Correct Answer:
kills the bacteria
Bactericidal
Correct Answer:
kills the bacteria and stops the growth or spread of the infection
Bacteriostatic drugs
Correct Answer:
clindamycin
macrolides
sulfonamides
tetracyclines<\/p>\n\n\n\n
![\"\"](\"https:\/\/learnexams.com\/blog\/wp-content\/uploads\/2024\/01\/Screenshot_97-1024x749.png\")
<\/figure>\n\n\n\nBactericidal drugs
Correct Answer:
ahminoglycosides
beta-lactums
fluroquinolones
Metronidazole
Streptogramins
vancomycin
anti-microbial resistance
Correct Answer:
1.) not knowing if the pt had recent use of antibiotics
2.) provider overuse of broad=spectrum antibiotics
3.) not performing susceptibility testing
4.) Age younger than 2 years or older than 65 years
5.) Daycare center attendance
6.) Exposure to young children
7.) Multiple medical co-morbidities
8.) Immunosuppression
Pharmacodynamics of Beta-lactam PCNs
Correct Answer:
inhibit biosynthesis of bacterial wall (beta-lactam ring)<\/p>\n\n\n\n
subclasses of Beta-lactams PCNS
Correct Answer:
natural PCNS
aminopenicillins
anti-staphylococcal PCNs
extended Spectrum PCNs
1st line therapy for Strep pharyngitis.
Correct Answer:
penicillin V
1st line therapy for all bites
Correct Answer:
Amoxicillin\/Clavulanate (Augmentin)
Natural PCN’s, Drugs
Correct Answer:
Penicillin V potassium (ledercillin) Penicillin G sodium (PCN G-Na)
Penicillin G procaine (Duracillin)
Penicillin G benzathine (Permapen)
Penicillin G potassium (Pfizerpen)<\/p>\n\n\n\n
Natural PCNs active against
Correct Answer:
aerobic gram (+) organisms
Aminopenicillins active against
Correct Answer:
Gram (-) organisms
Aminopenicillins Drugs
Correct Answer:
Amoxicillin
Ampicillin
Combinations:
Amoxicillin-clavulanate (Augmentin)
1st lines therapy for acute otitis media (AOM) & sinusitis
Correct Answer:
Amoxicillin
When aminopenicillins are combined with beta-lactamase inhibitors
Correct Answer:
their spectrum in broadened<\/p>\n\n\n\n
lab levels that indicate a pituitary tumor
normal\/elevated TSH
increased FT4 and T3<\/p>\n\n\n\n
lab levels that indicate primary hypothyroidism
low TSH
normal FT4
elevated T3<\/p>\n\n\n\n
lab levels that indicate exogenous T4 ingestion
low TSH
high FT4
normal T3<\/p>\n\n\n\n
normal T4 levels
4.5-12.5<\/p>\n\n\n\n
normal FT4
0.9-2<\/p>\n\n\n\n
normal T3
80-220<\/p>\n\n\n\n
normal FT3
230-620<\/p>\n\n\n\n
normal TSH
0.3-6<\/p>\n\n\n\n
timeframe for re-check of labs after starting levothyroxine
6-8 weeks<\/p>\n\n\n\n
s\/s of hypothyroidism
Hyporeflexia, slow thought process, weight gain, constipation, cold intolerance<\/p>\n\n\n\n
S\/S of hyperthyroidism
Hyperreflexia, mind racing, weight loss, diarrhea, heat intolerance<\/p>\n\n\n\n
Tx of thyroid storm
Methimazole and propylthiouracil<\/p>\n\n\n\n
Result of not treating hypothyroidism during pregnancy
Can decrease IQ and other aspects of neurophysical function in the child<\/p>\n\n\n\n
Meds that can decrease absorption of levothyroxine
H2 receptor blockers (cimetidine), PPI, carafate, cholestyramine (Questran), colestipol (Colestid), aluminum-containing antacids (Maalox), calcium supplements, iron supplements, mag salts, Xenical<\/p>\n\n\n\n
Meds that accelerate levothyroxine metabolism
Phenytoin, carbamazepine (Tegretol), rifampin, zoloft, phenobarbital<\/p>\n\n\n\n
Interaction between warfarin and levothyroxine
Accelerates degradation of vitamin K dependent clotting factors (enhances warfarin effect)<\/p>\n\n\n\n
Interaction between catecholamines and levothyroxine
Increases cardiac responsiveness<\/p>\n\n\n\n
How to confirm a DM dx
FBG >\/= 126
Random BG >\/= 200 plus s\/s of DM
OGTT >\/= 200
A1C 6.5% or ><\/p>\n\n\n\n
A1C goal for DM pts
< 7%<\/p>\n\n\n\n
Pre-meal BG goal
70-130<\/p>\n\n\n\n
Peak post-meal BG goal
< 180<\/p>\n\n\n\n
What time interval should A1C be rechecked?
