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120 Cards in this Set
- Front
- Back
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What is the causative organism behind Tuberculosis? What are some characteristics?
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Mycobacterium tuberculosis
Humans are the only reservoir Acid-fast bacteria Spread by airborn droplets, after inhalation is ingested by macrophages which transport bacteria to the lymph nodes. |
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How significant is Tuberculosis worldwide?
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#1 ID killer worldwide
~2 billion people are infected 3 million deaths per year Resurgence began in the 80's Peaked in the US in 1993 ~16k cases in the US in 2001 |
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How does Tuberculosis enter the US?
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Usually from foreign-born individuals from Vietnam, Philippines, India, China, Mexico, and Haiti
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What is a PPD? What constitutes a positive result?
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Purified protein derivative - an intradermal injection
A wheal is formed at the site of injection, and if negative it fades within 48-72 hours post-injection If the wheal shows signs of a hypersensitivity reaction when read 48-72h later, considered a positive result. |
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How does a PPD test for Tuberculosis?
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The PPD induces a hypersensitivity reaction driven by CD4+ T-lymphocytes specific for Tuberculosis - suggesting at the least prior exposure, at most infection.
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What is Anergy?
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The inability to mount an appropriate hypersensitivity response to an antigen - such as tuberculin. In these cases, patients may have tuberculosis but reactive negative to the PPD test.
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Describe Latent TB infection (LTBI).
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A positive PPD, no physical findings of disease, and CXR that is normal or reveals healed infection.
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Describe TB disease - what is required for one to be diagnosed with TB?
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Patient with infection and S/S or radiographic manifestations of disease
Disease may be pulmonary, extrapulmonary, or both. |
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How is infection control of TB managed in the outpatient setting?
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Review identification and isolation of potentially infectious patients with staff
Annual PPD screening of all health care workers Place surgical masks on at-risk patients |
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How is infection control of TB managed in the inpatient setting?
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Isolate the patient in a negative pressure room that exhausts outside, after being HEPA-filtered and treated with UV light
Six air exchanges per hour Personal respirator use |
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What are the five possible outcomes for a patient with LTBI?
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Patient remains asymptomatic
Granulomas develop Active pulmonary disease develops Reactivation disease develops There is hematogenous spread and extrapulmonary disease |
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If a patient has LTBI, how is it they remain asymptomatic?
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Normal immune response is capable of containing the organism, which may remain dormant until death
10% of asymptomatic LTBI may develop reactivation disease The patient will have a +PPD but a negative CXR They will either be reactors (never had a negative PPD) or converters (had a negative PPD but now have positive PPD) |
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If a patient has LTBI, how do they develop granulomas?
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The normal immune response contains the organism in a granuloma (tubercle).
May remain dormant death Patient will have +PPD, +CXR, and negative sputum acid-fast stain/culture The CXR may reveal Ghon Complex, peripheral lung granuloma and calcified hilar lymph nodes. |
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Which patients with LTBI develop active pulmonary TB?
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Not too common, usually in children
Patient presents with cough, fever, and infiltrates in CXR Patient may or may not have +PPD, CXR is positive, sputum stain and culture are positive. |
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Describe reactivation disease in LTBI patients.
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Reactivation disease occurs months or years after primary infection - most common form of clinically apparent disease.
10% of patients with LTBI will reactivate |
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When is there increased risk of reactivation of TB?
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1st two years post-infection, stress, immunological disease (HIV)
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What is hematogenous spread of TB?
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Seen more commonly in children and HIV-infected patients
May spread to a variety of distant organs May spread within the pulmonary system and cause miliary TB |
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Describe the CXR of miliary TB
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Reticulonodular pattern of TB granulomas in lung fields - diffuse
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What constitutes a positive PPD?
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A wheal of 5mm or greater 48-72h post-inoculation - erythema is irrelevant - only measure induration
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Who should be tested for TB?
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Those who have been in close contact with people with known or suspected TB
Foreign-born persons from areas with endemic TB Health care workers HIV positive individuals IV drug abusers Residents and employees of high-risk congregate settings Certain medically underserved, low-income populations (homeless) Children exposed to adults in high-risk categories |
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What size of induration from a PPD test is considered positive in all individuals?
