Evidence Based Practice Flashcards
Types of observational studies
Cohort studies
Case-control studies
Cross-sectional studies
Evidence based medicine (EBM) approaches a clinical dilemma as a clinical question using what pneumonic?
PICO
P-patients problem
I- clinical intervention
C- comparison of the intervention with at least one alternative
O- desired outcome used to compare interventions
Margination
A process in which white blood cells, or leukocytes, relocate from their normal central location in the bloodstream to the periphery along the endothelium wall. As margination progresses, leukocytes adhere to endothelial cells, before migrating from the blood to the tissue, where they are responsible for limiting the harmful stimuli and beginning the process of repair.
What type of questions is the PICO model best applied to?
Foreground questions (specified knowledge questions that affect clinical decisions)
Inflammation
Reaction of vascularized tissue in the body to local injury or insult.
Excessive inflammation can be pathogenic
Clinical signs: redness, fever, swelling, pain
Vascular and cellular components of inflammation
Vascular- following injury, the body increases blood flow to the site through dilation of the arterioles. This ultimately leads to dilation of the capillaries and venules. This allows increased permeability of macromolecules into the tissue space. This causes swelling/edema.
Cellular- as fluid is lost in the tissue space, large amounts of RBCs, WBCs, and platelets remain behind causing blood viscosity to increase. This increase in viscosity causes margination.
Histamine
Mediator of inflammation
Stored in granular tissue of mast cells
Once released, produces vasodilation and increased vascular permeability
Factor XII (Hageman factor)
Mediator of inflammation
Stored in an inactive form in plasma
Once activated, this plasma protein triggers the activation of 4 different cascades of systems important to inflammation and repair (coagulation cascade, kinin cascade, fibrinolytic cascade, complement cascade)
Coagulation cascade
leads to thrombin formation, which converts fibrinogen into fibrin, ultimately leading to clot formation
Kinin cascade
Leads to the production of bradykinin. Bradykinin is a peptide that causes vascular dilation and increases permeability
Fibrinolytic cascade
Involves the conversion of plasminogen into the active protease plasmin. Plasmin has two important functions: degradation of fibrin clots and activation of the complement cascade
Complement cascade
Has many important functions. Produces proteins that form the membrane attack complex, which attacks harmful microorganisms. Additional activated proteins in this cascade are mediators of inflammation causing vasodilation, increasing vascular permeability, promoting chemotaxis and phagocytosis, and initiating histamine release.
Arachidonic acid
A fatty acid found in many cell membranes. Two different pathways metabolize arachidonic acid, which results in the production of potent inflammatory mediators.
Prostaglandins and thromboxanes are produced from arachidonic acid through the cyclooxygenase pathway
Prostaglandins
Induce vasodilation and increase vascular permeability
Thromboxanes
Facilitate platelet aggregation, which is important to the healing and repair process.
Lipoxygenase pathway
results in the production of leukotrienes. Leukotrienes initiate chemotactic activities for WBC, causing vasodilation, and increase vascular permeability
Hemodynamics
Defined as the function of blood flow or circulation and the forces involved. Alterations or disturbances in the normal pattern of blood flow can be harmful to the organs and tissues of the body.
Edema
The abnormal accumulation of fluids in the interstitial spaces of cells or tissues
Water composition in the body
Intracellular compartment- contains approximately 2/3rds of total body water
Extracellular compartment- stores the remaining 1/3rd of total body water
The extracellular compartment is further divided into the interstitial space and plasma space, which are separated by the capillary wall.
What is normal exchange of water controlled by?
Controlled by hydrostatic and osmotic pressure, which is regulated by plasma proteins. Disruption of this normal exchange explains the etiology of edema
Causes of edema
Increased hydrostatic pressure Decreased osmotic pressure Increased vascular permeability caused by inflammation Obstruction of a lymphatic channel Sodium retention
Congestion
A passive process in which the drainage of blood from a given area is interrupted. An example of congestion can be seen in valvular stenosis. In this disorder, blood volume is increased in the cardiac chamber preceding the valve that is failing to open properly.
Increase in blood volume
Hyperemia
An active process in which blood flow is increased to a given area. An example of this process can be seen in acute inflammation.
Increase in blood volume.
Hemorrhage
the loss or escape of blood from the circulatory system. Accumulation of this lost blood may be external or enclosed within the tissue space of the body.
Hematoma
Referred to the accumulation of blood within the tissues and can range in severity for mild (bruise) to more severe (subdural hematoma)
Petechiae
Pinpoint hemorrhages seen most commonly on dermal or mucosal areas
Purpuras
Widespread hemorrhages slightly larger than petechiae usually found under the dermal surface
Ecchymoses
Larger, often blotchy hemorrhages that also are found on mucosal or dermal areas
Thrombosis
The pathologic process of formation of a blood clot within the circulatory system. The formed clot is referred to as a thrombus.