Every 3 months until under 7%, then every 6 months<\/p>\n\n\n\n
Action of insulin
Promotes conservation of energy and buildup of energy stores, such as glycogen. Promotes cell growth and division<\/p>\n\n\n\n
What insulin can be mixed?
NPH w\/ short-acting<\/p>\n\n\n\n
Baseline data prior to insulin
Random BG
FBG
A1C
Electrolytes
Urinary glucose and ketones<\/p>\n\n\n\n
What meds can raise BG
Sympathomimetics
Glucocorticoids<\/p>\n\n\n\n
What meds can lower BG
Sulfonyleureas<\/p>\n\n\n\n
Rapid-acting insulins
Humalog (Lispro)
Novalog (Aspart)
Apidra (Glulisine)<\/p>\n\n\n\n
Short-acting insulins
Regular (Humulin R, Novolin R)<\/p>\n\n\n\n
Intermediate acting insulins
Isophane (NPH)<\/p>\n\n\n\n
Long acting insulins
Lantaus (Glargine)
Levimir (Detemir)<\/p>\n\n\n\n
Pioglitazone considerations
Severe HF
Bladder CA or a hx of<\/p>\n\n\n\n
GLP1
glucagon-like peptide 1 receptor agonists<\/p>\n\n\n\n
TZD
Thiazolidinediones<\/p>\n\n\n\n
DPP4-i
Dipeptidyl peptidase-4 inhibitors<\/p>\n\n\n\n
SGL T2i
Sodium-glucose cotransporter 2 inhibitors<\/p>\n\n\n\n
What drug class should be considered for DM prior to insulin?
Biguanide<\/p>\n\n\n\n
Insulin correction dose calculation
Actual blood sugar – target blood sugar \/ correlation factor<\/p>\n\n\n\n
Correlation factor equation
Insulin sensitivity factor constant \/ TDD<\/p>\n\n\n\n
Insulin sensitivity factor
1500 for regular
1800 for rapid acting<\/p>\n\n\n\n
TDD equation
Pt’s kg x 0.6 units<\/p>\n\n\n\n
Examples of GLP-1
Exenatide (Byetta, Bydureon), liraglutide (Victoza), dulaglutide (Trulicity), Lixisenatide (Adlyxin), semaglutide (Ozempic)<\/p>\n\n\n\n
MOA of GLP-1
Lowers BG by slowing gastric emptying, stimulating glucose-dependent insulin release, suppressing postprandial glucagon release, and reducing appetite<\/p>\n\n\n\n
Adverse effects of GLP-1
Hypoglycemia
N\/v\/d
Pancreatitis
Renal insufficiency
Thyroid CA<\/p>\n\n\n\n
Examples of amylin mimetics
Pramlintide (Symlin)<\/p>\n\n\n\n
MOA of amylin mimetics
Delays gastric emptying and suppresses glucagon secretion, decreasing the postprandial rise in glucose<\/p>\n\n\n\n
Adverse effects of amylin mimetics
hypoglycemia, nausea, injection site reactions<\/p>\n\n\n\n
Examples of thiazolidinediones (Glitazones)
Pioglitazone (Actos)
Rosiglitazone (Avandia)<\/p>\n\n\n\n
MOA of thiazolidinediones
Decrease insulin resistance and thereby increase glucose uptake by muscle and adipose tissue and decrease glucose production by the liver<\/p>\n\n\n\n
Adverse effects of thiazolidinediones
Hypoglycemia, HF, bladder CA, fractures (women), ovulation<\/p>\n\n\n\n
Examples of glucosidase inhibitors
Acarbose (Precose)
Miglitol (Glyset)<\/p>\n\n\n\n
MOA of glucosidase inhibitors
Delay carb digestion and absorption, thereby decreasing the postprandial rise in BG<\/p>\n\n\n\n
Adverse effects of glucosidase inhibitors
flatulence, diarrhea, abdominal pain<\/p>\n\n\n\n
DPP-4i examples
Alogliptin (Nesina)
Linagliptin (Tradjenta)
Saxagliptin (Onglyza)
Sitagliptin (Januvia)<\/p>\n\n\n\n
MOA of DPP-4i
Enhance the activity of incretins by inhibiting their breakdown and therefore increase insulin release, reduce glucagon release, and decrease hepatic glucose production<\/p>\n\n\n\n
Adverse effects of DPP-4i
Pancreatitis, hypersensitivity reactions<\/p>\n\n\n\n
Examples of sulfonylureas
Glimepiride (Amaryl)
Glipizide (Glucotrol)
Glyburide (Glynase)<\/p>\n\n\n\n
Adverse effects of sulfonylureas
hypoglycemia, weight gain<\/p>\n\n\n\n
MOA of sulfonylureas
Promote insulin secretion by the pancreas; may also increase tissue response to insulin<\/p>\n\n\n\n
Examples of meglitinides (Glinides)
Nateglinide
Repaglinide<\/p>\n\n\n\n
MOA of meglitinides
Promote insulin secretion by the pancreas<\/p>\n\n\n\n