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15mm
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For which individuals is an induration of 5mm from a PPD test considered positive for TB?
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HIV positive individuals
Person in close recent contact with person with active TB People with CXR consistent with healed TB (Ghon Complex) Patients suspected to have TB Patients who are immunosuppressed (artificially, by disease, etc). |
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For which individuals is an induration of 10mm from a PPD test considered positive for TB?
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IV drug abusers
Patients with chronic illnesses at risk for reactivation Children < 4 years old Immigrants from endemic regions Residents and employees of high-risk congregate areas Persons from medically underserved low-income populations Health care workers |
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What are some factors that affect PPD accuracy?
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Tuberculin reactivity appears 2-12 weeks after infection - if a person has been exposed they should be given a PPD and if negative, retest in 3 months.
False positives - atypical mycobacterium infection (AIDS, children) False negatives (anergy) - age (<6months), poor nutrition, immunosuppression, viral infection, severe or disseminated (miliary) TB |
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How does the measles vaccine affect PPD accuracy?
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Measles vaccine (MMR) may cause anergy for up to 6 weeks
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What is the BCG vaccine? Describe it's purpose, usage, etc.
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A live virus vaccine, prepared from attenuated strains of Mycobacterium bovis - recommended by the WHO for administration at birth in selected 3rd world countries
Protects against miliary and meningeal TB in children (80%) and estimated to be 50% effective in preventing pulmonary TB Limited use in the US, highly variable efficacy, PPD reactivity may or may not occur after administration, interpretation of PPD should be the same in individuals with and without a history of BCG administration |
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If a patient has a positive PPD, what further questions should be asked?
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Determine if they have active symptoms: chronic cough, weight loss, night sweats
Obtain CXR including apical lordotic views |
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If a patient has a +PPD, negative CXR, and is asymptomatic, what kind of TB infection is it?
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Latent TB infection
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If a patient has a +PPD, is asymptomatic, but the CXR reveals granulomas, what kind of TB infection is it?
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Latent TB infection
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What tests must be done to confirm extrapulmonary TB?
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Acid fast stains and culture of CSF
Lymph node biopsies |
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If a patient has a positive PPD and they have LTBI, what steps should be taken?
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Report case to Health Department
Contact investigation - evaluate recent contacts and household contacts Treatment of LTBI Once a positive PPD is documented, patient should not receive further PPDs - if more screening needed, do CXR |
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How is LTBI treated?
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Daily Isoniazid in adults for 6-12 months - reduces rates 65-90%
Daily Isoniazid in children for 9-12 months reduces rates 100% ~300mg daily for 9 months is recommended regimen |
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If an asymptomatic child < 4 years old is in close contact with an individual with active TB, what steps should be taken?
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Do a PPD and CXR - even if both are negative, the child should be placed on an initial prophylactic therapy regimen of Isoniazid.
10-12 weeks later, a second PPD should be given. If that one is negative, patient is asymptomatic and over 6 months old, treatment may be stopped. |
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If an HIV infected patient is in close contact with a person with active TB, what steps should be taken?
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They should receive Isoniazid therapy regardless of PPD, CXR result.
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How do you prevent pyroxidine deficiency (and thus peripheral neuropathy)?
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Supplementation of Pyroxidine - particularly children on milk or meat deficient diets, HIV infected children, breast-feeding infants and their mothers.
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What are some symptoms that strongly indicate active pulmonary TB?
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Cough over 2 weeks duration
Bloody sputum and/or hemoptysis Weight loss Anorexia Fever Night Sweats |
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List the two forms of active pulmonary TB disease.
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Primary Pulmonary TB disease
Post-Primary (Reactivation) Pulmonary TB disease |
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Describe Primary Pulmonary TB disease.
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Peripheral infiltrates with hilar lymphadenopathy. More common in middle and lower lung zones. More common in children. May progress to pleural effusion, miliary pattern, or cavitation. May see atelectasis.