Virchows triad
Thrombus formation
- ) Decreased blood flow
- ) Injury or abnormality of the endothelial wall of the vessel
- ) Changes to the normal properties or processes of blood coagulation
Most thrombi are formed because of what?
decreased blood flow
On the venous side, blood pressure is lower (as compared to the arterial blood)
Embolism
the lodging of a detached mass, or embolus, from one area of the bloodstream to another. Most emboli are formed from blood clots and are referred to as thromboemboli
Infarction
the process of forming an ischemic necrosis within a tissue or organ
Shock
A serious condition involving decreased perfusion of tissues and organs because of inadequate blood flow. Signs and symptoms can include cold, mottled skin, mental status changes, and oliguria
Hypovolemic shock
Due to an inadequate volume of circulating blood most commonly caused by hemorrhage or trauma. In hypovolemic shock, cardiac output (CO) is reduced because of decreased venous return and systemic vascular resistance (SVR) is high because of compensatory vasoconstriction
Distributive shock
Due to an inadequate volume of circulating blood; however, fluid is not actually leaving the body as is seen in hypovolemic shock. Infections (septic), anaphylaxis (anaphylactic shock), and medications (neurogenic shock) are common causes of circulatory vasodilation leading to this type of shock.
CO usually is normal to elevated and SVR is reduced in distributive shock
Cardiogenic shock
Caused by cardiac malfunction and is most commonly seen in patient suffering myocardial infarction or cardiac arrhythmias. CO is reduced and SVR is increased in cardiogenic shocl
Shock can potentially progress through which 3 stages?
Nonprogressive stage-reflex neurohumoral mechanisms are activated, and normal circulation is restored
Progressive stage- tissue and organs remain hypoperfused, thereby increasing damage and decreasing likelihood of compensation. This condition can be seen in cases with severe blood loss.
Irreversible stage
Agenesis
the failure of organ formation during embryo formation
Aplasia
failure of organ or tissue development
Hyperplasia
the enlargement in the size of an organ or tissue because of cellular proliferation
The maintenance of blood pressure depends on what 2 factors?
Cardiac output and systemic vascular resistance
What is HTN most commonly caused by?
Increases in SVR
ANP
Atrial natiuretic peptide is secreted by the atria of the heart in response to increased blood flow. ANP increases urinary excretion of sodium and water thereby causing a decrease in blood pressure.
Nitric oxide
Potent vasodilator released by the endothelial cells in response to changes in blood pressure. Oxidative stress has been suggested to cause a deficiency in nitric oxide, and thus HTN
Endothelin
Vasoconstricting substance. Overstimulation can cause HTN
Insulin is necessary for
the transport of glucose into cells, where it is stored as glycogen to be used for energy
Insulin is produced
by the beta cells of the islets of Langerhans of the pancreas
In addition to glucose uptake, insulin stimulates
amino acid uptake, and thus, protein synthesis by muscle. It can also stimulate fatty acid storage in adipose tissues.
Symptoms of DM
polyuria, polydipsia, polyphagia, fatigue, weight loss
How do most cases of T1DM happen?
Most result from an immune-mediated destruction of beta cells of the pancreas by T-lymphocytes.
The majority of calories should come from
Fruits, vegetables, whole grains, legumes, and nuts
Intake of red meats and saturated fats should be limited
Calories recommended intake
1,800-2,000 kcal/day
Carb recommended intake
45-65% of total daily calories
Protein recommended intake
10-35% of total daily calories
Fat recommended intake
20-35% of total daily calories
Fish recommended intake
8 oz/week
Fiber recommended intake
14g/1000 calories eaten daily
Sodium recommended intake
<2,400 mg/day
Potassium recommended intake
4,700 mg/day
Whole grain recommended intake
> 3 ounce equivalents
Fat free or low fat dairy recommended intake
3 cups
Vitamin B12 recommended intake
2.4mcg/day (esp patients >50 years of age)
Folic acid recommended intake
400-600 mcg/day
Vitamin D recommended intake
25 mcg/day or 1000 IU/day
5 vegetable subgroups
dark green, orange, legumes, starches, and other
4.5 cups/day
What is the requirement to be whole grain?
Must be at least 51% whole grain ingredients by weight and be low in fat
Fat soluble vitamins
ADEK
Most dietary sources of fat should come from
Polyunsaturated fatty acids (PUFAs) and monounsaturated fatty acids (MUFAs)
Polyunsaturated fatty acids (PUFAs) include
Omega 6 fats- soybean, corn, safflower oils
Omega 3 fats- soybean, canola, and flaxseed oil, walnuts, fish
Avoid salt substitutes (potassium chloride) in patients with
kidney disease
BMI
Weight in kg/(height in m)^2
Obesity I
BMI 30-34.9
Obesity II
BMI 35-39.9
How much calorie reduction will prevent weight gain?
