Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Renal and CT > Flashcards

Renal and CT Flashcards

1
Q

Diuresis

A

increase in urine flow (mL/min) = UV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Natriuresis

A

increase in urinary sodium exctretion (UNaV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Kaliuresis

A

increase in urinary potassium excretion (UKV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Chloruresis

A

increase in urinary chloride excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Bicarbonaturia

A

increase in urinary bicarbonate excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Renin

A
  • from JG cells in afferent arteriole ⇒ angiotensin II
  • increased with sympathetic stimulation, renal hypoperfusion, ↑ cAMP, ↓ angII, ↑ intracellular Ca
  • renin-angiontensin system activated by diuretics.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Aldosterone

A
  • released from zona glomerulosa in adrenal gland.
  • ⇒ ↑ Na reabsorption via ENaC in distal nephron.
  • ↑ aldosterone whenever renin is ↑
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ADH

A
  • released from posterior pituitary gland when have ↑ plasma osmolality, ↓ BP
    • influenced more by osmolality than BP
  • ⇒ ↑ water reabsorption in collecting duct via V2 receptor stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ANF (Atrial Natriuretic Factor)

A
  • released from atrium in resopnse to volume expansion.
  • can ⇒ ↑ GFR and Na and water excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Angiontensin

A
  • constricts afferent arterioles ⇒ ↓ GFR.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Inulin

A
  • marker for GFR, not a natural substance.
  • presence in urine is an indication of filtration.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Sulfonilamide

A
  • carbonic anhydrase inhibitor.
  • has sulfonamide moiety for activity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Acetazolamide

A
  • carbonic anhydrase inhibitor
  • rapid onset (30 min)
  • excreted by tubular S2 segment but acts on S1 segment.
  • inhibits 85% of proximal tubular HCO3- reabsportion
  • inhibits 45% whole kidney HCO3- reabsorption
  • inhibits NHE3 on lumenal side of proximal convoluted tubule ⇒ ↓ Na inside cell ⇒ nonfunctional Na K ATPase on interstitial side. (prevents production of H+ needed for this antiport)
  • also affects Na HCO3- symport on interstitial side from ↓ Na inside cell ⇒ ↓ HCO3- brought to blood.
  • ⇒ ↑ HCO3- excretion, ↑ urinary pH, ↑ urine volume, ↑ Na excretion, ↑ urine K+, ↑ luminal negativity (promotes K excretion)
  • uses: glaucoma - ↓ ocular pressure
    • altitutde sickness prophylaxis - ↓ CSF pH
    • short-term diuretic for edema in CHF - potentiates distally-acting agents, corrects metabolic alkalosis
    • antiepileptic in catamenial epilepsy
    • corrects metabolic alkalosis
    • alkalinates urine - ↑ solubility of uric acid and cystein, ↑ aspirin excretion, ↑ urinary phosphate excretion
  • side effects: hyperchloremic metabolic acidosis, renal stone formation, hyperkalemia
  • contraindications: in K+ depletion, pts with hepatic cirrhosis (may ↑ excretion NH4+ ⇒ hepatic encephalopathy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dichlorphenamide

A
  • carbonic anhydrase inhibitor
  • uses: glaucoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Methazolamide

A
  • carbonic anhydrase inhibitor.
  • uses: glaucoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dorzolamide

A
  • topically active for glaucoma ⇒ ↓ intraocular pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Brinzolamide

A
  • topically active for glaucoma ⇒ ↓ intraocular pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mannitol

A
  • osmotic diuretic
  • does not cross water permeable membranes, ↓ fluid reabsoprtion (proximal tubules, thick ascending limb)
  • IV only
  • causes water to leave cells, keeps nephrons patent.
  • freely filtered, not reabsorbed by kidney.
  • uses: ↓ intraocular pressure in glaucoma, ↓ intracerebral pressure, anuria states (rhabdomyolysis)
  • side effects: hypovolemia
  • contraindications: CHF = ↓ kidney function so not filtered ⇒ hyponatremia, hypervolemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Urea

A
  • osmotic diuretic
  • not orally active
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Glycerin

A
  • osmotic diuretic
  • orally active
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Isosorbide