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Describe Post-Primary (Reactivation) Pulmonary TB disease.
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Due to endogenous reactivation of LTBI. Most commonly seen in apical segments. More commonly seen in adults. May proceed to cavitation.
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What are the three main steps in assessing a patient for pulmonary TB?
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1. H & P
2. PPD- remember, 10 - 40% of those with active infection will have anergy, and a negative PPD. 3. CXR- PA + Lateral, with apical lordotic views |
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What are some characteristics of late-stage TB CXRs?
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Cavitation, hilar adenopathy, multiple infiltrates
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In how many patients with active pulmonary TB is there a positive AFB sputum stain?
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70% of patients - presumptive evidence of TB
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How many sputum (or gastric aspirate) samples are required for testing for pulmonary TB?
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Three samples - for culturing acid fast bacilli, mycobacterial culture.
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How does TB appear in an acid fast bacterial stain?
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Red/pink rods
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What is the purpose of culturing TB?
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1. Confirm TB diagnosis
2. Obtain sensitivities for antibiotics Results may take 15-30 days |
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The recommended 4 drug therapy for TB (Isoniazid-Rifampin, Pyrazidamine, and Ethambutol or Streptomycin) is how effective at eradicating TB?
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AFter 2 months of therapy, 85% of patients will have negative TB cultures
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How do you monitor TB treatment?
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Monthly sputum cultures until they convert to negative
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After 32 months, if a patient still has positive TB sputum cultures, what next?
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Consider changing the drug regimen in case of resistance
Consider patient may be non-compliant with treatment regimen |
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Describe TB lymphadenitis (extrapulmonary).
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Most common site of extrapulmonary TB.
Cervical and supraclavicular most common sites. Painless swelling, at first discrete, may develop inflammation, fistula More common in children, women, HIV positive patients. |
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Describe Genitourinary TB (extrapulmonary).
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Second most common extrapulmonary site
May be asymptomatic or present with dysuria and frequency. UA is abnormal, with pyuria and hematuria (90%); routine culture is negative. Mycobacterial urine culture X 3 = positive in 90%. More common in women. May spread to involve fallopian tubes, epididymis. |
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Describe skeletal TB (extrapulmonary).
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Third most common site of extrapulmonary TB.
Most commonly seen in spine, hips, knees. More commonly seen in children. Spinal TB = Pott’s Disease |
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Describe TB meningitis (extrapulmonary).
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More commonly seen in young children and HIV infected patients.
Typically headache, mental changes evolve over 1-2 weeks Nuchal rigidity, cranial nerve palsy and hydrocephalus are common. CSF = increased WBCs and protein with low glucose; AFB stain positive in 20%. If unrecognized, 100% fatal; 25% will have persistent neurologic sequela after treatment. |
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List some forms of extrapulmonary TB.
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TB Lymphadenitis (Scrofula)
Genitourinary TB Renal TB Skeletal TB TB Meningitis GI TB - may simulate Crohn's disease Cutaneous TB - chronic ulcer, abscesses Uveitis Adrenal TB TB otitis Congenital TB - resembles TORCH infection |
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Are patients with LTBI contagious?
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No
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How is spontaneous respiration produced?
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Rhythmic discharge of motor neurons that innervate the respiratory muscles. Discharge is entirely dependent on nerve impulses from the brain.
Regulated by alternations in pO2, pCO2, H+ concentration |
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Where is the voluntary respiratory control center located? How does it work?
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The voluntary control center is located in the cerebral cortex and sends impulses to the respiratory motor neurons via the corticospinal tracts.
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Where is the automatic respiratory control center located? How does it work?
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The automatic system is driven by pacemaker cells in the medulla, and the impulses activate motor neurons in the cervical and thoracic spine that innervate inspiratory muscles. Cervical via phrenic activate diaphragm, and thoracic innervates external intercostal muscles
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How do changes on pCO2, pO2 and [H+] affect the medulla and respiration?
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A rise in pCO2 or [H+] or a drop in pO2 levels, results in increased respiratory motor activity in the medulla.