50-100kcal/day
What goal calorie reduction for weight loss?
500kcal/day reduction
What is the healthiest way to reduce calorie intake?
Reduce the amount of sugar, fat, and alcohol
Exercise
Resistance exercises (weight training or resistance bands) can reduce
osteoporosis as well as increase muscle strength and tone
A healthcare provider should be consulted before which individuals start an exercise program?
Men >40 and women >50
Individuals with a chronic disease
Individuals who have symptoms such as chest pain or pressure, dizziness, or joint pain
How is the smoking pack year calculated?
Calculated by the number of packs (20 cig/pack) smoked in a day x years smoke.
Example- if a person smokes 2 ppd for 5 years they have a 10 pack year smoking history
5 R’s used to encourage pts to quit smoking
Relevance Risks Rewards Roadblocks Repetition
In counseling pts, pharmacists should use the five A’s
Ask Advise Assess Assist Arrange
Withdrawal symptoms of smoking cessation
Peak 48 hours after cessation, gradually dissipate over the next 2-4 weeks, and completely resolve within 1 month. Increased appetite and weight gain may persist for 6 months
4 subsets of atherosclerotic disease
Coronary heart disease/ cardiovascular disease
Cerebrovascular disease
Peripheral arterial disease
Aortic atherosclerosis including thoracic or abdominal aortic aneurysm
Risk assessment for atherosclerotic disease should begin
at age 20 and be assessed every 4-6 years in low-risk patients and more often in those at higher risk (every 2 years). Risk assessment after age 79 is not necessary
Nonmodifiable heart disease risk factors
Age (>45 in men, >55 in women)
Gender (>men)
Ethnicity (AA at highest risk)
F/H (premature HD in male <55 years of age or females <65 years)
Which ASCVD risk score would benefit from statin therapy
> 7.5
Which ASCVD risk score would benefit from low dose aspirin?
> 10
Statin primary prevention
A pt with LDL > 190
A pt age 40-75 with DM and LDL > 70
A pt age 40-79 w/o DM and LDL >70 and ASCVD >7.5
High intensity statins
Atorvastatin 40-80 mg
Rosuvastatin 20-40 mg
Afib treatments
Rate control- beta blocker, non-dihydropyridine CCH (dilt or verapamil)
Rhythm- amiodarone
Which diuretics cause metabolic alkalosis and hypocalcemia?
Loop
CCBs AE
peripheral edema, constipation
Non-dihydropyridine CCB AE
bradycardia and heart block and can worsen HF
beta blocker AE
fatigue, bradycardia, heart block, and bronchconstriction in pts with lung disease
Congestive heart failure treatment
ACE or ARB
Beta blocker- metoprolol, carvedilol, bisoprolol
Hydralazine + isosorbide if AA
Spironolactone or epleronone
Digoxin is an add on
AE in HF treatments
Need to slowly titrate beta blockers to avoid worsening CHF symptoms Hyperkalemia with spironolactone Risk of toxicity form digoxin HA from isosorbide Lupus from hydralazine
Ischemic stroke treatment
Thrombolysis with alteplase is recommended in pts within 4.5 hours of symptom onset.
Aspirin within 24-48 hours
Anticoagulation with IV heparin or other agents not recommended
Venous thromboembolism treatment (DVT/PE)
IV heparin titrated to PTT or LMWH or subcutaneous fondaparinux
Heparin induced thrombocytopenia
Caused by heparin or LMWH. Can be lifethreatening
F/U VTE therapy
at least 3 months with oral anticoagulation.
Newer agents >warfarin
Asthma treatment
SABA prn
Add a low dose inhaled corticosteroid (ICS)
If more control needed, increase ICS dose or add LABA (salmeterol) or both
If more control needed, add oral corticosteroid, consider omalizumab to high dose ICS + LABA
COPD treatment
Use GOLD guidelines
- ) Begin with SABA prn plus LABA or long-acting anticholinergic (tiotropium)
- ) Add second long acting bronchodilator from class not used
- Consider addition of theophylline or roflumilast (if pt has chronic bronchitis)
What can worsen bronchoconstriction in COPD and asthma?
Non selective beta blockers
Peak expiratory flow rate
Used to monitor asthma severity
Spirometry
Used to monitor COPD, FEV1
CT scan of chest
Diagnostic of PE
Which drugs can cause esophagitis?