A
  • osmotic diuretic
  • orally active
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Furosemide

A
  • loop diuretic
  • aka Lasix
  • has sulfonamide group
  • bound to plasma proteins, filtration enhanced by proteinuria
  • secreted by S2 segment of proximal tubules
  • acts from luminal side of TAL
  • dosage: 20-40mg
  • given orally or IV
    • orally: onset of action = 30 min -1hr, duration = 6-8 hr
    • IV: onest of action = immediate, duration = 2hr
  • inhibits NKCC2 ⇒ ↓ lumen pos. potential ( back-leak of K into lumen) ⇒ ↑ Na, K, Cl in urine, ↓ resoprtion Ca, Mg.
  • ⇒ ↓ venous capacitance, ↓ concentrating ability (↓ NaCl reabsorption in medullary TAL), ↓ diluting ability (↓ NaCl resoprtion in cortical TAL), ↑ RBF and GFR
  • ⇒ ↑ Na and Cl excretion (Cl>Na), ↑ urine volume, isosthenuria, ↑ Ca and Mg excretion, ↑ PG and renin release, ↑ venous capacitance, block tubuloglomerular feedback, kaliuresis, ↓ osmotic gradient in medulla
  • uses: acute PE - ↓ pulm wedge pressure, ↓ LV filling pressure, in anephric pts, long term benefit, ↑ venous capacitance rapidly
    • edematous conditions: CHF, liver cirrhosis, nephritic syndrome, chronic heart failure, acute renal failure
    • acute hypercalcemia
    • hyperkalemia
    • acute renal failure
    • anion overdose
    • HTN
  • side effects: hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesia, allergic rxn, dehydration, hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ethacrynic Acid

A
  • loop diuretic
  • aka Edecrin
  • prodrug, adducts with cysteine group on methylene group
  • no sulfonamide group, has vinyl group
  • bound to plasma proteins, filtration enhanced by proteinuria
  • secreted by S2 segment of proximal tubules
  • acts from luminal side of TAL
  • given orally or IV
  • orally: onset of action = 30 min -1hr, duration = 6-8 hr
  • IV: onest of action = immediate, duration = 2hr
  • inhibits NKCC2 ⇒ ↓ lumen pos. potential ( back-leak of K into lumen) ⇒ ↑ Na, K, Cl in urine, ↓ resoprtion Ca, Mg.
  • ⇒ ↓ venous capacitance, ↓ concentrating ability (↓ NaCl reabsorption in medullary TAL), ↓ diluting ability (↓ NaCl resoprtion in cortical TAL), ↑ RBF and GFR
  • ⇒ ↑ Na and Cl excretion (Cl>Na), ↑ urine volume, isosthenuria, ↑ Ca and Mg excretion, ↑ PG and renin release, ↑ venous capacitance, block tubuloglomerular feedback, kaliuresis, ↓ osmotic gradient in medulla
  • uses: acute PE - ↓ pulm wedge pressure, ↓ LV filling pressure, in anephric pts, long term benefit, ↑ venous capacitance rapidly
    • edematous conditions: CHF, liver cirrhosis, nephritic syndrome, chronic heart failure, acute renal failure
    • acute hypercalcemia
    • hyperkalemia
    • acute renal failure
    • anion overdose
    • HTN
  • side effects: hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesia, allergic rxn, dehydration, hyperglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Bumetanide

