Brainscape's Knowledge GenomeTM

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


See full index

Block 2 > Pharm 2 > Flashcards

Pharm 2 Flashcards

1
Q

Antimicrobial agent. Subclass?

A

Substance produced by 1 microbe to inhibit growth of other microbe(s). Antibacterial/fungal/viral agents

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

3 characteristics of antibacterial activity

A

Bacteriocidal/static, spectrum, dose or time-dependent effects

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

Bacteriocidal vs bacteriostatic

A

Kills sensitive orgs at therapeutic doses; closer MIC & MBC —> more Bacteriocidal, MBC:MIC = 2-4:1 vs stop org growth by inhibiting protein synthesis or w/o killing at therapeutic doses; MBC:MIC = 16x greater —>MBC can’t be achieved by therapeutic doses

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

Broad vs narrow spectrum activity. Caveats?

A

Against gram pos & neg —> preferred empiric therapy in serious infxn vs limited types of pathogens —> preferred definitive therapy where pathogen is known. Variability in resistance

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

What factors play in dose or time dep effects?

A

Min inhibitory conc (MIC), min Bacteriocidal conc (MBC), dose-dependent killing rate, postabx effect (PAE)

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

MBC vs MIC

A

Lowest antimicrobial conc to kill pathogen; always higher than MIC; closer MBC & MIC values —> more cidal —> more kill vs lowest antimicrobial conc to prevent visible pathogen growth; doesn’t kill pathogen; breakpoint sets by CLSI that stay same across hospitals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lab tests for sensitivity: broth dilution vs Etest vs disk diffusion/Kirby Bauer

A

Put equal # of bacteria in serial diluted test tubes and find the first test tube that doesn’t have any growth —> MIC vs place Etest strip in agar cx of bacteria and find lowest MIC on zone of inhibition vs streak bacteria cx onto agar plate w/ abx disks —> find which abx disks have zone of inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is PAE?

A

Persistent effect on bacterial growth after antibacterial drug = removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is there abx resistance?

A

Suboptimal conc of abx, prolonged exposure of abx; impaired influx of ab —> inc efflux protein expression, mutation/mods/overprod in ab binding proteins, factor-associated protection, drug mods/degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Steps to find the right abx for pts

A

Get hx, PE, s/s, predisposing factors to confirm presence of infxn —> do gram stain, cx, sensitivity, collect a sample to ID pathogen —> consider infected site, host factors, drug factors to find empiric/presumptive therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prophylactic vs empirical vs definitive therapy + examples

A

Used to prevent dz for invasive procedures, dz transmission, immunocompromised; ex: amoxicillin before dental procedure for pt w/ prosthetic heart valve, giving antiviral to ppl exposed to flu vs tx pt to cover pathogens most likely present —> broad spectrum; ex: nitrofurantoin for UTI vs tx pt based on specific pathogen —> narrow spectrum, dec risk of abx resistance; ex: give amoxicillin for S. Pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Host vs drug factors

A

Age, preg, metab, organ dysfxn, concomitant drugs/drug interaction, concomitant dz states, allergy vs pharmacokinetics/dynamics, tissue penetration (CNS, bone, prostate, ocular = hard to penetrate), admin route, spectrum of activity, adverse effect profile (toxicities, sz, hematologic), cost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Combination abx therapy. Disadvantages?

A

Broaden spectrum coverage of empiric therapy, achieve synergistic activity, prevent resistance. Cost, adverse effects, superinfxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Antagonistic vs additive vs synergistic vs indifferent combination abx therapy

A

Combined effect < single effect of drug (2+2<2) vs combined effect = sum of single effects (2+2=4) vs combined effect > sum of single effects (2+2>4) vs combined effect = greatest effect by either drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Failures of abx therapy

A

Dz might not be bacterial, undetected pathogen, inappropriate drug selection/dose/admin route, immunosuppressive, surgical intervention, bacterial resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are new drugs discovered?

