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Year 2 PODT > Musculoskeletal conditions and inflammation > Flashcards

Musculoskeletal conditions and inflammation Flashcards

1
Q

describe the control in endocrine hormone systems

A

see corticosteroid lecture slide 4

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2
Q

describe the Hypothalamic-Pituitary-Adrenal (HPA) Axis

A

see corticosteroid lecture slide 5

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3
Q

Contrast Gluco versus Mineralocorticoid actions

A

-both produced from the adrenal cortex (zones??)

  • both bind to specific receptors in the body
  • Glucocorticoid receptor: widely expressed
  • Mineralocorticoid receptor: mainly expressed in epithelial cells in kidney, colon, bladder
  • glucocorticoids widely used in as anti-inflammatory drugs in medicine (see rest of lecture)
  • mineralocorticoids such as aldosterone regulate electrolyte balance in the kidney (e.g. fludrocortisone used in Addison’s disease)
  • Glucocorticoids have low activity in the kidney due to the action of the enzyme 11-b-hydroxysteroid dehydrogenase which inactivates GCs
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4
Q

give some examples of steroids both glucocorticoids and mineralcorticoids say their mode of action

A

Glucocorticoids: - hydrocortisone
- prednisolone, deflazacort Betamethasone, dexamethasone (potent) Beclomethasone (asthma)

  • Bind to the Glucocorticoid Receptor in the cytoplasm (widely expressed)
  • Anti-insulin

Mineralocorticoids:
- aldosterone, fludrocortisone

-Bind to the mineralocorticoid receptor expressed mainly in kidney,
epithelial cells of colon and bladder, regulate electrolyte balance

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5
Q

what is the precursor for mineralocorticoids and glucocorticoids

A

cholesterol

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6
Q

describe the properties of the glucocorticoid receptor

A

see corticosteroid lecture slide 11

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7
Q

How does the activated Glucocorticoid Receptor identify its target genes in the nucleus?

A

-GC receptor dimers bind to specific hormone response elements (HREs) on target genes

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8
Q

what are the actions of glucocorticoids

A
  1. Metabolic
  2. Anti-inflammatory
  3. Immunosuppressive
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9
Q

what happens when there’s too much corticosteroids and what happens when there’s too much corticosteroids

A

see corticosteroid lecture slide 16

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10
Q

describe the metabolic effects of glucocorticoids

A

“protecting glucose-dependent tissues (brain and heart) from starvation”

  • effect carbohydrate and protein metabolism
  • Liver: decrease glucose uptake and utilization increase gluconeogenesis
  • tendency towards hyperglycemia
  • Decreased protein synthesis andIncreased protein breakdown - cushings disease
  • provides amino acids and glycerol for gluconeogenesis
  • Long-term use can lead to fat redistribution (Cushing’s Syndrome)
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11
Q

describe the clinical use of glucocorticoids

A
  • Replacement therapy for Addison’s disease (adrenal failure)
    hydrocortisone (GC), fludrocortisone (MC)
  • anti-inflammatory/immunosupressive therapy
    prednisolone, dexamethasone
  • asthma: beclometasone (inhalation) ICBA2
  • eczema }
  • allergic conjunctivitis
  • rhinitis
  • autoimmune disease-rheumatoid arthritis, inflammatory bowel disease
  • transplant patients to prevent graft v host reactions

used in cancer:

  • combination with cytotoxic drugs e.g. Hodkins, leukemia
  • reduce cerebral oedema in patients with brain tumor (dex)
  • anti-emetic therapy in conjunction with chemotherapy - weight gain to stimulate appetite (cachexia)
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12
Q

Give details of the uses of steroids to treat rheumatoid arthritis and other muscle/bone inflammation

A
  • Rheumatoid Arthritis
  • Systemic Lupus Erythematosus (SLE) -Juvenile Idiopathic arthritis
  • all autoimmune diseases of joints, connective tissue etc.
  • treatment with supraphysiological doses of steroids reduces inflammation

How do corticosteroids reduce inflammation in SLE/RA?