A decrease in pCO2 or [H+] or increase on pO2 has the opposite effect. |
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What chemoreceptors are most sensitive and responsive to pO2 changes?
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Carotid and Aortic bodies
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What do the medullary chemoreceptors monitor?
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pCO2 and [H+]
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How do the carotid bodies monitor blood chemistry?
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They measure changes in pressure and composition of arterial blood flowing past.
They recognize the partial pressures of O2 mostly - and send signals to the medulla. |
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What chemoreceptors become the primary driver of ventilation in people with chronic hypercapnia (like emphysema)?
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Carotid bodies
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Which chemoreceptors are most sensitive to pCO2?
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Medullary chemoreceptors
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What are the normal ABG values for...
Blood pH? pCO2? pO2? HCO3-? |
7.35-7.45
35-45 mm Hg 80-105 mm Hg HCO3- 22-26 |
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What is the hallmark of hypoventilation?
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Elevation of the alveolar pressure of carbon dioxide - arterial pCO2 increase
Thus producing respiratory acidosis |
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What are symptoms of an acute rise in CO2?
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Anxiety
Dyspnea Confusion Psychosis Hallucinations Coma |
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What are symptoms of chronic hypercapnia?
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Sleep disturbances
Headache Loss of memory Daytime somnolence Personality changes Impaired coordination |
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How does chronic hypoventilation manifest when it reaches severe levels?
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Cyanosis
Stimulates erythropoesis and induces secondary polycythemia |
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What are some effects of hypoxemia in combination with hypercapnia?
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Pulmonary vasoconstriction
Right heart hypertrophy Congestive heart failure Impaired sleep quality - morning fatigue, daytime somnolence, mental confusion, intellectual impairment |
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What are some causes of chronic hypoventilation?
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Impaired respiratory drive - message centers not working
Defective neuromuscular system - support structure not working Impaired ventilatory appartus - respiratory mechanism itself not working |
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What may cause impaired respiratory drive?
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Peripheral and central chemoreceptor dysfunction - such as carotid body trauma, metabolic alkalosis
Brainstem respiratory neuron dysfunction - as in brainstem infarction, bulbar poliomyelitis, primary hypoventilation syndrome, central sleep apnea |
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What is primary alveolar hypoventilation?
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A condition of unknown origin, probably genetic defect, seen in men 20-25 yo
Characterized by chronic hypercapnia and hypoxemia in absence of identifiable neurological disease, respiratory muscle weakness, or mechanical ventilatory defects Failure in the automatic respiratory control system resulting in diminished central respiratory drive |
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How does primary alveolar hypoventilation develop?
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Develops insidiously, though may come to attention as severe respiratory depression after taking a sedative, anesthesia
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What are treatments for primary alveolar hypoventilation?
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When awake, patients are able to voluntarily hyperventilate to reduce their CO2 levels
CPAP - diaphagmatic pacing at night |
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What may produce a defective respiratory neuromuscular system?
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Spinal cord injury at the cervical level or motor neuron disease (amyotrophic lateral sclerosis (Lou Gehrig's Disease))
Respiratory muscle dysfunction due to myasthenia gravis or muscular dystrophy. |
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What may produce an impaired ventilatory apparatus?
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In the chest wall...kyphoscoliosis, ankylosing spondylitis, obesity hypoventilation syndrome (OHS)
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What is Kyphoscholiosis?
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Scoliosis and kyphosis - can be pretty severe
Often congenital, neuromuscular (cerebral palsy, MD), idiopathic form in adolescents (possible genetic predisposition) |
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What is Ankylosing Spondylitis?
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A form of arthritis affecting the spine, though other joints can become involved. Inflammation can lead to severe, chronic pain - can be new bone formation on the spine causing the spine to fuse in a fixed immoveable position, sometimes creating a forward stooped posture.
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What is Obesity Hypoventilation Syndrome?
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Defined by extreme obesity and alveolar hypoventilation during wakefulness. In its classic form, characterized by hypersomnolence, dyspnea, hypoxia, pulmonary HTN with right ventricular failure and peripheral edema
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What is the pathophysiology behind Obesity Hypoventilation Syndrome?