A

Chem mods, random screening, drug design/biotech, random chance, toxicity/AE/safety assessment, animal studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Safety testing: acute tox vs subacute/chronic tox vs chronic tox vs reproductive performance vs carcinogenic potential vs mutagenic potential

A

2 species, 2 routes; determines no effect dose and max tolerated dose vs 2 species, 3 doses; longer duration of expected clinical use —> longer subacute test vs 1 rodent + 1 nonrodent for >/= 6mo; run concurrently w/ clinical trials vs 2 species; on mating behavior, reproduction, birth defects vs 2 species, 2 yrs; determine pathology vs determine genetic stability and mutation in bacteria (Ames test)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Limitations of animal models

A

Expensive, large # of animals needed, diff species —> diff ADME than humans, not good at detecting AE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What makes a good clinical trial?

A

Using scientific method: good testable hypothesis; picking pts (in/exclusion criteria), ctrl, sample size; pt compliance; finding meaningful indices of drug, choose effects for observation; observations must be converted to valid data

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

bactericidal fluoroquinolones: cipro vs levo vs moxi vs delafloxacin

A

gram neg w/ Pseudo, atypical, poor gram pos vs gram pos/neg w/ Pseudo, resp Q vs gram pos/neg W/O Pseudo, resp Q, not for UTI b/c no renal elim vs gram pos w/ MRSA, gram neg w/ Pseudo, some anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

bactericidal nitroimidazoles: metronidazole MOA vs preg cat vs indications vs contraindications vs AE vs drug interaction

A

prodrug reduced in ANAEROBES to reactive reduction products –> lose DNA helix structure –> disrupt DNA/nucleic acid synthesis vs preg cat B –> don’t use vs intraabd anaerobic infxn, STI, aspiration PNA, SSTI, prophylaxis vs don’t use w/in 3d of alc or propylene glycol –> disulfiram rxn vs N/V/D, HA, metallic taste vs warfarin, alc, propylene glycol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

bactericidal rifampin MOA vs preg cat vs spectrum of activity vs indication vs AE vs drug interaction

A

antitubercular agent; inhibits DNA-dep RNA polymerase –> no chain formation for RNA synthesis vs preg cat C vs staph, mycobacteria vs TB, meningococcal prophylaxis, prosthetic valve endocarditis vs orange urine, tears, sweat; blood dyscrasias; hep/jaundice, GI, flu like sxs vs induces CYP enzymes, 3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

bactericidal nitrofurantoin MOA vs preg cat vs spectrum of activity vs indication vs contraindication vs AE

A

reduced by bacterial flavoproteins to reactive intermediates that inactivate/alter bacterial ribosomal proteins –> inhibit DNA/RNA/cell wall/protein synthesis, aerobic metab vs preg cat B –> hemolytic anemia in newborn vs E coli, E faecalis, K pneu, staph saprophyticus vs uncomplicated cystitis vs renal impairment –> avoid use w/ CrCl <30-60mL/min d/t urine and neurotox vs hemolytic anemia –> avoid in G6PD defic, pulm tox, GI upset, yellow/brown urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

1 vs 2 vs 3 vs 4 vs 5 gen cephalosporins fight against?

A

gram pos cocci, some gram neg vs gram pos, more gram neg; IV = the only cephalosporins against gram neg anaerobes vs gram pos, even more gram neg w/ Neisseria; ceftazidime only does Pseudo (no gram pos or other gram neg) vs gram pos, resistant gram neg w/ Pseudo vs gram pos, lose some gram neg than gen4, MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Know lec 14/15, slide 19

A

know all them infxns that cephalosporins tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

cell wall inhibitors examples

A

beta lactams: PCN (amino, antistaph, antipseudo), cephalosporins, carbapenems, monobactams; vancomycin (glycopeptides), lipoglycopeptides (dalbavancin, oritavancin, telavancin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

lipoglycopeptides: dalbavancin vs oritavancin vs telavancin

A

MRSA and Strep SSTI; renal dose adjustment vs MRSA, gram pos SSTI, E faecalis (not VRE); don’t use w/ heparin for 48h vs same w/ ortiavancin; prolong QT interval, metal taste

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

drug interactions by PCN: probenecid vs tetracycline vs methotrexate & mycophenolate