  • steroids suppress all phases of early inflammation
  • decrease in numbers of activated macrophages, T-cells especially T-helper (CD4+) cells
  • decreased IL-1, IL-2 production (lymphocyte activators)
  • decreased transcription of COX-2, PLA2, IL-2R (mediators of inflammation) via inhibition of AP-1, NFkB signalling
  • suppression of chronic inflammation
    a) increased annexin-1 (lipocortin) levels in leukocytes, inhibition of phospholipase A2
  • reduced arachadonic acid levels
  • reduced prostaglandin, leukotriene levels
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13
Q

List the common side-effects of steroids, and the features of Cushing’s syndrome

A

Side-Effects/Adverse Drug Reactions of Glucocorticoids:

  • mainly due to large doses and prolonged administration
  • exogenous GC suppress normal H-P-A response to illness
  • withdrawal from GC needs to be phased
  • patients need to carry a steroid card alerting doctors to the fact that they are on steroid therapy

Main side-effect of glucocorticoids is suppression of the HPA axis

side effects see slide 32 corticosteroid lecture

Adverse effects:

Physiological:

  • Adrenal and/or pituitary suppression
  • Pathological

Cardiovascular;
Increased blood pressure Gastrointestinal
Peptic ulceration exacerbation (possibly)
Pancreatitis Renal
Polyuria
Nocturia Central nervous
Depression Euphoria Psychosis Insomnia
Endocrine
Weight gain Glycosuria/hyperglycaemia/diabetes Impaired growth in children
Bone and muscle
Osteoporosis
Proximal myopathy and wasting Aseptic necrosis of the hip Pathological fractures
Skin
Thinning
Easy bruising Eyes
Cataracts (including inhaled drug) Increased susceptibility to infection
(signs and fever are frequently masked) Septicaemia
Reactivation of TB
Skin (e.g. fungi-oral thrush)

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14
Q

Why do glucocorticoids cause osteoporosis?

A
  • osteoporosis and increased fractures seen with steroid therapy
  • important to consider when using e.g. prednisolone
  • GCs regulate Ca2+/PO4– metabolism
  • GCs regulate collagen synthesis by osteoblasts
  • GCs inhibit Vit D3 induction of genes in osteoblasts
  • GCs inhibit osteoblasts (bone formation) and activate osteoclasts (digestion of bone matrix)
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15
Q

what causes cushings syndrome

A
  • arises from excess circulating glucocorticoids
  • mainly caused by increased circulating levels of GC or ACTH
  • ACTH from pituitary (65 % of cases-Cushing’s Disease)
  • ACTH from non-pituitary tumor (10 % of cases)
  • excess secretion of GC from adrenal tumor (25 % of cases)
  • suppression of ACTH secretion
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16
Q

name some Important NSAIDs commonly in use in medicine

A
  • aspirin
  • ibuprofen
  • Naproxen (Alleve)
  • Indomethacin-powerful NSAID with wide ranging use/side-effects -Diclofenac
  • Paracetamol
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17
Q

describe the mechanism of action of NSAIDs

A

reduce inflammatory response and pain

-NSAIDs work by inhibition the action of cyclooxygenase (COX) enzymes -2 main isoforms: COX-1 and COX-2

  • NSAIDs work by inhibiting COX enzymes, lowering levels of prostaglandins e.g. PGE2, PGI2
  • Prostaglandins cause:
  • vasodilation
  • oedema
  • pain (increasing Bradykinin-mediated nociception)

General Rule of Thumb:

  • Majority of anti-inflammatory effects of NSAIDs occur via COX-2 inhibition
  • Most side-effects of NSAIDs occur via COX-1 inhibition
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18
Q

Appreciate the different roles of COX-1 versus COX-2 inhibition

A

-2 main isoforms: COX-1 (constitutively active) COX-2 (inducible)

COX-1:

  • expressed in most tissues including platelets general “housekeeping” COX enzyme
  • Prostaglandins produced by COX-1 involved in
    a) protection of gastric mucosa
    b) platelet aggregation
    c) renal blood flow autoregulation

COX-2:
- inducible form of enzyme
expressed in activated inflammatory cells e.g. basophils, eosinophils

Other points to consider:

  • COX-1 and COX-2 have approximately 60 % sequence identity
  • both have similar ability to induce arachidonic acid oxidation
  • differences in COX tissue expression define their different roles/side-effects
  • most NSAIDS are non-selective between COX-1 versus COX-2
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19
Q

List the main medical uses of NSAIDs

A
  • anti-inflammatory
  • analgesic
  • anti-pyretic

also:

Anti-platelet: Aspirin (COX-1 inhibition)

  • Stroke prevention
  • MI prevention
  • Unstable angina
  • Deep venous thrombosis (DVT) prevention

Colon cancer prevention:
- low dose, long-term (5 years) aspirin may reduce the risk of colon and other GI cancers - not sure how this works

