inflammatory cytokines); can also inhibit other cytokines and T-cell activity
•VERY expensive
•Generally only effective in combination with non-biologics (MTX)

26
Q

Naturopathic Approaches:

2.Correct underlying causes, imbalances and triggers (6)

A

a) Dysbiosis/microbial triggers
b) Diet/lifestyle triggers
c) Stress (physical/mental/emotional)
d) Nutritional imbalances
e) Hormone imbalances
f) Xenobiotic/heavy metal exposure and accumulation

27
Q

Naturopathic Approaches:

Bacterial Dysbiosis: 6

A
  • Dietary modifications (low carbohydrates): Specific carbohydrate diet, GAPS diet, low FODMAP diet.
  • Herbal antibiotics:
  • Berberine: 1,000 – 5,000mg po qd (hydrogen producing bacteria)
  • Garlic: 450mg TID (methane producing bacteria).
  • Conventional antibiotics
  • Rifaximin: 1650mg/day (550mg TID) x 2 weeks – nonabsorbable antibiotic
28
Q

Naturopathic Approaches: 5

Intestinal Candidiasis:

A
  • Dietary modifications: reduce intake of sugars including carbohydrates, dairy and processed sugars.
  • Herbal anti-fungals:
  • Caprylic acid (time release): 1,000 – 2,000mg po cc
  • Berberine: 1,000mg – 5,000mg per day
  • Oregano oil: 150mg TID
29
Q

Naturopathic Approaches:
Hormone Imbalances:
•Prolactin – high •Prolactin lowering agents: 2

A
  • Vitex astus-cagnus: 40 – 160mg TID of chaste tree extract

* Bromocriptine (dopamine agonist): 2.5mg po qd – main pharmacologic treatment.

30
Q

Naturopathic Approaches:
Hormone Imbalances:
•Estrogen – high
•Estrogen regulating strategies: 4

A
  • Promote weight loss if patient is overweight or obese.
  • Reduce alcohol consumption
  • Promote healthy liver function (improves estrogen metabolism)
  • Supplementation – Indole-3-carbinol, DIM,
31
Q 
Naturopathic Approaches:
Hormone Imbalances:
   •Prolactin – high/low?
   •Estrogen – high/low?
   •Insulin - high/low?
   •Testosterone - high/low?
   •Cortisol - high/low?
   •DHEA-S - high/low?
   •Thyroid hormone - high/low?
A
  • Prolactin – high
  • Estrogen – high
  • Insulin - high
  • Testosterone - low
  • Cortisol - low
  • DHEA-S - low
  • Thyroid hormone – low or high
32
Q

Naturopathic Approaches:

Heavy Metal Exposure: 2

A
  • Mercury can induce autoimmunity, immune complex formation and deposition and the formation of ANAs.
  • Chelating or otherwise detoxing metals and xenobiotics may stimulate autoimmune responses.
33
Q

Naturopathic Approaches:

Nutritional Supplementation: 11

A
  • Multivitamin/multimineral supplementation
  • Vitamin D:
  • Essential fatty acids:
  • Probiotics:
  • Green Tea Extract:
  • Lipoic Acid:
  • Niacinamide:
  • Glucosamine Sulfate:
  • Chondroitin Sulfate:
  • SAMe:
  • Methylsulfonylmethane (MSM):
34
Q

Naturopathic Approaches:

Acute Treatment: 3

A
  • Capsaisin
  • Bromelain:
  • Curcuma:
35
Q

•Environmental triggers for autoimmunity: 6

A
  1. Hormone production (Reproductive & Cortisol)
  2. Infections
  3. Microbial flora (skin, GI, vaginal…etc)
  4. UV radiation
  5. Toxic exposure (heavy metals, pharmaceuticals…etc)
  6. Diet and lifestyle (obesity, food allergies…etc)

Rheumatolgy (14 decks)

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