A

inhibit renal tubular secretion of PCN –> inc PCN conc vs slows bacterial growth –> dec PCN effect on fast growing bacteria vs myelosupression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

streptogramin: quinupristin + dalfopristin MOA vs PD vs spectrum of activity vs indication vs AE vs drug interaction

A

bind to 50S –> no protein synthesis –> no aa incorporation vs bactericidal but each agent alone = static vs gram pos, MRSA, VRE (E. faecium) vs SSTI vs NVD, arthralgia, myalgia vs weak CYP3A4 inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

lefamulin MOA vs PD vs spectrum of activity vs indication vs AE

A

binds to peptidyl transferase center in domain V of 23s rRNA of 50S –> prevent tRNA from binding vs gram pos, MRSA, VRE, gram neg, atypical vs community acquired PNA vs NVD, inc LFT, QT prolong, embryo tox, C diff diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

glycylglycines: tigecycline and eravacycline spectrum of activity vs AE

A

broad spectrum: gram pos, MRSA, VRE, gram neg (no Pseudo), atypical vs inc mortality, pancreatitis, don’t use in bloodstream infxns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

sulfa drug: TMP-SMX MOA vs PD vs preg cat vs spectrum of activity vs indication vs contraindication vs AE vs drug interaction

A

inhibit folic acid synthesis: SMX inhibits converting paraminobenzoic acid to dihydropteroic acid by inhibiting dihydropteroate synthase; TMP inhibits redux of dihydrofolic acid to tetrahydrofolate vs cidal but static alone vs C-D –> don’t use 1st trimester b/c no folic acid, or 3rd trimester b/c kernicterus vs staph, MRSA, gram neg, Pneumocystis jirovecii vs UTI, prostatitis, GI infxn vs sulfa allergy, preg/BF, folic acid defic anemia vs dermatologic rxns (SJS, TEN, rash), hemolytic anemia, crystalluria/stones, photosensitivity, inc BUN/inhibit tubular secretion of Cr, hyperkalemia vs 2C8/9 inhibitor, warfarin can inc INR; meds causing hyperkal: ACE inhibitors, aldosterone receptor blockers, aldosterone antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

posaconazole SOA vs how to take it

A

Asper, Candida, Coccidio, Cryptococcus, Mucormycosis vs take suspension w/ high fat meal –> maximize oral aborsorption; give to pts PO if CrCl<50ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how to take itraconazole?

A

soln taken w/o food; tab and capsules taken w/ food. don’t use in pts w/ HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Allylamines/squalene epoxidase inhibitor MOA vs preg cat vs indication vs AE vs drug interaction

A

inhibit squalene epoxidase –> no ergosterol synthesis vs B (topical) vs dermatomycosis, onychomycosis vs HA, GI, inc LFT, rash/pruritus vs CYP2D6 substrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

echinocandins AE

A

anaphylaxis or histamine rxns, infusion rxn, phlebitis, NVD, anemia, inc LFT, fever, nephrotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

adrenal cortex vs adrenal medulla releases?

A

corticosteroids vs adrenaline/epi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

glucocorticoids: the 5 R’s

A

ready innate immunity, reinforce innate immunity, repress proinflamm and adaptive immunity, resolve inflamm (block IL’s and cytok), restore antiinflamm macs and homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

reasons for diet supplements

A

improve/maintain health, supplement diet, support bone health, lower chol, improve immunity

40
Q

most popular herbal diet supplements

A

turmeric, wheat/barley, aloe vera, spirulina

41
Q

diet supplement = regulated by what 2 agencies?

A

FDA (safety), FTC (advert, label, health claims)

42
Q

Dietary Supplement Health and Education Act of 1994

A

define diet supplement under each food category, remove them from consideration as a drug or diet additive, regulate safety not efficacy; must contain Supplement Facts labels on food

43
Q

Dietary Supplement an Nonprescription Drug Consumer Protection Act 2006

A

mandatory reporting of AE of diet supplements and OTC meds by manufacturers and retailers to FDA MedWatch; AE: birth defects, life threatening event, hosp, death

44
Q

how do 3rd parties review supplements?

