Other PCM Final Flashcards
Sympathetic heart
Parasympathetic heart
T1-T5
Vagus
Sympathetic lungs
Parasympathetic lungs
T2-7,
Vagus
Sympathies effect heart lungs
Causes bronchodilation, decreased secretions, coronary artery vasodilation, increase heart rate
Parasympathetic effect heart and lungs
Bronchoconstriction, increased secretions, coronary artery vasoconstriction, decreased heart rate.
Pain tolerance is lowered due to what
Hyperactivity of SNS
Normalize sympathetic tone!!!
BE CAREFUL WITH ARRHYTTHMIAS
Myocardium chapman
2nd ICS along sternal border
Intertransverse space between T2 and 3
Bronchus chapman
2nd ICS along sternal border
Lateral to T2 spinous process
Vacuum
Contraindicated in COPD
Heart failure OM
Consider fluid status before treating-can the heart tolerate increased fluid return/circulation/stress
Diaphragm
S1, S2, AR, MR, friction rub high pitched
Bell
S3, S4, MX carotid bruit
Low pitched
S3
Dull, low pitched, best heard with bell
Due to high pressures and abrupt deceleration of inflow across the mitral valve at the end of the rapid filling phase
Physiologic in children/young adults
Pathologic >40 Kentucky
S4
Dull, low pitch, best heard with bell
Atrial gallop from forceful contraction of atrial against a stiffened (low compliant) ventricle
Can be normal in trained athletes (tennesee)
Systolic murmur
AS< PS, MR, TR
Diastolic murmur
AR< PR< MS, TS
Weber
Lateralization
Sound lateralize to one ear-conduction loss int hat ear of sensorineural loss in opposite
Rinse
Compare air and bone conduction
AC.BC normalAC=BC or BC>AC conductive loss to that ear
When do frontal sinus form
7 years old
Aphthous ulcers
Canker sores
Cheilitis
B12 or iron defiency , red cracks at corners of mouth
Gators palatines
Benign lump on hard palate
Generalizer hperresonance
COPD emphysema
Unilateral hyperresonance
Large pneumothorax, large air filled bulla in lung
Decreased breath sounds
Decreased air flow (COPD, muscular weakness)
Poor transmission of sound (COPD, pleural effusion, pneumothorax)
Wheeze
Narrowed airway COPD bronchitis, asthma
Crackles
Fine-Velcro -interstitial pulmonary fibrosis
Ronchi
Secretions in airway
Strider
Inspiratory wheeze, partial obstruction larynx or trachea
Pleural friction rub
Inflamed pleura
Bronchophony
Consolidation
Spoken words louder or clearer
Egophony
We sound a
Pneumonia
Whisper
99 louder
Lung sound normal
Vesicular
Lobar pneumonia
Whispered sound louder increased fremitis, bronchial sounds
NonTB mycobacteria infection (NT, M kansaii)
Fatigue, dyspnea, occasional hemoptysis,
Diagnose NTM
Sputum culture and molecular diagnostics
Fungal infection
Varies by etiology but can present with pneumonia, nodules, cavitation
Diagnose fungal infection
Results, regional exposure
Lung cancer
Fever, cough, chest pain, hemoptysis, dyspnea
Diagnose lung cancer
Hisopathology
Lymphoma
Fever, night swears, weight loss
Diagnose lymphoma
Histopathology
Sarcoidosis
Hilar lymphadenopathy, can have cavitary lesions
Diagnose sarcoidosis
Histopatholog-noncaseating granulomas
Septic emboli
Extrapulmonary infection (typically endocarditis) embolizing to lung
Diagnose septic emboli
Blood culture, echocardiogram
Lung abscess
Fever, cough, sputum production
Lung abscess cxr
Air fluid levels in a cavitary lesion, other pulmonary infiltrates
Who is at risk for TB
Know someone with TB
Immigrants ( from less than 5 years)
Resident or employees of high risk area (jail, prison, nursing homes, homeless shelters, healthcare facilities, drug treatment facilities)
Medically underserved, drug treatment facilities
IV drug
HIV AIDS
BCG (bacilli calmetter guerin) vaccine
The IFN-y release assay can be used when a patient has a positive TST test with a history of a BCG vaccination
INF-y release assay test TB vs BCG
Most people who have had BCG vaccine will have TST reaction
3-19 mm (2-3 months after vaccine)
What if TST test over ten years after vaccine
