Lecture 2 (Rheum)-Exam 1 Flashcards
1
Q
Extended-Release Products:
* Who is it reserved for?
* What does it decrease?
* Allow for what?
* What is there a high risk of?
A
- Reserved for patients with severe chronic pain – usually cancer patients
- Decreased dosing frequency
- Allow for more even steady state with less peaks and troughs
- High risk for overdose of accidently ingested or breach of extended-release mechanism (e.g., crushing, cutting, chewing)
2
Q
What is a muscle spasm vs muscle spasiticity?
A
Muscle Spasm
* Sudden / involuntary
* Secondary to fatigue or injury
Muscle Spasticity
* Sustained contraction
* Decreased dexterity from the CNS
* Multiple sclerosis
* Cerebral palsy
* Stroke
* Spinal cord damage
3
Q
What are approved muscle relaxants for muscle spasms?
A
- Carisoprodol (Soma)
- Chlorzoxazone (Parafon)
- Cyclobenzaprine (Flexeril)
- Metaxalone (Skelaxin)
- Methocarbamol (Robaxin)
- Orphenadrine (Norflex)
- Tizanidine (Zanaflex)
- Diazepam (Valium)
4
Q
What are approved muscle relaxants for muscle spasticity?
A
- Baclofen
- Dantrolene
- Tizanidine
- Diazepam
5
Q
How does a muscle contract happen?
A
Action potentials travel down the UMN from the central nervous system
* Cause release of excitatory neurotransmitters (glutamate, norepinephrine)
* Synapse with the LMN
* Activate muscle contraction
6
Q
What is the inhibitory interneuron?
A
Regulates excitation of the LMN
7
Q
Central inhibition of muscle contraction:
* How does Gaba work?
A
GABA – inhibitory neurotransmitter
* Binds to GABA receptors
* Causes cell hyperpolarization
* Decrease frequency of cell depolarization
* Decreasing muscle contraction
8
Q
How does Benzodiazepines (diazepam, et al ) work?
A
- Bind to GABA A receptors
- Increases of Cl- influx
- Hyperpolarization and decreased excitation
Work on CNS
9
Q
How does baclofen work?
A
Binds to GABA B receptors
* Postsynaptic – increased K+ efflux
* Hyperpolarization
-
Presynaptic – decrease release of excitatory neurotransmitters (NE and glutamate)
* Less action potentials
Work on CNS
10
Q
How does Tizanidine work?
A
- Alpha-2 agonist
- Binds to alpha-2 receptors on presynaptic neurons of the UMN
- Results in less release of exitatory neurotransmitters
Work on CNS
11
Q
What are the four anti spasticity agents?
A
Baclofen, dantrolene, diazepam and tizinidine
12
Q
A
13
Q
What is the MOA of baclofen?
A
Binds GABAb receptors on:
1. LMN increasing K+ efflux, hyperpolarization, decreased action potential
2. Presynaptic UMN inhibiting release of excitatory NT glutamate and norepinephrine
14
Q
What is the MOA of Dantolene?
A
Inhibits ryanodine receptors on the skeletal muscle cells; prevents Ca2+ release from SR preventing contraction
WORKS ON SKELETAL MUSCLE SO MORE PNS
15
Q
What is the MOA of diazepam (Valium)?
A
Binds BDZ receptor on inhibitory GABAa receptor on LMN; increasing Cl- influx, hyperpolarization, decreased action potentials
16
Q
What is the MOA Tizanidine (Zanaflex)?
A
Alpha-2 receptor agonist; binds to presynaptic UMN inhibiting release of excitatory NT glutamate and norepinephrine
17
Q
What is unique about Dantrolene (Dantrium)?
A
Hepatotoxicity with high doses
18
Q
What are the 6 antispasmodics medicine?
A
- Carisoprodol (soma)
- Chlorzoxazone (parafon)
- Cyclobenzaprine (flexeril)
- Metaxalone (Skelaxin)
- Methocarbamol (Robaxin)
- Orphenadrine (norflex)
19
Q
A
20
Q
What drug is a schedule IV that is antispasmodics?
A
Carisoprodol (soma)
21
Q
What are the side effects of central muscle relaxants?
A
22
Q
What are the Unique SE of central muscle relaxants?
A
- Dizziness/ lightheadedness
- Hypotension
- Arrythmias
23
Q
What are anticholinergic side effects?