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1) Work of breathing is increased, such that normal ventilation is no longer physically possible because of obesity
2) There may be decreased drive to breathe because it's too much work for the body - body decides it is more efficient to tolerate an elevated PaCO2 by resetting the set-point of the CNS chemoreceptors. |
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What is Pickwickian syndrome?
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Another name for Obesity Hypoventilation Syndrome
Named after a character in Charles Dickens' first novel - the Pickwick papers - which described a character with OHS. |
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What are the two main types of sleep apnea?
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Central
Obstructive |
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Describe central sleep apnea.
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It starts in the brain and features a sudden loss of the normal drive to breathe
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Describe obstructive sleep apnea.
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Starts as an upper airway blockage despite airway drive being present
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Which is more common, central sleep apnea or obstructive sleep apnea?
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Obstructive sleep apnea
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How does central sleep apnea work?
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Due to breathing instability, caused by a variety of conditions, there is transient loss of central drive from the brainstem to the ventilatory muscles, resulting in hypoventilation.
Key to Dx - apneic episodes are not accompanied by any respiratory effort - patient suddenly stops breathing. Cheyne-Stokes breathing pattern observed |
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In which kind of sleep apnea is Cheyne-Stokes breathing seen?
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Central sleep apnea
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What is another name for obstructive sleep apnea?
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Obstructive sleep apnea-hypopnea
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How many people with OSAH are estimated to go undiagnosed?
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80%
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How causes OSAH to happen, and in what patient demographic?
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Caused by repetitive upper airway obstruction during sleep due to narrowing and/or collapse of the respiratory passages though the patient maintains respiratory effort. Sleep is associated with pharyngeal narrowing, increased respiratory resistance, and decreased muscle tone - combined with gravity, it produces snoring.
Most patients are obese - have peri-pharyngeal fat infiltration - have large necks - large tongue or soft palate Some patients have a very receding jaw which alters tongue placement |
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What is the link between OSAH and snoring?
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4% of men and 2% of women who snore have OSAH
More often in older people |
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What is the difference between mere snoring and OSAH?
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In OSAH patients, the pharynx is abnormal in size and/or collapsibility
OSAH patients often have further decreased muscle tone during sleep, pull of gravity in a supine position aggravates the anatomic factors even more |
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How does a patient experience OSAH?
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Complete obstruction occurs, there is continued ventilatory drive, lasting more than 10 seconds
The apnea creates asphyxia/hypoxia until there is brief arousal from sleep which restores normal breathing This sequence can repeat several hundred times each night, unrecognized by the patient except in the form of fragmented sleep. |
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What is the primary cause of daytime hypersomnolence in OSAH patients?
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Sleep fragmentation from repetitive arousals
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What are typical complaints when a patient has OSAH?
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Ongoing, worsening daytime sleepiness and/or their bed partner or family member complains of excessive snoring, or witnessed some apnea
Sleep is worse after using alcohol or sedatives May feel more alert before going to bed than after waking up May complain of memory loss, intellectual impairment, mood disturbance |
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What are concerns for the physician who is caring for a patient with OSAH?
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Development or worsening of already present
systemic hypertension, and/or pulmonary HTN Risk of developing cardiac arrhythmias Worsening of left ventricular function in someone with congestive heart failure (CHF) Development of cor pulmonale (right heart failure) Development of dilated cardiomyopathy Increased number of strokes (CVAs) Death |
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What are some consequences/risks associated with sleep apnea?
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Hypertension
MI Stroke Diabetes Work-related accidents Depression |
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What is the link between cardiorespiratory system and OSAH?
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Cardio-respiratory problems are the most common major sequelae of OSAH.
Thought to be related to... Nocturnal asphyxia Extreme bradycardia > 10 second alternating with tachycardia Abrupt increases in BP during arousals >300 mmHg Increased ventricular afterload during each apneic event Elevated sympathetic and adrenal activity, increased vagal tone secondary to hypoventilation and respiratory acidosis |
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How many apneic patients develop mild pulmonary HTN? Cor pulmonale?