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20
Q

what are the main side effects of NSAIDs

A
  • gastric irritation
  • compromised renal blood flow
  • increased bleeding
  • increase risk of MI (COX-2)
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21
Q

describe the mode of action of NSAIDs as anti-inflammatory drugs

A

Anti-inflammatory-NSAID inhibition of COX-2 predominantly

NSAIDs: decreased PGE2, PGI2 levels which:

  • decreases blood flow
  • decreases pain
  • decrease swelling

Clinically useful in:

  • Inflammatory arthritis
  • Dental pain
  • Oro-facial pain
  • Post operative pain
  • Bone metastases in cancer

NB-NSAIDs have no effect on the disease causing the inflammation e.g. RA

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22
Q

describe the mode of action of NSAIDs as analgesic drugs

A

Analgesic-mild/moderate pain due to inflammation or tissue damage

Mechanism:
i) decreased Prostaglandins, reduced sensitization of Bradykinin nociception (reduced pain reception)

  • Effective in arthritis, muscle pain, toothache, dysmenorrhea postpartum pain, cancer metastasis in bone pain
  • Headache: NSAIDs reduce PG-induced vasodilation in brain
  • reduce postoperative pain, reduce the amount of opioids needed by up to 30 %
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23
Q

describe the mode of action of NSAIDs as anti-pyretic drugs

A

Anti-pyretic: decreased PG production in the hypothalamus

“NSAIDs reset the bodies thermostat” (paracetamol primarily used)

How?
- not sure - could be -vasodilation, sweating (COX-3) - NB-no effect on normal body temperature

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24
Q

list some side effects of NSAIDs

A
  • high burden of side-effects with NSAIDs
  • due to the inhibition of COX activity and PG production in non-inflammatory tissues
  • common side-effects include:
  • GI disturbances*
  • Adverse Renal Effects*
  • Rashes
  • CNS effects
  • Bone Marrow effects
  • Aspirin sensitive asthma
  • Liver toxicity (paracetamol)
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25
Q

describe GI disturbances with NSAIDs

A

Gastrointestinal Disturbances-perforations, ulcers, bleeds
- diarrohea, constipation, nausea, vomitting also common
-occurs in approximately 1/3 of patients taking NSAIDs
- approx 100,000 people in the USA hospitalised as a result of GI effects of NSAIDs
- 15 % of these people die-tend to be older patients taking NSAIDs for arthritis
- Cause: NSAIDs inhibit gastric COX-1 which generates PGE2 that stimulates mucus production and inhibits acid secretion from the parietal cells in the stomach:
> limit this effect by giving Misoprostol which is a PGE1 analogue (avoid in pregnancy!!)
> other types of ulcer protection also used (PPIs, antacids)
ICBA 2

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26
Q

describe adverse renal effects with NSAIDs

A
  • in healthy patients, no risk to kidney function
  • patients with compromised renal function-NSAIDs can cause acute renal failure
  • neonates, elderly, heart, liver, kidney disease patients at risk of this side-effect

Cause:
- COX inhibition, reduced PGE2, PGI2 production, altered renal blood flow

  • Na+ retention, leading to hypertension
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27
Q

describe some drug interactions of NSAIDs

A
  • Increased risk of bleeding with 2 NSAIDs especially if one is aspirin
  • Increased risk of gastro-intestinal bleeding with anticoagulants, and anti- depressants (aspirin and SSRIs ,venlafaxine)
  • Reduced effectiveness of diuretics and antihypertensive agents
28
Q

When are NSAIDS contraindicated?

A
  • Patients with peptic ulcer disease
  • Patients with a history of gastrointestinal bleeding
  • Those receiving anticoagulants
  • To be used with caution in patients with renal impairment, heart failure or hypertension
  • used with caution in pregnancy, especially during the third trimester (can cause closure of the ductus arteriosus in utero, PH in baby)
  • ibuprofen can be used to close the PDA in premature infants (JAMA)
  • Those with a previous history of allergic reactions e.g. asthma
29
Q

what is the ending for ace inhibitors

A

-pril

Enalapril Lisinopril

30
Q

what is the ending for ARBs

A

-artan

Losartan Valsartan

31
Q

what is the ending for Ca2+ channel blockers

A

Amlodipine Aranidipine

  • dipine
32
Q

what is the ending for COX-2 inhibitors

A

Celecoxib Paracoxib

  • coxib
33
Q

Describe DMARDs, giving three examples and their MOA

A

Disease-Modifying Anti-Rheumatic Drugs (DMARDs)