A
  • loop diuretic
  • aka Bumex
  • has sulfonamide group
  • bound to plasma proteins, filtration enhanced by proteinuria
  • secreted by S2 segment of proximal tubules
  • acts from luminal side of TAL
  • 40x more potent than furosemide
  • given orally or IV
  • orally: onset of action = 30 min -1hr, duration = 6-8 hr
  • IV: onest of action = immediate, duration = 2hr
  • inhibits NKCC2 ⇒ ↓ lumen pos. potential ( back-leak of K into lumen) ⇒ ↑ Na, K, Cl in urine, ↓ resoprtion Ca, Mg.
  • ⇒ ↓ venous capacitance, ↓ concentrating ability (↓ NaCl reabsorption in medullary TAL), ↓ diluting ability (↓ NaCl resoprtion in cortical TAL), ↑ RBF and GFR
  • ⇒ ↑ Na and Cl excretion (Cl>Na), ↑ urine volume, isosthenuria, ↑ Ca and Mg excretion, ↑ PG and renin release, ↑ venous capacitance, block tubuloglomerular feedback, kaliuresis, ↓ osmotic gradient in medulla
  • uses: acute PE - ↓ pulm wedge pressure, ↓ LV filling pressure, in anephric pts, long term benefit, ↑ venous capacitance rapidly
    • edematous conditions: CHF, liver cirrhosis, nephritic syndrome, chronic heart failure, acute renal failure
    • acute hypercalcemia
    • hyperkalemia
    • acute renal failure
    • anion overdose
    • HTN
  • side effects: hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesia, allergic rxn, dehydration, hyperglycemia
25
Q

Torsemide

A
  • loop diuretic, is a sulfonylurea
  • aka Demadex
  • has sulfonamide
  • bound to plasma proteins, filtration enhanced by proteinuria
  • secreted by S2 segment of proximal tubules
  • acts from luminal side of TAL
  • given orally or IV
  • orally: onset of action = 30 min -1hr, duration = 6-8 hr
  • IV: onest of action = immediate, duration = 6-8hr
  • inhibits NKCC2 ⇒ ↓ lumen pos. potential ( back-leak of K into lumen) ⇒ ↑ Na, K, Cl in urine, ↓ resoprtion Ca, Mg.
  • ⇒ ↓ venous capacitance, ↓ concentrating ability (↓ NaCl reabsorption in medullary TAL), ↓ diluting ability (↓ NaCl resoprtion in cortical TAL), ↑ RBF and GFR
  • ⇒ ↑ Na and Cl excretion (Cl>Na), ↑ urine volume, isosthenuria, ↑ Ca and Mg excretion, ↑ PG and renin release, ↑ venous capacitance, block tubuloglomerular feedback, kaliuresis, ↓ osmotic gradient in medulla
  • uses: acute PE - ↓ pulm wedge pressure, ↓ LV filling pressure, in anephric pts, long term benefit, ↑ venous capacitance rapidly
    • edematous conditions: CHF, liver cirrhosis, nephritic syndrome, chronic heart failure, acute renal failure
    • acute hypercalcemia
    • hyperkalemia
    • acute renal failure
    • anion overdose
    • HTN
  • side effects: hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesia, allergic rxn, dehydration, hyperglycemia
26
Q

Hydrochlorothiazide

A
  • thiazide diuretic
  • 10x more potent than chlorothiazide
  • inhibits NCC in distal convoluted tubule ⇒ ↓ intracellular Na ⇒ slowed Na K ATPase ⇒ absorb Ca ⇒ hypocalcuria
  • ↓ ability to produce dilute urine, ↓ free water formation
  • uses: edema from CHF, HTN, calcium nephrolithiasis and osteoporosis,
    • mainstay for: nephrogenic diabetes insipidus*****
  • side effects: extracellular volume depletion, hypotension, hypokalemia, dilutional hyponatremia, ↓ glucose tolerance, hyperlipidemia, allergic rxns (sulfonamide group), ↑ risk digoxin toxicity, ↑ risk quinidine-induced torsades de pointes.
27
Q

Indapamide

A
  • non-thiazide diuretic
  • inhibits NCC in distal convoluted tubule ⇒ ↓ intracellular Na ⇒ slowed Na K ATPase ⇒ absorb Ca ⇒ hypocalcuria
  • ↓ ability to produce dilute urine, ↓ free water formation
  • uses: edema from CHF, HTN, calcium nephrolithiasis and osteoporosis,
    • mainstay for: nephrogenic diabetes insipidus*****
  • side effects: extracellular volume depletion, hypotension, hypokalemia, dilutional hyponatremia, ↓ glucose tolerance, hyperlipidemia, allergic rxns (sulfonamide group), ↑ risk digoxin toxicity, ↑ risk quinidine-induced torsades de pointes.
28
Q