A
- Fever
- Dry mucous membranes
- Flushing
- Blurred vision
- mydriasis
- Hallucinations
- Sedation
- Tachycardia
24
Q
How are steroids produced?
* Released when?
* What type of effects?
A
Endogenous steroids produced in the adrenal gland (MC cortisol)
* Released in response to stress and inflammation
* Anti-inflammatory and immunosuppressive effects
25
What is the MOA of steroids?
**Inhibit the production of inflammatory cytokines**
* Bind to glucocorticoid receptors inside cells
* Bind to sites on DNA
* Down regulate cytokine production
**Inhibit the production of inflammatory mediators**
* Inhibit phospholipase A2
* Prevents the production of arachidonic acid
* Decreasing prostaglandins, leukotrienes, thromboxane
**Immunosuppression**
26
For steroids effects, what happens to the inflammatory response?
Suppress inflammatory response to all noxious stimuli
* Pathogens
* Chemical / physical
* Immune mediated / hypersensitivity
27
For the effects of steroids, how is inflammation reduced?
Reduce inflammation by **DECREASING**:
* Cytokine production – including various interleukins, tumor necrosis factor alpha
* Recruitment of WBCs and monocytes to sites of inflammation (neutrophil demargination)
* Lymphocyte, monocytes, basophil, eosinophil, mast cell production / function
* T-lymphocyte activity
* Production of prostaglandins, bradykinins, leukotrienes (inhibition of phospholipase A2)
## Footnote
Underlying cause of disease NOT corrected-> just a bandage
28
What is the short term adverse effect of steroids?
* Increased appetite
* Acne
* Insomnia
* Hyperglycemia – induction of gluconeogenesis and insulin resistance-> Caution with diabetes
* Increased fluid retention, edema, and blood pressure
* Mineralocorticoid effects
* Mood / Psychiatric changes
* Steroid psychosis
29
What is the long term adverse effect of steroids?
* Hypothalamic – pituitary-adrenal axis suppression
* Cushing syndrome – moon facies, buffalo hump, central obesity
* Growth suppression (in younger people)
* Muscle wasting
* Skin atrophy
* Immunosuppression (issues with infection)
* Cataracts / glaucoma
* Decreased bone mineral density (need to watch closer)
* Gastrointestinal bleeding
30
What are the big effects of glucocorticoids and mineralocorticoids?
Glucocorticoids
* Glucose metabolism
* Anti-inflammatory
Mineralocorticoids
* Sodium retention
* Fluid retention
31
32
What drug is high glucocorticoid and no mineralocorticoids?
Dexamethasone
33
# Tapering
What is the recommedation following prolonged use/higher doses of steroids?
Recommended following prolonged use / higher doses
* Prednisone ≥ 30 mg daily (or equivalent) for ≥ 2 weeks
* Any dose systemic steroid for ≥ 4 weeks
* Signs and symptoms of HPA suppression present
34
Why do you need to taper steriods?
Used to avoid disease flare or adrenal crisis/insufficiency (HPA suppression)
35
# LOW YIELD
What is the general taper for steroids?
36
What is the signs and symptoms of adrenal insufficiency?
37
Osteoporosis:
* What is the mechanism?
* What is less?
* Who is at higher risk of fracture?
* What is thinning?
* Osteoclasts break down bone faster than osteoblasts rebuild it
* Fewer trabeculae
* Bones with higher percentage of trabecular bone at increased risk of fracture – spine, wrist, ribs
* Cortical bone thinning
38
What is the most common casues of osteoporosis?
* Postmenopausal dt decreased estrogen
* Age related
39
How does postmenopausal cause osteoporosis?
Postmenopausal - decreased estrogen
* Increased proliferation, differentiation, and activation of osteoclasts (more breakdown)
* Increased calcium excretion (increase Ca in pee)
* Decreased calcium absorption from the GI tract
40
How is age related issues cause osteoporosis?
* Osteoblasts lose ability to form bone
* Osteoclasts retain activity
41
What are the risk factors of osteoporosis?
* Decreased estrogen
* Decreased serum calcium
* Alcohol consumption
* Smoking
* Medications (steroids, heparin)
* Physical inactivity
42
What is the t-scores and diagnostic criteria for osteoporosis?
43
Who needs to be screened for osteoporosis?