TST reaction typically <10 mm
What is BCG and getting repeated TST
Reaction can get bigger than 10 mm
Booster phenomenon *healthcare workers, yearly TST in those with history of BCG vaccine)
Interferon gamma release assay (IGRA) are affected by BCG (like quantiferon T GOld)
NOOOOOOO
Signs and symptoms of active pulmonary T
Fever (can be diurnal), night sweats, cough (>2 weeks) (productive or hemoptysis) weight loss, lymphadenopathy
PPD(purified protein derivative)
TST( tuberculin skin test)
Ok
PPD >5 mm induration
HIV, close contact with actively infected person, cxr with fibrotic changes consistent with TB, immunosuppression (TNFa inhibitors, chronic glucocorticoids, chemotherapy, organ transplant)
PPD>10 mm
Persons with clinical conditions that increase risk of reactivationL silicosis, DM, chronic renal failure with dialysis, malignancies, malnourished, IV drug, kids less than 4, from country with high prevalence, residents/employees in high risk setting L jail)
> 15 mm
Health individual >4 with low likelihood of true TB infection
Anergy PPD
No rxn secondary to immune unresponsiveness
Diagnosis T
Sputum culture-MICROBIAL diagnosis
3 separate morning sputum samples are taken for culture on liquid and solid media.
How long for sputum culture TB results
6-8 days slow grower!
Gold standard Tb dianosis
Sputum culture
Sputum staining TB bc have to ask for it!!
Acid fast
Rhodamine-auramine stain-initial screening stain for TB
Ziehl-neelsen or kinyun stain-confirmatory AFB
PPD (TST)
Utilized to determine if person is currently infected or has been previously infected with M TB.
PPD diagnose T
Nope. Supports
Most widely used screen for Tb
PPD
Each, easy, sensitive not specific
Interferon gamma release assay ORGA
Indicates if there has been a cellular response to BT
Who is IGRA used for
People who have gotten BCG (as a vaccine or for cancer therapy)
Can be used to test people who have been exposed to ppl with Tb
Chest x ray Tb for reactivation T
Cavitary lesions typically involve the spices of the lungs
NAAT (nuclei acid amplification test) Tb
In conjunction with a smear that is positive for AFB while cultures are pending .
NAAT-TB
Detects TB genetic material
NAAT-R
Detects INH and rifampin resistance
How long do you have to treat Tb with meds
6 months
Four drugs Tb
Rifampin isoniazid athambutol, pyrazinamide
Side effect rifampin
Red orange fluid, NV rash, hepatitis, Steven johnson
Isoniazid AE
Hepatitis, NV, peripheral neuropathy (give B6), rash
Pyrazinamide AE
Urticaria, hyperuricemia/gout, hepatitis, joint aches
Ethambutol
Optic neuritis color blind
What monitor while on B meds
Kidney and liver function
AE
What should laboratory baseline include before treat T
Hepatic enzymes, CBC, serum, creatinine, uric acid
What test for before Tb treat
Hep B and C in at risk and counseling and test for HIV
What test do if ethambutol
Visual acuity and red green discrimination
Is sputum gotten to monitor efficacy
Yup
Delay treatment for sputum
Don’t delay if clincial diagnosis and awaiting sputum
-start 4 drug tract if active tb
Clinical diagnosis active Tb
Clincial symptoms, assess risk, order radiography, sputum, don’t delay
Latent Tb considerations
Clinically silent (no symptoms, but positive IGRA or TST0 but can become active
Get screening PPD or IGRA->positive->check CXR to make sure there is no active TB
Cxr negative->treat as latent TB with 9 months of INH
Who need to report
Ppl confirmed or suspected Tb must be reported to a state or local public health authority promptly (in many states, this period is 24)
Are labs required to report diagnostic specimens for Tb
Yup to provider and to public health authority
The public health authority can provide a link to expert medical consultation for diagnosis or management
This may be especially useful in regions with limited local expertise or where Tb is not common
CDC
Sponsor regional centers where consultatio is available