Chlorthalidone

A
  • non-thiazide diuretic with more Carbonic Anhydrase inhibitory action
  • inhibits NCC in distal convoluted tubule ⇒ ↓ intracellular Na ⇒ slowed Na K ATPase ⇒ absorb Ca ⇒ hypocalcuria
  • ↓ ability to produce dilute urine, ↓ free water formation
  • uses: edema from CHF, HTN, calcium nephrolithiasis and osteoporosis,
    • mainstay for: nephrogenic diabetes insipidus*****
  • side effects: extracellular volume depletion, hypotension, hypokalemia, dilutional hyponatremia, ↓ glucose tolerance, hyperlipidemia, allergic rxns (sulfonamide group), ↑ risk digoxin toxicity, ↑ risk quinidine-induced torsades de pointes.
29
Q

Metolazone

A
  • thiazide diuretic
  • inhibits NCC in distal convoluted tubule ⇒ ↓ intracellular Na ⇒ slowed Na K ATPase ⇒ absorb Ca ⇒ hypocalcuria
  • ↓ ability to produce dilute urine, ↓ free water formation
  • uses: edema from CHF, HTN, calcium nephrolithiasis and osteoporosis,
    • mainstay for: nephrogenic diabetes insipidus*****
  • side effects: extracellular volume depletion, hypotension, hypokalemia, dilutional hyponatremia, ↓ glucose tolerance, hyperlipidemia, allergic rxns (sulfonamide group), ↑ risk digoxin toxicity, ↑ risk quinidine-induced torsades de pointes.
30
Q

Quinethazone

A
  • thiazide diuretic
  • inhibits NCC in distal convoluted tubule ⇒ ↓ intracellular Na ⇒ slowed Na K ATPase ⇒ absorb Ca ⇒ hypocalcuria
  • ↓ ability to produce dilute urine, ↓ free water formation
  • uses: edema from CHF, HTN, calcium nephrolithiasis and osteoporosis,
    • mainstay for: nephrogenic diabetes insipidus*****
  • side effects: extracellular volume depletion, hypotension, hypokalemia, dilutional hyponatremia, ↓ glucose tolerance, hyperlipidemia, allergic rxns (sulfonamide group), ↑ risk digoxin toxicity, ↑ risk quinidine-induced torsades de pointes.
31
Q

Chlorothiazide

A
  • thiazide diuretic
  • inhibits NCC in distal convoluted tubule ⇒ ↓ intracellular Na ⇒ slowed Na K ATPase ⇒ absorb Ca ⇒ hypocalcuria
  • ↓ ability to produce dilute urine, ↓ free water formation
  • uses: edema from CHF, HTN, calcium nephrolithiasis and osteoporosis,
    • mainstay for: nephrogenic diabetes insipidus*****
  • side effects: extracellular volume depletion, hypotension, hypokalemia, dilutional hyponatremia, ↓ glucose tolerance, hyperlipidemia, allergic rxns (sulfonamide group), ↑ risk digoxin toxicity, ↑ risk quinidine-induced torsades de pointes.
32
Q

Amiloride

A
  • K+ sparing Diuretic
  • blocks ENaC in principal cell ⇒ blocks effects of aldosterone
  • promotes acidosis, spares (H+), makes less negative lumen for K+ sparing.
  • uses; Liddle’s syndrome (HTN, ↓ renin, metabolic alkalosis, hypokalemia, normal aldosterone), Lithium induced nephrogenic diabetes insipidus, with thiazides for HTN and edema.
33
Q

Triamterene

A
  • K+ sparing diuretic
  • blocks ENaC in principal cell ⇒ blocks effects of aldosterone
  • promotes acidosis, spares (H+), makes less negative lumen for K+ sparing.
  • uses; Liddle’s syndrome (HTN, ↓ renin, metabolic alkalosis, hypokalemia, normal aldosterone), Lithium induced nephrogenic diabetes insipidus, with thiazides for HTN and edema.
34
Q