* All adults ≥ 50 years with history of fracture
* USPSTF: all women ≥ 65 years
* Endocrine society: all men ≥ 70 years
44
What is a bone healthy lifestyle?
* Weight-bearing exercises with resistance training – 30 to 40 min, three times a week
* No Smoking
* Limited ETOH
* Fall prevention
45
How much calcium should women take pre and postmenopausal?
* 1000 mg daily – premenopausal women and men 50 to 70 years of age
* 1200 mg daily – postmenopausal women and men 71 years and older
46
How much vitamin D should women and men take? What does it do?
* 600 international units/ day men and women 51 to 70 years
* 800 international units / day – men and women > 70
* Reduce bone loss and fracture rate in older men and women taking adequate calcium
47
How much protein do you need to intake for osteoporosis prevention?
0.8 g/kg/day
48
What are the high risk patients of osteoporosis?
1. Patients with osteopenia and a history of fragility fracture at the hip or spine
2. Patients with a t-score of -2.5 or less in the lumbar spine, femoral neck, total hip
3. Patients with a T-score between -1 and -2.5 if the FRAX 10-year probability of major osteoporotic fracture ≥ 20% and hip fracture ≥ 3%
49
What is the first line therapy of osteoporosis? How does it work?
Bisphosphonates
MOA:
* Reduce bone resorption by:
* Stimulating osteoclast apoptosis
* Decrease cholesterol synthetic pathway which decreases osteoclast function
| Osteoclasts are either killed or unfunctional
50
What is the pharmacokinetics of bisphosphonates?
Bioavailability poor - < 1%
* Worse with concomitant food intake
Amount absorbed
* 50% eliminated renally
* 50% remains for months to years
51
What are the side effects of bisphosphonate?
* **Esophagitis**
* **Esophageal irritation**
* **Heartburn**
* **Abdominal pain**
* **Diarrhea**
* Hypocalcemia
* Renal dysfunction
* **Osteonecrosis of the jaw** – rare, prolonged, high doses, invasive dental procedures ⭐️
* Flu-like symptoms (fever, muscle aches) with IV therapy
52
Bisphosphonates:
* What are the oral medicine?
* What should you do to increase bioavailability and decrease SE?
Oral (alendronate, risedronate, ibandronate)
* Take on empty stomach in the morning – increases poor bioavailability
* Full glass of water
* Remain upright for at least 30 minutes
53
What are the IV bisphosphonates?
Intravenous
* Zoledronic acid
* Pamidronate
54
What are drug holidays for bisphosphonates?
* After 3 to 5 years treatment – patients mild to moderate fracture risk
* After 6 to 10 years – patients at high fracture risk
* ≤ 5 year holiday with BMD Q 2 to 4 years
| You can stop taking the medicine
55
What are the second line treatments of osteoporosis?
* Denosumab
* Ralonifene
* Teriparatide
| Patients who cannot tolerate or have contraindications bisphosphonates
56
How are specific agents determined for osteoporosis?
Specific agent depends on patient co-morbidities, T-scores, adverse effects, patient preference
57
What is densumab used for?
Patients at **high risk** for fracture (eg, osteoporosis by BMD in the absence of fragility fracture, T-score >-2.5 with a fragility fracture, single vertebral fracture)
| Osteoporosis
58
What is raloxifene used for?
Patients with no history of fragility fractures, especially in women at high risk for breast cancer
| osteoporosis
59
What is teriparatide used for
Patients at very high risk of fracture (eg, T-score of ≤-3.5, T-score of ≤-2.5 plus a fragility fracture, severe or multiple vertebral fractures)
| osteoporosis
60
What is the mechanism of action and CI for denosumab, teriparatide and raloxifene?
61
What are the adverse effects and specific features of denosumab, teriparatide and raloxifene?
62
Osteoporosis
* What do you need to obtain after therapy?
* When does less frequent monitoring for osteoporosis occur?
* Obtain a follow-up dual-energy x-ray absorptiometry (DXA) of the hip and spine after two years
* Less frequent monitoring if BMD better or stable
63
What do you need to evaluate the patient for if they have clinically significant BMD decrease or a new fracture after therapy?
Evaluate patient for:
* Poor adherence
* Inadequate gastrointestinal absorption
* Inadequate intake of calcium and vitamin D
* Development of a disease or disorder with adverse skeletal effects.