Tetracycline abx, biphosphanates
Which drugs worsen GERD by decreasing lower esophageal sphincter tone
Beta blockers. CCBs. and caffeine
PUD treatment
Clindamycin plus either metronidazole or amoxicillin
Plus
PPI for 10-14 days
NSAID induced ulcers are treated with H2RAs or PPIs and the NSAID is stopped or changed to celecoxib. PPIs or misoprostol can be used to prevent NSAID induced ulcers
Which drugs cause hepatic dysfunction
acetaminophen, amiodarone, statins, phenytoin, carbamazepine, valproic acid, azole antifungals, Isoniazid
AST >ALT in
alcohol induced liver disease
Alkaline phosphatase and bilirubin are present in
elevated levels in cholestatic liver disease
Otitis media treatment
10 days of high dose amoxicillin 1st line
Oral cephalosporins, macrolides, and clindamycins used in allergy
Sinusitis treatment (abx)
Amoxicillin, doxycycline (adults only)
Resp FQ or clindamycin + cefepime if high risk
Pharyngitis treatment
Pen VK, amoxicillin, cephalosporins, azithromycin, clindamycin
CAP treatment outpatient
Doxycycline or azithromycin or clarithromycin
With comorbidities- rep quinolone or high dose Amoxicillin/ clavunate added to above
CAP treatment inpatient
Respiratory quinolone or a combo of cephalosporin (ceftriaxone) plus azith, clarith, or doxy
CAP in ICU
Pts require anti-pseudomonal coverage
Cefepime, Pip/Tazo, meropenem
And possible MRSA coverage
Vanc
Skin and soft tissue infections abx
Nonpurlent, use penicillin, cephalexin, or clindamycin
Severe- Pip/Tazo plus vancomycin
Purulent infections should target MRSA
Doxy or TMP-SMX used for moderate purulent infections, vanc, linezolid, daptomycin, or ceftaroline used for severe
CDiff associated diarrhea (CDAD) treatment
10-14 days with oral or IV metronidazole if less severe or oral vanc if more severe
Most severe- metronidazole + oral vanc
Recurrence treated with same agent or fidaxomicin.
Frequent recurrences treated with long term oral vanc, fidaxomicin, or fecal microbiota transplant
Uncomplicated cystitis treatment
Nitrofurantoin for 5 days or TMP-SMX for 3 days
Alternatives include quinolone x 3 days or fosfomycin x 1 day
Outpatient pyelonephritis treatment
quinolone for 7 days or TMP-SMX for 14 days
Hospitalized UTI treatment
Quinolone
Anti-pseudomonal Beta lactam
Or both
Aminoglycoside can be added but carry risk of nephrotoxicity
Endocarditis treatment
Most commonly caused by streptococcus viridans, staphylococci, and enterococci
Pen G or ceftriaxone for 2-4 weeks. Alternative is vanc
Prosthetic valve endocarditis requires combo with aminoglycoside and rifampin for 2-6 weeks
Meningitis treatment
Pneumococcus and Neisseria meningitides
Empiric therapy of ceftriaxone + vancomycin for children >3 months and adults
Ampicillin is added for listeria coverage if > 60 years old
Ampicillin +cefotaxime or aminoglycoside added if <3 months old
Surgical prophylaxis
start within 60 minutes of incision (120 min for quinolones and vanc)
Drugs should be redosed every 2 1/2 lifes during surgery (4 hours for cefazolin)
Prophylaxis should not exceed 24 hours
Cefazolin is DOC
Clinda and vanc are alternates.
Add metronidazole in colorectal surgery
Sepsis treatment
Rapid, aggressive crystalloid (NS, LR) fluid resuscitation to maintain MAP >65 mmHg and normalize hyperlactetemia
Albumin in pts with higher fluid requirements
For persistent shock, NE is vasopressor of choice, which addition of vasopressin or another catecholamine based on hemodynamic needs.
Low dose corticosteroid can be considered for pts failing vasopressors
C. glabrata, C. krusei treatmetn
Echinocandins (caspofungin), amphotericin B, coriconazole
DOC for asperigillus
voriconazole
Histoplasma, blastomyces, coccidioides, cryptococcus tx
fluconazone or itraconazole if mild
amphotericin B +/- flucytosine for serious
Mucorales (zyhomycetes, rhizopus) tx
amphotericin B or isavuconazole
Aminoglycosides and vancomycin are
nephrotoxic
Linezolid can cause
anemia
thrombocytopenia
neuropathies- do not give with serotonergic drugs
Nephrotoxic drugs
aminoglycoside antibiotics, vancomycin, amphotericin B, IV contrast dye, NSAIDs, ACEIs and ARBs, β-lactams (notably piperacillin–tazobactam), and loop diuretics.
Low therapeutic index agents
phenytoin, carbamazepine, warfarin, digoxin, aminoglycosides, thyroid supplements, cyclosporine, tacrolimus, theophylline, lithium