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20% develop pulmonary HTN
10% develop cor pulmonale |
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What are the clinical symptoms of apnea?
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Loud snoring
Severe sleepiness (may be denied by patient) Other symptoms: night sweats, dry mouth or sore throat in morning, personality change, morning confusion, intellectual impairment, impotence, morning headaches, physically restless sleep |
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What is the prototype OSAH patient?
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A middle aged male
hypertensive obese large neck structurally abnormal or crowded airway |
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What may contribute to a crowded upper airway?
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Enlarged tonsils
Micrognathia Retrogniathia Large tongue |
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How do you diagnose someone with sleep apnea?
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Patient must be evaluated while sleeping - a polysomnograph - the gold standard for diagnosis
Some controversy because despite the commonness and morbidity, it's expensive to do a polysomnograph. |
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What are some alternatives to the sleep study?
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Arterial O2 saturation oximetry can be tested all night - and used to confirm the dx if there are at least 10-15 episodes of apnea/hour
Negative results do not exclude the diagnosis - and a full sleep study would be needed if there is still suspicion. |
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What is monitored in a polysomnograph?
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EEG - level of sleep
EOG - electrocculogram - REM EMG - at chin for teeth grinding, on calves for movement Airflow thermocouple sensor at nose to detect apneic episodes Chest belt with sensor to record respiratory effort Abdominal belt with sensor to record respiratory effort Cardiac rhythm leads to follow rate and rhythm O2 sat monitor |
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What is the AI index?
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the # of apneic episodes per hour
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What is the AHI index?
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The total number of apneic and hypopneic episodes/hour
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What is hypopnea?
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Diminished movement of air for > 10 seconds
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What are normal, mild, moderate, moderately severe, and severe values for the AHI?
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Apnea Hypopneic Index
Normal < 5 events per hour Mild 5-15 events per hour Moderate 16-30 events per hour Moderately severe 31-39 events per hour Severe > 40 events per hour |
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Treatment for apnea is reimbursed if ...?
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AHI > 15
AHI between 5 and 14, and one or more complications attributable to apnea and hypopnea are present, which include... excessive sleepiness, impaired neurocognitive function, mood disorders, insomnia, or cardiovascular disease, such as HTN, ischemic heart disease, or a history of cerebrovascular disease |
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How is mild OSAH treated?
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Weight loss
Avoidance of alcohol, sedatives Try OTC treatments like Breathe Right strips, if nasal obstruction is present Consider mandibular repositioning device |
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What is the treatment for OSAH which has the most dramatic results?
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WEIGHT LOSS
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What is the most frequently employed approach to treating OSAH?
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An airway device
In mild-moderate cases, sometimes mandibular repositioning devices are all that is needed |
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What are some treatments for moderate-severe OSAH?
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CPAP
Surgery - UPPP Surgery - Jaw Tracheostomy |
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What is CPAP?
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Continuous positive airway pressure
Provides a pneumatic splint to keep the airway from collapsing. Improves mood and functionality in patients. Decreases incidents of MVA. Requires sleep studies to adjust the pressure. Varying rates of compliance. |
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What is a UPPP?
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Uvulopalatopharyngoplasty
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What are some other surgeries besides UPPP used to treat severe OSAH?
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Radiofrequency Tissue-Volume Reduction of the Tongue
Hyoid Suspension/Advancement Maxillomandibular Advancement Genioglossus Advancement Tracheostomy |
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What percent of apneic crashes are caused by MVAs?
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20%
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Some states require reporting of patients with severe apnea - what are we required/recommended to report?
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Patients who insist on driving before treatment
Patients who wont comply with treatment Patients in driving occupations with higher risk (bus drivers, truckers of hazardous waste) |
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What are the physician responsibilities with regard to sleep apnea?
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Diagnose sleep apnea
Assess the risk for motor accidents Inform the patient of these risks (write it down for them) Treat the patient Have a plan of follow-up to determine the effectiveness of treatment |