64
What do you need to do with patients who have a decrease in BMD (<5 percent) no discernible contributing factors after osteoporosis treatment?
* Continue the same therapy and repeat BMD two years later OR
* Switch therapies
65
What is the treatment goals of osteoarthritis?
* Minimize pain
* Optimize function
* Slow the process of joint damage
66
What is the the mainstay of OA management and should be tried first?
Nonpharm interventions:
* Weight management and exercises
* Physical therapy for knee OA; not effective for hip OA
* Braces and foot orthoses not recommended
* Glucosamine / chondroitin not recommended
67
What is the first line therapies for OA?
* Acetaminophen
* Topical NSAIDS
* Systemic NSAIDS
* Capsaicin
68
why is acetaminophen given as a first line for OA?
Acetaminophen less effective than NSAIDs but initial trial
appropriate given superior safety profile
69
Why is topical NSAIDs use as a first line for OA after acetaminophen?
Topical NSAIDS (e.g., diclofenac) moderately effective
* Trial recommended for minimal joint involvement (knee)
* Recommended over systemic NSAIDs for patients ≥ 75 years of age
70
Why are systemic NSAIDs given as a first line drug for OA after acetaminophen and topical NSAIDs?
* Systemic NSAIDs effective; give at lowest effective dose to minimize side effects; as needed dosing appropriate
* Patients < 75 years
* Patients at low risk for gastrointestinal or cardiovascular events
71
What drug is used for hand osteoartrisitis only?
Capsaicin
72
* What are the drugs are second line of OA? Explain why you use them
Tramadol
* Patients not responding to acetaminophen, NSAIDs (alone or in combination)
* Patients with high GI or CV risk
* Minimal role for other opioids
Duloxetine
* Moderate efficacy for knee OA
* Add on therapy for patients with low to moderate response to first-line therapies
73
What can be used as first line for OA if local ?
Intra-articular corticosteroid injections
* Patients not responding to acetaminophen, NSAIDs (alone or in combination)
* Improve function and provide short-term pain control; no improvement in QOL
* Triamcinolone or methylprednisolone
* Frequency – every 3 months
* Risk of greater cartilage loss
74
What is last line for OA?
Surgery
* Last line therapy
* Improve function and provide pain relief for patients with moderate to severe pain and radiographically confirmed OA
75
For RA, what is the disease process?
76
What are the different types of DMARDs? (synthetic and biologic)
77
What is the first line for RA? And how does it work?
Methotrexate
* Inhibits tetrahydrofolate reductase; inhibits DNA synthesis / cell proliferation
* Primarily rapidly dividing inflammatory cells
78
# methothrexate
What are the contraindications, SE and what do you need to mointor?
79
What is the moa, contraindication, SE and monitoring needed for Lefluomide?
For RA-synthetic DMARDs
80
What is the DOC for pregnancy for RA-synthetics?
* What are the SE and what do you need to monitor?
81
What is the sulfasalazine's MOA, contraindication, SE and monitoring?
RA-Synthetic DMARDs
82
# LY
Jannus Associated Kinase (JAK) inhibitors – tyrosine kinase inhibitors
* How does it work?
* What is an example?
* What are the side effects?
83
What are antibodies and what are monoclonal antibodies?
Monoclonal antibodies: antibobies made in the lab that target certain receptors
84
What are the sites of action for Rituzimab, Tocilixumab, abatacept, and anakinra?
85
RA-biologic DMARDs:
* What is there is increase risk of?
* What do you need to screen for?
* What do you need to give before therapy?
* What do you not give during therapy?
Increased risk of infection – reactivation of TB / varicella zoster
* Screen patient for TB, hepatitis B and C, HIV, and vaccine status prior to initiation
* Give appropriate vaccination before therapy initiation
* Give influenza and pneumococcal vaccines as needed during therapy
* Do not give live vaccines during therapy
86
RA-biologic DMARS:
* What do you need to monitor for?
* Regimen may require holding depending on what?
* What is a common reaction?
* Monitor patient closely for signs / symptoms of infection
* Regimen may require holding depending on severity of infection
* Infusion reactions common – patients may require premedication and rescue medication
* Hydrocortisone - diphenhydramine - epinephrine
87
What is the same across the board for biologic DMARDs for RA?
ALL are subcutanous or IV
88
How do you figure out the severity of RA?