How is TB most likely to be transmitted in health care
When health care workers and patients come in contact with persons who have unsuspected TB who are not receiving adequate treatment, and who have not been isolated from others
All healthcare setting need an infection control program designed to ensure the following
Prompt detection of TB disease
Airborne precautions
Treatment of people who have suspected or confirmed Tb disease
A Tb infection control program should be based on ehwta
Three level hierarchy of control measures
Administrative controls
Management measures intended to decrease the risk or exposure to persons with infections TB
Minimize the number of areas where exposure to m Tb may occur
Environmental controls (why we admit to negative pressure rooms)
To prevent the spread and reduce the concentration of infectious droplet nuclei
Controlling the source of infection by using local exhaust ventilation (hoods) and diluting and removing contaminated air by using general ventilation
Controlling the airflow to prevent contamination of air in areas adjacent to the source airborne infection isolation rooms; and cleaning the air by using high efficiency particular air HEPA filtration, or UV germicidal irradiation
Use respiratory protective equipment
Respiratory controls
Consists of the use of personal protective equipment in situations that pose a high risk of exposure to TB disease
Use of respiratory protection equipment can reduce risk of exposure of health care workers to infectious droplet nuclei that ave been expelled into the air from a patient with infectious T disease
The following measures can be taken to reduce the risk for exposure
-implementing a respiratory protection program
-training health care workers on respiratory hygiene and the importance of cough etiquette procedures
Room air
FiO2=21%
Fraction if inspiraed oxygen
Nasal cannula
1-6 liters-FiO2=40-70% (similar to NC. Amount of oxygen adjusted on wall)
Venturi mask
3-15 liters-aerosol mask-FiO2=34-50% (oxygen amount adjusted by the aperture aka fixed orifice device)
Non rebreather
15 liters, bag reservoir-FiO2 80-100%
What effects the respiratory protection
The level os respiratory protection selected
The fit characteristics of the respiratory model
The care in using the respiratory and
The adequacy of training and fit testing program
Nonpowered respirators
With filters
Powered air purifying respiratory
With high efficiency filters
Fit testing performed
During the initial respiratory protection program training and periodically thereafter, in accordance with federal state and local regulations
Acute T OMM
Contraindicated
Can Spears the bacteria to the lymph nodes causing them to be sore of swollen
Complications from lymph node involvement include sepsis, a dangerous infection of the bloodstream, and fistulas, which are abnormal openings, either between organs or between an organ and the body’s exterior
After acute phase
Tart
CS, ME, BLT ribs-thoracic cage and diaphragm impediments
Lymph
ST MFR
Phrenic nerve tract
Increasing air movement and diaphragmatic function
Cardiovascular causes of chest pain
Acute coronary syndrome -unstable angina, NSTMI, STEMI, pericarditis, pericardial tamponade, aortic dissection, valvular heart disease
Pulmonary causes of chest pain
PE, pneumothorax, pleurisy, asthma COPD exacerbation, resp infection
GI causes of chest pain
GERD, esophageal spasm, esophagitis, esophageal rupture (boerhaave SBS), hiatal hernia
Mak causes of chest pain
Costochondritis, rib fracture, spasm
Endocrine cause of chest pain
Hyperthyroidism
Psychiatric chest pain
Severe anxiety, panic attacks, cocain induced vasospasm
Other causes of chest pain
Sickle cell, rheumatic diseases, sarcoidosis, herpes zoster
Chest pain of acute coronary syndrome
Pressure, squeezing, sharp, burning
Radiation acute coronary syndrome presentation