A

Consumer Lab: randomly pulls supplementss from store sshelves o test potency, ID, purity; CODEX = intl agency created by Food & Agricultural Org and WHO

45
Q

Quality issues in diet supplements

A

quantity (megadoses –> toxic), formulation (capsules, tab, gel, liquid, powder), excipients (extra ingredients to inc bulk, flavor, color), vit (active/methylated/phosphorylated forms, synthetic or natural), minerals (chelated, carbonates and oxides = taken w/ food to inc absorption)

46
Q

diet supplements affecting blood clot

A

omega 3 FA, vit C&E –> should be dc’d 10-14d prior to surgery or certain medical tests

47
Q

vit/minerals vs antioxidant vs herb supplements for athletes

A

enhance performance w/ defic vs attenuates exer-induced ROS prod and oxidative dmg vs lack consistency in herb prep, studied in only animals

48
Q

how does iron affect sport performance? types of sports anemia? at risk pop?

A

iron helps deliver O2 –> critical for sport performance. hemodilution, iron defic anemia, foot strike anemia. rapidly growing male adolescent, female athlete w/ heavy menses, athletes on energy-restricted diet, training w/ heavy sweating in hot climates, “stacking” mult products together like caffeine

49
Q

why do military use protein supplements vs MTV?

A

inc muscle mass, physical performance, energy/endurance, wt loss vs improve overall health

50
Q

3 types of protein supplements? whey vs casein vs soy

A

protein concentrates, isolates, hydrolysates. dairy based, quickly digested, rich in BCAA vs dairy based, slowly digested (forms gel in stomach) vs plant based, complete source of protein

51
Q

when are nutrient drug interactions sig?

A

alters therapeutic drug response, compromises nutrition status –> malnutrition

52
Q

supplement drug interactions vs drug supplement interactions?

A

ginseng, echincea influence transport and/or enzymes –> alter drug effect vs antiepileptic drugs affect vit D metab –> impact bone health, inc vitB6 catab; corticosteroids dec Ca2+ resorption and impair vit D metab

53
Q

fxnal foods vs nutraceuticals vs pharmaceuticals

A

food constituents having biological effect influencing health and susceptibility to dz (fiber, omega3, cranberry juice, tumeric) vs any food product w/ extra health benefits vs cmpd made as medicinal drug

54
Q

diet supplement vs ergogenic acid

A

substance taken orrally to add nutrition to diet (tab, liquid, powder) vs any supplement, food product, dietary manipulation enhancing work capacity or athletic performance

55
Q

therapeutic advances of COVID19

A
  • Therapies targeting inflamm
  • Therapies for acute resp failure
  • Therapies targeting RAAS
  • Antiviral therapies
  • Antithrombotic therapies
  • Neutralizing ab therapies
  • Vit supplements
56
Q

hypothal-pituitary-adrenal (HPA) axis

A
  • Hypothalamus secretes corticotropin releasing hormone (CRH) →
  • Stimulates the anterior pituitary gland to secrete adrenocorticotropic hormone (ACTH) →
  • Stimulates the adrenal cortex to secrete cortisol, aldosterone, androgens
57
Q

what suppresses vs stimulates HPA axis?

A

endogenous (cortisol) or exogenous glucocorticoids; Sudden withdrawal from glucocorticoids → adrenal insufficiency vs Stress; ↑ production of adrenal steroids → initially enhances body’s resistance to stress

58
Q

is aldosterone regulated by HPA axis?

A

nope, by renin-angiotensin-aldosterone system

59
Q

3 layers of adrenal cortex

A
  • Zona glomerulosa (outer layer) –> Mineralocorticoids: aldosterone (salt)
  • Zona fasciculata (middle layer) –> Glucocorticoids: cortisol (sugar)
  • Zona reticularis (inner layer) –> Adrenal androgens: dehydroepiandrosterone (sex)
60
Q

metabolic effects of glucocortoicoids

A

inc blood glu for f/light –> inc gluconeogenesis, dec insulin; promote lipogenesis d/t long term glucocorticoids; muscle protein catab –> lymphoid/ connective tissue/fat/skin wasting, osteoporosis

61
Q

antinflamm effects of glucocorticoids (limits inflamm, not correct the dz)