Severity
* Multiple methods to determine
* Disease Activity Scale (DAS – 28)
* Number of swollen joints
* ESR or CRP level
* Global Patient Health Score (0 to 100)
* < 2.6 = remission
* 2.6 to 3.2 = low
* > 3.2 = moderate to severe
89
What are the treatment goals of RA?
Treat to target
* Remission
* Low disease activity
90
How do you give inital symptomatic relief as a bridging therapy for RA?
NSAIDS and / or steroids
* **Rapid onset of action**
* Control inflammation and decrease pain
* NSAIDS do not modify disease process
* Steroids considered disease modifying antirheumatic drugs (DMARDs) but risk of long-term use outweigh benefits
## Footnote
Symptom relief but does not control disease progression
91
How do you control the disease progression of RA?
DMARDS
* Inhibiting immune response and blocking proliferation endothelial cells and fibroblasts at involved joint
* Specific mechanisms vary
* **Slow onset of action – weeks to months**
* Stop or slow the disease process – remission is possible
## Footnote
NSAIDs+steroids with DMARDs then tapper off steroids
92
What is the first line of RA?
Methotrexate
* Oral administration conditionally preferred over subcutaneous injection
93
For RA treatment:
* What is not recommended?
* Why is methotrexate recommended?
* What is there strong evidene of?
* What is methotrexate similar to?
* HCQ and SSZ not recommended – limited disease modifying effects
* Easy dosing/inexpensive since once a week
* Strong evidence supporting use in combination therapy
* Similar efficacy to biologic DMARDS with better safety profile and lower financial burden
94
When should you do monotherapy and combination therapy for RA?
* Monotherapy appropriate if low disease activity
* Combination DMARD therapy if moderate to high disease activity
95
What is also added for initial therapy for moderate to high RA?
Glucocorticoids
* Short-term therapy recommended in addition to DMARD therapy for patients who require for symptom resolution
* Therapy initiation
* Disease flairs
* Toxicity > benefit for long-term use in all patients
* Long-term therapy NOT recommended
* Lowest dose for shortest time
96
What is the second line monotherapy for RA? What is the dual therapy?
Second-line monotherapy - biologic or tofacitinib
* No specific biologic recommended
Dual therapy (add bio to methotrexate)
* May be required for patient with moderate to high disease activity
* MTX + biologic DMARD
* MTX + tofacitinib
97
RA:
* What is triple therapy?
* All therapies have what?
* Choice of drug depends on what?
* When switching therapies for lack of efficacy, what do you do?
**Triple therapy** = MTX/HQ/SSZ
**All therapies with similar long-term outcomes**
* Choice dependent on resource setting and patient comorbidities
* When switching therapies for lack of efficacy; switching to biologic DMARD of different class recommended
98
What is the treatment for Juvenile idiopathic arthritis (JIA)- Oligoarthritis?
99
What is the treatment for juvenile idiopathic arthritis (JIA)-Polyarthritis?
100
What are the non-pharmacotherapy and first line therapy for acute gout flare?
Non-pharmacotherapy:
* Ice / rest
First-line pharmacotherapy:
* NSAIDs – any NSAID is appropriate; including COX-2 specific agents
* Systemic corticosteroids – prednisone most common but could use alternatives
* DOC if NSAID contraindications
* Colchicine
101
What are the second line therapy for acute gout flare?
Intra-articular corticosteroids – monoarticular disease, rule out septic arthritis
102
* What is the treatment (dosages)?
* When should you consider switching drugs?
103
Colchicine:
* What is the MOA?
* When most effective?
* Anti-inflammatory – disrupts microtubule formation preventing activation, degranulation, and migration of neutrophils
* Most effective when started within 36 hours of symptom onset
104
What is the contraindications of colchicine?
P-glycoprotein or strong CYP3A4 inhibitors – mostly protease inhibitor used for the treatment of HIV (e.g., ritonavir)
105
What are the adverse reactions of colchicine?
* Diarrhea
* Nausea / vomiting
* Pharyngolaryngeal pain
* Bone marrow suppression (leukopenia, granulocytopenia, thrombocytopenia, aplastic anemia)
| GI SE!!!!!!
106
What are the lifestyle modifications for chronic treatment of gout?
107
When is urate lowering therapy recommended or not recommended for chronic gout?
