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Renal and CT Flashcards

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1
Q

Diuresis

A

increase in urine flow (mL/min) = UV

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2
Q

Natriuresis

A

increase in urinary sodium exctretion (UNaV)

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3
Q

Kaliuresis

A

increase in urinary potassium excretion (UKV)

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4
Q

Chloruresis

A

increase in urinary chloride excretion

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5
Q

Bicarbonaturia

A

increase in urinary bicarbonate excretion

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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.
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7
Q

Aldosterone

A
  • released from zona glomerulosa in adrenal gland.
  • ⇒ ↑ Na reabsorption via ENaC in distal nephron.
  • ↑ aldosterone whenever renin is ↑
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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
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9
Q

ANF (Atrial Natriuretic Factor)

A
  • released from atrium in resopnse to volume expansion.
  • can ⇒ ↑ GFR and Na and water excretion
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10
Q

Angiontensin

A
  • constricts afferent arterioles ⇒ ↓ GFR.
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11
Q

Inulin

A
  • marker for GFR, not a natural substance.
  • presence in urine is an indication of filtration.
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12
Q

Sulfonilamide

A
  • carbonic anhydrase inhibitor.
  • has sulfonamide moiety for activity.
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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)
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14
Q

Dichlorphenamide

A
  • carbonic anhydrase inhibitor
  • uses: glaucoma
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15
Q

Methazolamide

A
  • carbonic anhydrase inhibitor.
  • uses: glaucoma
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16
Q

Dorzolamide

A
  • topically active for glaucoma ⇒ ↓ intraocular pressure
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17
Q

Brinzolamide

A
  • topically active for glaucoma ⇒ ↓ intraocular pressure
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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
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19
Q

Urea

A
  • osmotic diuretic
  • not orally active
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20
Q

Glycerin

A
  • osmotic diuretic
  • orally active
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21
Q

Isosorbide

A
  • osmotic diuretic
  • orally active
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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
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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
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24
Q

Bumetanide

Study These Flashcards
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
**Torsemide**
* **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
**Hydrochlorothiazide**
* **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
**Indapamide**
* **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
**Chlorthalidone**
* **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
**Metolazone**
* **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
**Quinethazone**
* **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
**Chlorothiazide**
* **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
**Amiloride**
* **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
**Triamterene**
* **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
**Eplerenone**
* **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
**Spironolactone**
* **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
**Conivaptan**
* **ADH antagonist.** * **works on V1a and V2 receptors** in collecting tubule. * **⇒ ↓ water reabsorption**. * IV only * _uses_: **hyponatremia, CHF**.
37
**Tolvaptan**
* **ADH antagonist.** * **works on V2 receptor** in collecting duct. * take **orally**, lasts 12-24hr. * _uses_: **hyponatremia and SIADH**.
38
**NSAIDs**
* _use_: osteoarthritis, RA, SLE.
39
**Glucocorticoids**
* _use_: osteoarthritis, RA, SLE.
40
**Methotrexate**
* **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
**Azothioprine**
* non-biologic DMARD
42
**Chloroquine (Hydroxychloroquine)**
* **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
**Cyclosporine**
* non-biologic DMARD
44
**Leflunomide**
* non-biologic DMARD
45
**Mycophenolate Mofetil**
* non-biologic DMARD
46
**Sulfasalazine**
* **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
**Cyclophosphamide**
* non-biologic DMARD * _use_: SLE
48
**Abatacept**
* **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
**Rituximab**
* biologic DMARD * B cell
50
**Tocilizumab**
* biologic DMARD * IL-6R
51
**TNFR1-associated Periodic Fever Syndromes**
* **autosomal dominant** * mutations that **presents cleavage of TNF receptors** * _presentation_: episodes of fever and severe localized inflammation. fever, peritonitis, soft tissue inflammation.
52
**Belimumab**
* 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
**Etanercept**
* 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
**Infliximab**
* 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
**Adalimumab**
* 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
**Golimumab**
* 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
**Certolizumab Pegol**
* 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
**Prednisone**
* _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)

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