A

suppresses T cells, cytok prod, inflamm mediators; dec prostacyclin –> dec cap permeability –> promote vasconstrict; dec lymphocytes/adaptive immunity and inc innate immunity

62
Q

Physiologic effects of mineralocorticoids

A

regulate sodium reabsorption in excretory sites; In kidney collecting duct, aldosterone promotes sodium retention and potassium excretion by increasing the expression of:
o Na+ channels in apical membrane (lumen)
o Na+/K+ ATPase in basolateral membrane (interstitium)

63
Q

corticosteroids MOA

A
  • Corticosteroids diffuse into cells (b/c lipophilic) and bind to cytosolic receptors (glucocorticoid and mineralocorticoid receptors)
  • The steroid-receptor complex translocates into nucleus and binds to specific DNA sequence
  • Binding stimulates or inhibits the transcription of specific genes
64
Q

gluco vs mineralocorticoid receptors

A

broad tissue, high affinity for cortisol and prednisone, low affinity for aldosterone vs excretory sites (sweat/salivary glands, kid, colon), high affinity for cortisol and aldosterone

65
Q

primary vs secondary adrenal insufficiency

A

adrenal cortex destroyed by autoimmune rxns, Addison’s dz vs hypothal or pituitary d/o –> dec CRH or ACTH prod, prolonged admin of exogenous glucocorticoids –> neg feedback on CRH and ACTH, dec cortisol and androgens

66
Q

adrenal insufficiency clinical pres

A
  • Weakness
  • Weight loss
  • Increased pigmentation
  • Postural hypotension/dizziness
  • Hypoglycemia
67
Q

congenital adrenal hyperplasia. tx?

A

enzyme deficiencies that impair synthesis of cortisol and aldosterone
o Steroid 21-α hydroxylase deficiency
o Decreased cortisol (90%) and aldosterone (75%)
o Increased adrenal androgens → prenatal virilization (hirsutism in females)
* Treated by hydrocortisone to suppress ACTH secretion and fludrocortisone to provide mineralocorticoid activity

68
Q

Cushing’s syndrome

A
  • Secretion of excessive glucocorticoids
    o ACTH-secreting pituitary adenomas –> inc prodof cortisol
    o Ectopic secretion of ACTH by small cell lung ca
    o Cortisol-secreting adenoma or carcinoma of adrenal cortex
  • Iatrogenic/medically induced Cushing’s syndrome
    o Secondary to the pharmacologic treatment with exogenous glucocorticoids, HIV protease inhibitors
69
Q

glucocorticoid AE vs contraindication

A
  • Infections
  • Osteoporosis
  • Weight gain
  • Impaired glucose metabolism
  • Hypertension
    vs live vax, desmopressin
70
Q

glucocorticoids admin routes: systemic vs local. know how to describe each route

A
  • Oral
  • Parenteral
    vs
  • Intraarticular
  • Topical
  • Inhalation
71
Q

EXAM QUESTION: W/DRAWAL FROM STEROID TX

A
  • Chronic glucocorticoid therapy should ALWAYS be tapered slowly with gradually decreasing doses
  • Long-term steroid therapy suppresses the release of hypothalamic CRH and pituitary ACTH, → atrophy of adrenal cortex
  • Sudden cessation may induce acute adrenal crisis or exacerbation of underlying inflammatory disease → treat with IV glucocorticoids
72
Q

is aldosterone itself a therapeutic agent?

A

no b/c high 1st pass hepatic metab despite being endogenous mineralocorticoid –> use fludrocortisone (exogenous minerlaocorticoid) instead

73
Q

osilodrostat (corticoid synthesis inhibitor) MOA vs indic vs AE vs drug interaction

A

inhibits 11 B-hydroxylase vs Cushing where surgery is not an option vs adrenal insufficiency, hypokal vs QT prolong meds, 3A4 inducers & inhibitors

74
Q

what do mineralocorticoid receptor antagonists do? know the 3 types and their stuff

A

block aldosterone effects in renal tubules –> diuretic. spironolactone, eplerenone, drospirenone

75
Q

Tocilizumab (MOA, AE, serious AE)
Barcitinib (MOA, AE, serious AE)
Molnupiravir (MOA)