-diverse set of unrelated agents that have different mechanisms of action -all have the potential to improve the symptoms of rheumatoid arthritis

decrease disease severity, improve symptoms

  • decrease number of swollen joints
  • reduced pain score
  • decrease serum levels of IgG
34
Q

describe the mode of action of Methotrexate

A

Methotrexate-folic acid antagonist with immunosuppressant activity

  • used to treat Crohn’s disease
  • used as an anti-metabolite in cancer therapy, inhibits DNA synthesis
  • blocks expansion of T cells
  • potent anti-rheumatoid activity, common first-choice DMARD
  • ROA-orally, im, iv
  • 6 week onset of action
  • potential side-effects include blood disorders, liver cirrhosis, nephrotoxicity, GIT damage neural tube defects
  • long term therapy common (>5 years), most commonly used DMARD for RA - not to be used in pregnancy/avoid conception 3 months post therapy due to teratogenic effects
35
Q

describe the mode of action of Leflunomide

A

immunosuppresant drug, specific inhibitor of activated lymphocytes

  • Inhibitor of dihydroorotate dehydrogenase, blocks pyrimidine production
  • blocks clonal expansion of T-cells, other cells can bypass this blockade
  • well absorbed orally, long half-life (4-28 days)
  • main s/e are anaemia, hepatotoxicity, diarrohea, nausea
  • blood monitoring essential
  • onset of action in 4 weeks
  • can be given to patients who don’t respond to MTx
  • contraindicated in pregnancy, breast feeding
  • Needs a 2 year wash out period, best avoided in premenopausal women
36
Q

describe the mode of action of Anti-tumour necrosis factor-a (TNFa) antibodies

A
  • Infliximab-monoclonal antibody against TNFa
  • Etanercept-recombinant TNFa receptor-IgG fusion protein
  • used for RA, Crohn’s Disease
  • NICE guidelines - use these drugs after at least 2 DMARDs have been tried
  • Infliximab used in combination with MTx
  • If MTx cant be used due to C/I, use etanercept as monotherapy
  • Major therapeutic advance in the treatment of rheumatoid arthritis
  • s/e include reactivation of TB, increased infections
  • very expensive drugs: one year of therapy costs about £20,000 per patient
37
Q

describe the mode of action, classification, indications and adverse effects of paracetamol

A

analgesic L , s 10

Classification: analgesic, antipyretic, misc. not an NSAID

Mechanism: inhibits prostaglandin synthesis via CNS inhibition of COX3 (not peripheral)— doesn’t promote ulcers, bleeding or renal failure; peripherally blocks generation of pain impulses, inhibits hypothalamic heat-regulation center

Mode of action:

  • Analgesic
  • Weak prostaglandin inhibitor

Indications:
- Mild to moderate pain without inflammation

Adverse effects:

  • Rare at normal dosage
  • Caution in liver impairment/low body weight
  • Liver/renal toxicity in over dosage
38
Q

describe the pharmacological effects of opioids

A

Sedation and anxiolytic:

  • Drowsiness and lethargy
  • Apathy
  • Cognitive impairment
  • Sense of tranquility

Depression of respiration:

  • Main cause of death from opioid overdose
  • Combination of opioids and alcohol is especially dangerous

Cough suppression:
- Opioids suppress the “cough center” in the brain

Pupillary constriction: pupillary constriction in the presence of analgesics is characteristic of opioid use

Nausea and vomiting:

  • Stimulation of receptors in an area of the medulla called the chemoreceptor trigger zone causes nausea and vomiting
  • Unpleasant side effect, but not life threatening

Gastrointestinal symptoms:
- Opioids relieve diarrhoea as a result of their direct actions on the intestines

Other effects:

  • Opioids can release histamines causing itching or more severe allergic reactions including bronchoconstriction
  • Opioids can affect white blood cell function and immune function
39
Q

describe the mechanism of action of opioids

A

Activation of peripheral nociceptive fibers causes release of substance P and other pain-signaling neurotransmitters from nerve terminals in the dorsal horn of the spinal cord

Release of pain-signaling neurotransmitters is regulated by endogenous endorphins or by exogenous opioid agonists by acting presynaptically to inhibit substance P release, causing analgesia

40
Q

describe the mechanism of action of opioids

A

analgesic lecture slide 17

Activation of peripheral nociceptive fibers causes release of substance P and other pain-signaling neurotransmitters from nerve terminals in the dorsal horn of the spinal cord

Release of pain-signaling neurotransmitters is regulated by endogenous endorphins or by exogenous opioid agonists by acting presynaptically to inhibit substance P release, causing analgesia

41
Q

describe the target, action, effect and overall effect of morphine

A

Target: G-protein coupled opioid ‘mu’ receptors in the CNS and peripheral nervous system

Action: Full agonist (high affinity for receptors)

Effect: Closure of N-type voltage-dependent calcium channels and opening of calcium-dependent inwardly rectifying potassium channels – this increases potassium conductance. Opioids also presynaptically inhibit the release of pain-signalling neurotransmitters such as substance P.

Overall effect: Membrane hyperpolarisation and reduced neuronal excitability, reduction or inhibition of pain neurotransmission.

42
Q

describe the three types of mu-receptor opioid receptors

A

Mu-1:
- Responsible for central interpretation of pain

Mu-2:
- Responsible for respiratory depression, spinal analgesia, physical dependence, and euphoria

(Mu-3 only opioid alkaloids)

43
Q

describe kappa opioid receptors

A
  • Only modest analgesia
  • Little or no respiratory depression
  • Little or no dependence
  • Dysphoric effects
44
Q

describe delta opioid receptors

A
  • It is unclear what delta’s responsible for
  • Delta agonists show poor analgesia and little addictive potential
  • May regulate mu receptor activity
45
Q

how do you calculate the breakout dose for opioids

A

The breakthrough dose should be equivalent to a 4 hourly dose (i.e. 1/6th of the daily dose)

May need to titrate dose according to patient needs: 5% to 25% of total daily opioid dose

Generally use the same opioid as being used for regular regimen

46
Q

what are the contraindications for opioids

A

Patients with impaired pulmonary function

Patients with impaired hepatic and/or renal function

Patients with hypothyroidism

Patients with recent head injury

47
Q

list some clinical uses of opioid analgesics

A

Analgesia for severe visceral pain

Acute pulmonary edema

Cough suppression

Diarrhoea

Pre-medication

Regional anaesthesia

48
Q

what type of tolerance occurs in opioids

A

Physiological tolerance involves changes in the binding of a drug to receptors or changes in receptor transductional processes related to the drug of action

49
Q

describe cross tolerance in opioids

A

Cross-tolerance occurs with all opioids and relates to tolerance to a currently administered opioid that does not extend completely to other opioids when switching. It may lower the required dose of the second opioid.

May need to adjust switch dose down by 25-50% initially and re-titrate with the new second opioid

50
Q

describe dependence

A

Physiological dependence occurs when the drug is necessary for normal physiological functioning – this is demonstrated by the withdrawl reactions

Withdrawl reactions are usually the opposite of the physiological effects produced by the drug

51
Q

list some withdrawal symptoms associated with opioids

A

Acute Action:

  • Analgesia
  • Respiratory
  • Depression
  • Euphoria
  • Relaxation and sleep
  • Tranquilization
  • Decreased blood pressure
  • Constipation
  • Pupillary constriction
  • Hypothermia
  • Drying of secretions
  • Reduced sex drive
  • Flushed and warm skin

Withdrawl Sign:

  • Pain and irritability
  • Hyperventilation
  • Dysphoria and depression
  • Restlessness and insomnia
  • Fearfulness and hostility
  • Increased blood pressure
  • Diarrhoea
  • Pupillary dilation
  • Hyperthermia
  • Lacrimation, runny nose
  • Spontaneous ejaculation
  • Chilliness and “gooseflesh”
52
Q

name an opioid antagonist and how it works

A

Naloxone

Opioid antagonists are used to treat opioid overdose

Strong binding affinity for the Mu receptor

Work by competitive inhibition site blocking agonist activity

53
Q

describe treatment for constipation

A
  • Increase fluid intake
  • Improve mobility
  • Increased fibre intake (unless d/t opioids)
  • Stopping constipating drugs
  • Excluding underlying pathology
54
Q

list some laxatives and their methods of action

A

Macrogols: osmotic laxative

Docusate: faecal softener - increases intestinal fluid secretion

fybogel: bulk laxatives - swells and distends the colon

bisacodyl and Senna: stimulant (irritant) laxatives - stimulate the enteric nervous system

55
Q

describe management of constipation

A
  • Pre-empt constipation by putting everyone at risk (eg patients on opioids) on regular laxatives
  • Treat reversible causes eg give analgesia if pain on defecation, alter diet, ↑ fluid intake
  • Adjust any constipatingmedication, if possible.
  • Advise the person about increasingdietary fibre, drinking an adequate fluid intake, and exercise.

Offer oral laxatives if dietary measures are ineffective, or while waiting for them to take effect.

  • Start treatment with a bulk-forming laxative (Fybogel)(adequate fluid intake is important).
  • If stools remain hard, add or switch to an osmotic laxative (macrogols (Movicol))
  • If stools are soft but the person still finds them difficult to pass or complains of inadequate emptying, add a stimulant laxative (Bisacodyl, senna, (sodium picosulfate/ enema).

If the person has opioid-induced constipation:

  • Avoid bulk-forming laxatives.
  • Use an osmotic laxative (macrogols (Movicol))(or docusate which also softens stools) and a stimulant laxative (Bisacodyl, senna, (sodium picosulfate/ enema)

Advise the person that laxatives can be stopped once the stools become soft and easily passed again.

56
Q

What are Biologics?

A
  • derived from living material (plant, animal or microorganism)
  • usually based on protein and/or nucleic acid
  • used for the treatment of diseases in humans
57
Q

what are the clinical concerns with biologics

A
  • Species specificity limits standard pre-clinical models for safety testing
  • Usually injected
  • Immunogenicity:
    Macromolecules (proteins) like biologic drugs are Capable of triggering an immune response with varying but unpredictable consequences:
  • Antibodies may have no clinical effect
  • Antibodies may neutralize the molecule making it therapeutically ineffective
  • Rare but serious autoimmune responses can be life- threatening
  • Small changes in a macromolecule can completely shift its immunogenicity profile
58
Q

what do cytokines do?

A
  • Inflammatory effects (e.g. IL-1, TNF)
  • T and B cell regulation ( e.g. IL-2, interferon gamma)
  • Anti-inflammatory effects ( e.g. IL-4)
  • Haematopoietic effects ( G-CSF)
  • Chemo attractant activity (> 50 cytokines termed chemokines due to ability to influence movement of immune cells
59
Q

Medicines that Affect Cytokines

A

• TNF antagonists
• Interleukin antagonists
• Monoclonal antibodies (mab) when used as medications given generic name ending in - mab
• Antecedent u (-umab) = human antibody
• Antecedent xi (- ximab) = mixed human/murine (chimeric) Antibody
Fusion proteins end in – cept e.g. Ertanercept (anti-TNF)

60
Q 
• Recognise the class of biological agent based on
standard nomenclature rules
A

• Monoclonal antibodies (mab) when used as medications given generic name ending in - mab
• Antecedent u (-umab) = human antibody
• Antecedent xi (- ximab) = mixed human/murine (chimeric) Antibody
- Fusion proteins end in – cept e.g. Ertanercept (anti-TNF)

61
Q

How are the new biologic drugs used?

A
  • Must be given by injection - they are proteins
  • Must be monitored closely - potential side effects
  • Must be used long term – NOT a cure- stopping therapy
  • can cause disease flare
  • Initiate after non-biologic DMARDs have failed to work
62
Q

Benefits of Anti-TNF Drugs

A

• Decrease disease activity by 20-70%
• Decrease blood markers of inflammation
• Improves strength and patient vitality
• May induce complete disease remission – 15%
• Prevents progression and permits healing of radiographic bone
damage

63
Q

Adverse Effects of Biologic Therapy

A

• Local site reactions/allergic reactions
• Infection-unusual organisms-tuberculosis, fungi, listeria-monitor
regularly
• Blood disorders-low WBC, platelets
• Liver toxicity
• Induced auto-immune diseases – SLE, MS
• Malignancy-lymphomas

64
Q

Biologic Therapy: Major Safety Issues

A
  • Infections
  • Infusion/injection-sitereactions
  • Autoimmunediseases
  • Malignancy
  • Immunogenicity,blockingantibodies
  • Use in pregnancy
  • Use in patients with congestive heart failure
  • Use in patients with cardiovascular diseases
65
Q

risk factors for serious infections in rheumatoid arthritis

A

biologics lecture slide 39

66
Q

Autoimmune diseases induced by biologics

A

don’t need to know all

  • SLE or lupus-like syndromes
  • Vasculitis
  • Psoriasis
  • Sarcoidosis
  • Demyelinating CNS Disease
  • Demyelinating peripheral neuropathies
  • Antiphospholipid syndrome or APS-like features
  • Interstitial lung diseases
  • Ocular Autoimmune Diseases
  • Autoimmune Hepatitis
  • Inflammatory myopathies

Year 2 PODT (14 decks)

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