Back, jaw, shoulders, arms, upper abdomen
Palpitations acute coronary syndrome
Possible
Nausea acute coronary syndrome
Secondary to vagal stimulation
Diaphoresis acute coronary syndrome
Secondary to sympathetic discharge
Dyspnea acute coronary syndrome
May/may not improve with Ian or rest
Other possible findings of acute coronary syndrome
Hypotension, HTN, diaphoresis with cool, clams skin, JVD , S3, S4, rales
How does acute coronary syndrome present
Pressure-type retrosternal chest paint hat typically occurs at rest or with minimal exertion lasting >10 min
Can radiate to either or both arms, the neck or the jaw
-pain ma also occur in these areas independent of chest pain
Unexplained new onset or increased exertional dyspnea is the most common angina equivalent
Older patients (>75 years old) and women usually present with typical symptoms of acs, the freque cy of atypical presentations is increased int hese groups as well as in patients with DM, impaired renal function and dementia** -atypical symptoms, including epigastric pain, indigestion, stabbing or pleuritic pain,and increasing dyspnea in the absence of chest pain should raise concern
What do when come in
Thorough cardiovascular exam
Also look at hepatojugular reflux, rales in the lung bases or egophony (sign of heart failure) and/or dependent edema
Risk cvd
Aging, men, family history, cigarettes or have quit less than 6 months ago, or env smoke
Sedentary lifestyle
Obesity
Stres
HTN >140/90
Dyslipidemia LDL>130 HDL<40, or meds, or TC>200
Pre diabetes IFG>100 or OGTT>140 and ,199 done in 2 dif measurements
Negative risk factor cvs
HDL>60
Nonmodifiable risk factors
Factors that increase the risk of developing a condition that cant be changed: age, gender, family
Stable angina
Intermittent chest paint hat can be brought on by exertion or duress. Improves with rest and/or nitroglycerin. Episodes tend to be similar in nature. Episodes generally 2-5 minutes
Unstable angina
Chest pain that can occur at rest, pain tends to escalate over time, episodes last 10 minutes, does not respond to rest of nitroglycerine, high risk of ae: NSTEMI, STEMI
noonspecific ekg findings (may have inverted t wave)-ekg changes are typically transientnormal cardiac enxymes
NSTEMI (least common)
Complete occlusion of minor coronary artery or partial occlusion of major coronary artery that causes ischemia, tissue damage, and possible myocyte damage/necrosis.
**ekg findings are variable-normal or may have St depression, t wave inversion **elevated cardiac enzymes
Stemi(most common
Complete vascular occlusion of major coronary artery leading to ischemia and myocardial damage/necrosis **ST segment elevations affiliated with area of heart where blood flow is affected. May also have new lbbb **elevated cardiac enzymes, severe symptoms
Immediate treatment for ACS
MONA-B
MONA-B
Morphine, O2, nitroglycerina, asprin (Asa), beta blocker
Still give O2 if O2 looks ok
Year..heart is distressed and demanding more
Labs acs
CBC(anemia) CMP(electrolyte imbalance, liver of kidney prob)
Cardiac markers
Troponin I or T immediately upon patient presentation and q6hx3
Ekg
Immediately on presentation, then ekg q8hx3
Cxr
Evaluate potential causes for cp
Lipid panel
Fasting in am (is there HDL? Has patient responded to HDL to) this is not an immediate assessment during the acs evaluation, but rather information to be used for prevention/risk management once the patient is stabilized
Urine drug screen
Consider-are there substances that indicated presentation
Uncontrollable chest pain, new LBBB or stemi
Stat cath lab
Nitroglycerin and hposphodiesterase inhibitors (sildenafil-viagara)
Absolute contraindication secondary to hypotensive effects secondary to systemic vasodilation. Can result in severe hypotension or even death. Use PDE inhibitors within 24 hours of presentation is contraindication to use ntg
Contraindication ntg
PDE inhibitor within 24 hours