A
  • MOA: binds to receptors for IL6 –> inhibits it
  • AE: neutropenia, HTN, dyslipidemia, elevated transaminases
  • Serious AE: GI perforation
  • MOA: oral JAK inhibitor
  • AE: thrombocytosis
  • Serious AE: thromboembolism, stroke
  • MOA: oral ribonucleoside analog that potently inhibits replication of COVID
76
Q

Nirmatrelvir + Ritonavir
Remdesivir

A
  • Nirmatrelvir
    o MOA: SARS-CoV-1 main protease inhibitor
  • Ritonavir
    o MOA: HIV1 protease inhibitor and CYP3PA inhibitor –> tx mild COVID
  • MOA: sterically interact w/ viral RNA dependent RNA pol
  • IV
  • Clinical trial: 200mg loading dose by IV on day 1  100mg maintenance dose
77
Q

Penciclovir (topical)
Trifluridine (topical)
Docosanol (topical)

A
  • MOA: To penciclovir 3P to inhibit HSV polymerase competitively w/ deoxyguanosine 3P
  • Topical cream for herpes labialis/cold sores
    vs
  • MOA: inhibit thymidylate synthetase –> incorporate viral DNA in place of thymidine
  • Topical
  • Ophthalmic prep instilled in eye q2hrs
  • HSV keratoconjunctivitis, recurrent epithelial keratitis
    vs
  • MOA: inhibit lipid-enveloped HSV from fusing to plasma membrane  no viral entry into host cells  no viral replication
  • Pharmacokinetics: topical applied 5x QD
  • Indication: cold sores, fever blisters
78
Q

new drugs for HSV/VZV

A
  • Pritelivir & amenamevir
    o Helicase-primase inhibitors; for HSV
  • Valomaciclovir
    o Viral DNA pol inhibitor; for VZV and EBV
79
Q

HSV/VZV vs CMV drugs

A

o Acyclovir (PO, IV, topical)
o Valacyclovir (PO)
o Famciclovir (PO)
o Penciclovir (topical)
o Trifluridine (eye)
o Docosanol (topical)
vs
val/ganciclovir, cidovir, foscarnet (all IV but val = PO)

80
Q

characteristics vs risks factors of OA

A
  • Degenerative joint disease
  • Loss of productivity
  • Decreased quality of life, disability
  • Higher in older age groups
    VS
    o Obesity
    o Occupation
    o Certain sports
    o Joint trauma
    o Genetic predisposition
81
Q

Pathophysiology of OA

A
  • Cartilage damage → ↑ chondrocyte activity → imbalance between breakdown and re-synthesis of cartilage → further cartilage loss → joint space narrowing
  • Pain due to activation of nociceptive nerve endings by mechanical and chemical irritants
  • Distention of the synovial capsule, microfracture, periosteal irritation, damage to ligaments or the meniscus
82
Q

desired outcomes vs nonpharm tx of OA

A
  • Relieve pain and stiffness
  • Maintain or improve joint stability
  • Limit functional impairment
  • Maintain or improve quality of life
  • Begin tx with the safest and least invasive therapies
    vs
  • Weight loss → reduces disability
  • Bracing/splinting → support painful or unstable joints
83
Q

gout. clinical spectrum of dz:

A

urate crystals in the joints –> inflammatory response. hyperuricemia, Recurrent attacks of acute arthritis associated with monosodium urate crystals in synovial fluid leukocytes, Deposits of crystals in tissues and around joints, Interstitial renal disease, Uric acid nephrolithiasis

84
Q

clinical pres vs labs of gout

A

acute, inflammatory monoarthritis; fever, intense pain, erythema, warmth, swelling vs ↑ serum uric acid, leukocytosis; Monosodium urate crystals in synovial fluid; kidney stones

85
Q

risk factors of gout

A
  • ↑ age
  • ↑ serum creatinine
  • ↑ blood urea nitrogen
  • ↑ blood pressure
  • Male
  • Obesity
  • Drugs: diuretics, niacin, ethanol, cytotoxins
86
Q

5 therapeutic strategies of gout: NSAIDs or glucocorticoids vs Colchicine
vs Allopurinol or febuxostat
vs Probenecid and sulfinpyrazone vs
Pegloticase

A

-Inhibiting inflammatory responses; start at onset of sxs and taper off 2-3d
-Inhibiting recruitment of inflammatory cells to the joints; corticoids = equivalent to NSAID, taper off 10-14d; can do systemic intraarticular injections
-Inhibiting uric acid synthesis
-Inhibiting uric acid reabsorption → increasing uric acid excretion
-Metabolism of uric acid to allantoin by recombinant uricase

87
Q

prophylaxis of gout

A
  • Goal: < 6 mg/dL
  • Indicated with 2 or more attacks per year
  • Patients with tophi (deposit of urates in tissues)
  • Wait for 6 – 8 weeks after acute attack to start
  • Overproducer vs. underexcreter of uric acid?
88
Q

colchicine vs allopurinol vs febuxostat for MOA vs PK vs AE vs DI

A

antimitotic; disrupt microtubules –> no leuk migration or phag vs readily absorbed –> excreted in bile or urine, renal dose adjustment vs diarrhea, myelosuppression –> aplastic anemia, agranulocytosis vs P glycoprotein, 3A4 inhibitor
Xanthine oxidase inhibitors: lower serum urate levels in a dose-dependent manner in over/underexcreters vs renal dose adjust vs rash, Leukopenia, HA, “Hypersensitivity syndrome”: severe rash, hepatitis, interstitial nephritis, and eosinophilia vs Metabolized to oxypurinol (active metabolite) in the liver; Inhibits the metabof warfarin, azathioprine
same as allopurinol vs renal dose adjustment for CrCl<30ml/min vs Nausea, Arthralgias, ↑ minor liver enzymes, ↑ risk of thromboembolism vs Metabolized to inactive metabolites, Contraindicated with azathioprine and mercaptopurine

89
Q

tramadol for acute gout

A

oral opioid analgesic/agonist and serotonin-norepi reuptake inhibitor; risk w/ sz and suicidal tendency

90
Q

misc tx for gout. nonpharm tx for gout

A

fenofilbrate: inc clearance of hypo/xanthing, dec serum urate; losartan: angiotension II receptor antag for HTN, inhibits uric acid reabsorption in renal tubule and inc urinary excretion –> alkalizes urine. exer, wt loss, PT, assisted devices

91
Q

RA + clinical pres + risk factors

A

Autoimmune disorder characterized by symmetrical inflammation of joints → chronic inflammation leads to erosions of the bone and cartilage → joint destruction
* Clinical presentation: pain/stiffness in multiple joints > 6 weeks, fatigue, weight loss, low-grade fever
* Risk factors: fhx, females, tob, genetic susceptibility (HLA-DR4)

92
Q

pathophysiology of RA

A
  • Synovial T cell activation
  • APCs activate CD4+ T cells → activate B cells
  • B cells differentiate to autoantibody producing plasma cells
  • RF and anti-CCP antibodies produced
  • T effector cells also stimulate the synovial macrophages and fibroblasts to secrete proinflammatory mediators (TNF-alpha, IL-1, and IL-6)
93
Q

nonpharm vs pharm tx of RA

A
  • Exercise as tolerated
  • Rest, adequate sleep
  • Splinting
  • Emotional support
    VS
  • Disease Modifying Antirheumatic Drugs (DMARDs)
  • Prednisone (glucocorticoids)
94
Q

nonbiologic vs biologic agents of RA

A
  • Etanercept
  • Infliximab
  • Adalimumab (TNF alpha inhibitors)
  • Anakinra (IL1 receptor blocker)
  • Abatacept (Tc activation inhibitor)
    VS
  • Sulfasalazine
  • Leflunomide
  • Tofacitinib
  • Hydroxychloroquine
  • Methotrexate
95
Q

comp vs noncomp inhibitors for antivirals

A

acyclovir, penciclovir, cidofovir vs foscarnet

96
Q

which drugs are glucocorticoid vs mineralocorticoid receptor antag?

A

mifepristone vs spironolactone, eplerenone, drospironone

Block 2 (16 decks)

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