**Urate lowering therapy (ULT) strongly recommended for patients with:**
* ≥ 1 subcutaneous tophi
* Radiologic evidence of damage attributed to gout
* ≥ 2 acute gout flares/year
**Urate lowering therapy (ULT) conditionally recommended for patients with:**
* Greater than one but less than two acute gout flares/year
**Urate lowering therapy (ULT) NOT recommended for patients after first flare except for under specific circumstances – see guidelines**
108
What is the first line therapy and alternative therapies for chronic treatment?
First line therapy: Allopurinol
* All patients – including those with stage ≥ stage 3 CKD
Alternative therapies
* Febuxostat
* Probenecid
* Colchicine
109
# GOUT – CHRONIC TREATMENT (ULT)
* When should chronic gout treatment be started?
* What is concomitant initial therapy with?
* What is target uric acid levels?
**All therapies should be started after resolution of acute gout flare**
* Concomitant initial therapy with anti-inflammatory prophylaxis for 3 to 6 months is strongly recommended (low dose colchicine or NSAIDs)-> because increase risk of acute flare
* Doses should be increased to a target serum uric acid level of <6mg/dL
110
Hyporicemics:
* What are the exampes and what is the MOA?
* What are the SE?
Allopurinol and febuxostat:
* Decrease formation of uric acid by inhibiting xanthine oxidase
Allopurinol side effects:
* Rash
* Acute gout flare
* Nausea/vomiting
* Hepatic failure/hepatic necrosis
111
Uricosurics:
* What are the examples?
* What is the MOA?
* Increase risk of what?
Probenecid and sulphinpyrazone
* Decreased uric acid reabsorption from the kidneys by competing for uric acid transporter
* Increased risk of kidney stone formation
112
Pseudogout:
* What are the non-pharmcotherapy txt?
* What is the pharmcotherapy for acute flare? Chronic ?
113
What are the treatment goals of reactive arthritis?
* Identify triggering infection STD
* Treat ACTIVE infection (ex. STI)
* Prompt treatment of organism can prevent initiation and persistence of arthritis
* Less evidence for treating of post-enteric infections (GI bug)
114
# Reactive arthritis?
When treating of organism can prevent initiation and persistence of arthritis, what is the treatment for PRC positive chlamydial infections?
Best data PCR positive Chlamydial infections
* Prolonged treatment (3 to 6 months) recommended
* Doxycycline + rifampin OR azithromycin + rifampin
* Symptom remission and PCR negativity
115
What is first line, second line txt of reactive arthritis?
First-line NSAIDs
* Two to 4-week trial on full dose prior to changing NSAIDs
Second-line glucocorticoids - patients who do not respond to NSAIDs
* Intra-articular preferred for mono or oligoarthritis
* Systemic treatment indicated for patients with polyarthritis
* Three to 6-month trial before moving to next step
116
What are the symptoms for reactive arthritis?
117
What is the treatment for chronic forms for reactive arthritis?
* Conventional systemic DMARDs – methotrexate / azathioprine
* Biologic DMARDs – etanercept / infliximab
| Reactive into chronic
118
What are the treatment goals of fibromyalgia?
* Confirm diagnosis
* **Patient education KEY**
* Evaluate and treat / control the major symptoms § Chronic widespread pain
* Fatigue
* Insomnia
* Cognitive dysfunction
* **Goal = improve quality of life**
119
* What are the symptoms of fibromyalgia?
* How should treatment be dealt with?
Treatment should be individualized, multidisciplinary, and involving both nonpharmacologic and pharmacologic therapy in most patients
120
What are the non-pharm treatments for FM?
* Acupuncture
* Biofeedback
* Cognitive behavioral therapy
* Exercise
* Hypnotherapy
* Massage
* Meditation
* Guided imagery
121
Fill in the pharmacotherapy for FM
122
What is polymyositis and dermatomyositis?
123
What is inital therapy for polymyositis?
124
What are additional therapies and what do you need monitor for polymyositis?
125
What is polymyalgia rheumatica?
126
What is the initial therapy of POLYMYALGIA RHEUMATICA?
127
What are additional therapies and what needs to be monitor for POLYMYALGIA RHEUMATICA?
128
What is POLYARTERITIS NODOSA (PAN)?
129
What is the initial therapy of PAN (servere and non-severe)
Methylpresidone
130
What are adiitional therapies and monitoring needed for PAN?
131
What is the treatment for Sjogren's
* **Mainly symptomatic with goal of keeping mucosal surfaces moist**
* **Artificial tears or saliva, increased hydration, ocular and vaginal lubricants**
* **Pilocarpine improves symptoms by stimulating the exocrine glands**
* Cyclosporine may improve ocular symptoms
* Hydroxychloroquine-may help arthralgias
* Glucocorticoids-not effective for sicca symptoms but may have role in treatment of extraglandular manifestations
132
SJOGREN’S DISEASE – SICCA SYMPTOMS
133
Cyclosporine (restasis):
* What does it cause?
* What type of drug is it?
* How much time do you need to wait inbetween eye drops?
* Increase tear production in keratoconjunctivitis sicca-associated ocular inflammation
* Immunomodulator / anti-inflammatory
* Inhibition of T-cell activation
* Allow ≥15mins between dosing of lubricant eye drops.
134
What are the adverse reactions of cyclosporine (restasis)
* Ocular burning
* conjunctival hyperemia
* Eye pain
* Foreign body sensation
* Pruritus, stinging, blurring
135
PILOCARPINE (SALAGEN):
* What does it cause?
* What are contraindications?
* What are precautions?
Cholinergic agonist; increases secretion of exocrine glands
Contraindications:
* Uncontrolled asthma
* Miosis undesirable (iritis, acute angle- closure glaucoma)
Precautions:
* Severe hepatic impairment
136
PILOCARPINE (SALAGEN):
* What are the interactions?
* What are adverse reactions?
Interactions:
* Cardiac conduction disturbances with β- blockers.
* Antagonizes anticholinergics (eg, atropine, ipratropium)
Adverse Reactions:
* Sweating
* Nausea
* Rhinitis
* Flushing
* Urinary frequency
* Abnormal vision
137
Scleroderma symptoms?
138
Scleroderma:
* Is there a cure?
* How is treatment individualized?
* What is the goal?
* Multiple specialist involvement due to what?
* Treatmet is aimed at what?
139
SCLERODERMA – RAYNAUD’S:
* What do you need to educate your patient on?
* What is first line therapy?
Reduce frequency and severity of attacks
Patient education:
* Smoking cessation
* Cold avoidance
* Avoid vasoconstricting medications
First-line therapy:
* Calcium channel blockers (dihydropyridine-type)
* Ex: Nifedipine or amlodipine
140
What is the MOA for calcium channel blockers?
* Bind to and blocks voltage-gated calcium channels
* Calcium does not enter the cell
* No depolarization
* Muscle does not contract
* Vasodilation
141
What are the symptoms of lupus?
142
What is the goals of lupus?
* Improve long-term survival
* Prevent organ damage
* Prevent disease flares
* Optimize quality of life
* Complete remission rare
Most patients can obtain partial remission / low disease activity in all or most organs
143
# LY
What is mild, moderate, severe lupus?
Based on systemic lupus erythematosus disease activity index
144
What is the adjunct, treatment of non renal systemic lupus erythematosus? What are the goals?
145
What is first line of SLE?
First-line (Grade A):
* Hydroxychloroquine (DMARD)
* Glucocorticoids (e.g., prednisone)
* Rapid symptom control
* Short-term therapy recommended or daily dose of ≤ 7.5 mg/day
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What is second line of SLE?
Methotrexate or azathioprine
* Methotrexate more effective
* Azathioprine compatible with pregnancy
Cyclosporine (CNI)
Mycophenolate mofetil
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What is the txt for patients with SLE and extra renal disease? What is the MOA?
Belimumab (Grade A moderate refractory)
* MOA: B-lymphocyte stimulator antagonist
* Recommended for:
* Patients with inadequate control of extra renal disease
* Ongoing disease activity or frequent flare
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Belimumab is more likely to respond in patients with what?
* SLEDAI score > 10
* Prednisone dose > 7.5mg/day
* High complement levels
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What are drugs that are high and low risk of drug induced lupus?
150
Drug induced lupus:
* What are the clinical features?
* When does it start?
* All patients ahve what?
* Improvement when?
* Clinical features predominantly constitutional, joint, & pleuropericardial
* Rare CNS & renal disease
* Months to years after starting offending agent
* ALL patients have antinuclear antibodies (ANA)
* Improvement following withdrawal of offending drug