Eplerenone

A
  • Mineralocorticoid-receptor Antagonist, K+ sparing.
  • t1/2= 5hr.
  • does not compete with DHT for androgen receptor
  • uses: 1° aldosteronism, 2° aldosteronism, ↓ morbidity and mortality in pts with NYHA class III and IV heart failure, with thiazides for HTN
    • drug of choice for mobilizing edema from hepatic cirrhosis*******
  • side effects: hyperkalemia, drowsiness, lethargy, ataxia, confusion.
35
Q

Spironolactone

A
  • Mineralocorticoid-receptor Antagonist, K+ sparing.
  • t1/2= short, Cannenone (metabolite) has a longer one.
  • competes with DHT for androgen receptor at ↑ concentration ⇒ gynecomastia.
  • uses: 1° aldosteronism, 2° aldosteronism, ↓ morbidity and mortality in pts with NYHA class III and IV heart failure, with thiazides for HTN
    • drug of choice for mobilizing edema from hepatic cirrhosis*******
  • side effects: hyperkalemia, gynecomastia, impotence, ↓ libido, hirsutism, deepened voice, menstrual irregularities, diarrhea, gastritis, peptic ulcers, drowsiness, lethargy, ataxia, confusion.
36
Q

Conivaptan

A
  • ADH antagonist.
  • works on V1a and V2 receptors in collecting tubule.
  • ⇒ ↓ water reabsorption.
  • IV only
  • uses: hyponatremia, CHF.
37
Q

Tolvaptan

A
  • ADH antagonist.
  • works on V2 receptor in collecting duct.
  • take orally, lasts 12-24hr.
  • uses: hyponatremia and SIADH.
38
Q

NSAIDs

A
  • use: osteoarthritis, RA, SLE.
39
Q

Glucocorticoids

A
  • use: osteoarthritis, RA, SLE.
40
Q

Methotrexate

A
  • non-biologic DMARD
  • folate analog = blocks tetrahydrofolate-dependent steps in purine metabolism
  • lower doses = anti-inflammatory
  • high doses = cytotoxic (chemo)
  • ↑ adenosine formation ⇒ anti-inflammatory via **A2a and A2b receptors **⇒ ↑ cAMP
  • ⇒ ↓ IL-1 and IL-6; ↑ monocyte apoptosis, ↑ IL-1ra, ↑ IL-4 and IL-10, inhibit COX2 synthesis and neutrophil chemotaxis
  • use: first line for RA
  • side effects: hair loss, nausea, headaches, skin pigmentation
41
Q

Azothioprine

A
  • non-biologic DMARD
42
Q

Chloroquine (Hydroxychloroquine)

A
  • non-biologic DMARD
  • suppresses T cell response to mitogens, ↓ leukocyte chemotaxis, inhibits DNA and RNA synthesis.
  • takes 3-6 months to show effects
  • use: rheuamtic diseases and malaria, SLE.
  • side effects: binds to melanin-containing tissues so need eye monitoring.
43
Q

Cyclosporine

A
  • non-biologic DMARD
44
Q

Leflunomide

A
  • non-biologic DMARD
45
Q

Mycophenolate Mofetil

A
  • non-biologic DMARD
46
Q

Sulfasalazine

A
  • non-biologic DMARD
  • combo salicylate and sulfa antibiotic
  • metabolized to sulfapyridine (in RA) and 5-aminosalicylic acid (in IBD)
  • inhibits rheumatoid factor, suppresses T and B cell proliferation, ↓ inflammatory cytokines.
  • takes 1-3 months to show improvement in RA.
  • use: RA that doesn’t respond well to meds, ulcerative colitis
  • side effects: nausea, vomiting, headache, rash.
47
Q

Cyclophosphamide

A
  • non-biologic DMARD
  • use: SLE
48
Q

Abatacept

A
  • biologic DMARD.
  • recombinant fusion protein: extracellular domain of CTLA-4 and CH2 and CH3 domains of human IgG1.
  • binds CD80/CD86 ⇒ no co-stimulatory signal ⇒ blocks T cell activation.
  • use: monotherapy for RA or combo therapy for RA with DMARDs in mod-severe cases.
  • side effects: ↑ risk of infection.
  • don’t use with TNF antagonists.
49
Q