Adverse effects of meglitinides
hypoglycemia, weight gain<\/p>\n\n\n\n
examples of SGLT2
Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)<\/p>\n\n\n\n
MOA of SGLT2
Increase glucose excretion via the urine by inhibiting proteins in the kidney tubules, decreasing glucose levels and inducing weight loss by caloric loss through the urine<\/p>\n\n\n\n
Adverse effects of SGLT2
Genital mycoctic infections, orthostasis<\/p>\n\n\n\n
Examples of dopamine agonists
Bromocriptine (Cycloset)<\/p>\n\n\n\n
MOA of dopamine agonists
Activates dopamine receptors in the CNS<\/p>\n\n\n\n
Adverse effects of dopamine agonists
Orthostatic hypotension, exacerbation of psychosis<\/p>\n\n\n\n
Examples of biguanides
Metformin (Glucophage, Glucophage XR)<\/p>\n\n\n\n
MOA of biguanides
Decreases glucose production by the liver, increases tissue response to insulin<\/p>\n\n\n\n
Adverse effects of biguanides
Decreased appetite
N\/v\/d
Lactic acidosis<\/p>\n\n\n\n
Black box warning for metformin
Severe metabolic acidosis can occur w\/ accumulation of metformin<\/p>\n\n\n\n
What patients are at the greatest risk of metabolic acidosis
DM pts with significant renal impairment who take metformin<\/p>\n\n\n\n
Step 1 of DM tx
Lifestyle changes plus metformin<\/p>\n\n\n\n
Step 2 of DM tx
Add drug such as thiazolidinediones, SGLT2 inhibitor, DPP-4i, GLP-1 receptor agonist<\/p>\n\n\n\n
Step 3 of DM tx
Three drug combo<\/p>\n\n\n\n
Step 4 of DM tx
Combo injectable regimen inclusive of insulin<\/p>\n\n\n\n
What tx should a pt have if their A1C is 9% at dx?
Dual therapy<\/p>\n\n\n\n
What tx should a pt have if their A1C is 10% or FBG is 300 or more at dx?
Injectable therapy<\/p>\n\n\n\n
Who is at risk for toxicity from methylxanthines
Pts w\/ liver dysfunction<\/p>\n\n\n\n
Tx for methylxanthine toxicity
Activated charcoal and a cathartic<\/p>\n\n\n\n
Examples of methylxanthines
Theophylline
Aminophylline<\/p>\n\n\n\n
Therapeutic goal of methylxanthines
Bronchodilation to decrease the intensity and frequency of moderate to severe asthma attacks and to control COPD exacerbations<\/p>\n\n\n\n
Baseline data for methylxanthines
FEV1<\/p>\n\n\n\n
Contraindications for methylxanthines
Untreated seizure disorder or PUD<\/p>\n\n\n\n
Precautions for methylxanthines
Heart disease, liver dysfunction, seizure disorders, PUD<\/p>\n\n\n\n
Monitoring requirements for methylxathines
FEV1, frequency\/severity of attacks, HR and rhythm, EKG, levels to ensure they are in a therapeutic range<\/p>\n\n\n\n
Drug interactions that increase the effects of methylxanthines
Cimetidine
Fluoroquinolone ABX<\/p>\n\n\n\n
Drug interactions that decrease the effects of methylxanthines
Phenobarbital
Phenytoin
Rifampin<\/p>\n\n\n\n
Step 1 therapy for asthma and COPD
SABA PRN<\/p>\n\n\n\n
Step 2 therapy for asthma and COPD
SABA PRN + low dose ICS or comolyn\/montelukast\/theophylline<\/p>\n\n\n\n
Step 3 therapy for asthma and COPD
SABA PRN + low dose ICS + LABA\/medium dose ICS<\/p>\n\n\n\n
Step 4 therapy for asthma and COPD
SABA PRN + medium dose ICS + LABA<\/p>\n\n\n\n
Step 5 therapy for asthma and COPD
SABA PRN + high dose ICS + LABA and possibly omalizumab<\/p>\n\n\n\n
Step 6 therapy for asthma and COPD
SABA PRN + high dose ICS + LABA + oral glucocorticoids and possibly omalizumab<\/p>\n\n\n\n
Recommended step for initial tx of intermittent asthma
Step 1<\/p>\n\n\n\n
Recommended step for initial tx of mild persistent asthma
Step 2<\/p>\n\n\n\n
Recommended step for initial tx of moderate persistent asthma
Step 3<\/p>\n\n\n\n
Recommended step for initial tx of severe persistent asthma
Step 4<\/p>\n\n\n\n
Contraindications for beta agonists
Tachydysrhythmias or tachycardia associated w\/ digitalis toxicity<\/p>\n\n\n\n