Rituximab

A
  • biologic DMARD
  • B cell
50
Q

Tocilizumab

A
  • biologic DMARD
  • IL-6R
51
Q

TNFR1-associated Periodic Fever Syndromes

A
  • autosomal dominant
  • mutations that presents cleavage of TNF receptors
  • presentation: episodes of fever and severe localized inflammation. fever, peritonitis, soft tissue inflammation.
52
Q

Belimumab

A
  • aka Benlysta
  • biologic DMARD
  • humanized Ab against B-lymphocyte stimulator protein (BLyS)
    • BLyS made by inflammatory cells and binds receptors on B cells.
  • use: SLE
53
Q

Etanercept

A
  • aka Enbrel
  • fusion protein: Fc portion of human IgG1 and TNFR2 receptor chains.
  • binds TNF, makes it inactive
  • binds LT (TNFbeta) that binds the same receptor.
  • shorter t1/2 than natural IgG1 Ab.
  • t1/2 of TNF complexes longer than free TNF.
  • use: RA, psoriasis, chronic juvenile arthritis, ankylosing spondylitis, psoriatic arthritis, uveitis.
    • use with methotrexate in RA
  • side effects: bacterial infections, TB, opportunistic infections (histo or coccidiomycosis), may ↑ mortality in CHF.
  • careful when giving to those with demyelinating diseases and SLE.
54
Q

Infliximab

A
  • aka Remicade
  • give IV
  • chimeric monoclonal Ab against TNF (mouse and human)
  • does not bind LT
  • binds transmembrane TNF, TNF monomer, and active trimer
  • ⇒ caspase-3 activation and apoptosis of activated lymphocytes, reverse signaling via mTNF.
  • ⇒ ↓ number of swollen joints and severity of RA. blocks granulocyte migration into joint, ↓ circulating VEGF.
  • use: with methotrexate in refractory RA, Crohn’s disease. also juvenile chronic arthritis, ankylosing spondylitis, psoriasis, psoriatic arthritis, uveitis, IBD.
  • side effects: bacterial infections, TB, opportunistic infections (histo or coccidiomycosis), ↑ mortality with CHF.
  • be careful when using with demyelinating disease and SLE.
55
Q

Adalimumab

A
  • aka Humira
  • give subQ
  • recombinant human IgG1 monoclonal Ab for TNFalpha.
  • prevents binding of TNF to TNFR1 and TNFR2.
  • can fix complement and bind to Fc receptor.
  • ⇒ apoptosis of monocytes/macrophages and T cells.
  • use: Crohn’s disease, RA, juvenile chronic arthritis, ankylosing spondylitis, psoriasis, psoriatic arthritis, uveitis, IBD.
  • side effects: bacterial infections, TB, opportunistic infections (histo or coccidiomycosis).
  • careful when using with demyelinating disease and SLE.
56
Q

Golimumab

A
  • aka Simponi
  • give subQ
  • recombinant human IgG2 monoclonal Ab to TNFalpha.
  • prevents TNF binding to TNFR1 and TNFR2.
  • can fix complement and bind Fc receptor.
  • ⇒ apoptosis of monocytes/macrophages and T cells.
  • use: Crohn’s disease, RA, juvenile chronic arthritis, ankylosing spondylitis, psoriasis, psoriatic arthritis, uveitis, IBD.
  • side effects: bacterial infections, TB, opportunistic infections (histo or coccidiomycosis).
  • careful when using with demyelinating diseases or SLE.
57
Q

Certolizumab Pegol

A
  • aka Cimzia
  • recombinant humanized protein with mouse anti-TNF sequences in human VH and VL framework
  • no Fc region ⇒ no compliment fixation or ADCC
  • PEGylation ⇒ ↑ t1/2
  • use: RA, juvenile chronic arthritis. ankyosing spondylitis, psoriasis, psoriatic arthritis, uveitis, IBD.
  • side effects: bacterial infections, TB, opportunistic infections (histo or coccidiomycosis)
  • careful when using in pts with demyelinating disease or SLE.
58
Q

Prednisone

A
  • use: drug of choice for SLE.
  • start with low dose.
  • increase dose if have: arthritis not responding well to NSAIDs, pleuritis, pericarditis, nephritis.

Pharmacology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions