Family med Flashcards
[USPSTF] Grade A and B recs for: Screening 1. Lung ca 2. Colon ca 3. Cervical ca 4. Breast ca 5. BRCA
Screening
1. Lung ca - Low-dose CT every year for those between 55- 80 yo who have 30+ pack-year hx and smoke or quit <15 years
- CRC screening - from 50 - 75 years
- FOBT yearly
- stool DNA testing (cologard) q3yrs
- sigmoidoscopy q5yrs with FOBT q3yrs
- colonoscopy q10yrs - Cervical cancer screening - 21+ screening with pap smear q3 yrs, starting at 30 can do q5yrs pap smear and HPV screening - until age 65 (can stop earlier if mammo for non-HPV reasons eg fibroids)
- if ASCUS - do reflex high risk HPV DNA testing –> if (-), continue routine screening, if (+) –> colpo
- if ASC, LSIL, or HSIL –> do colpo - Breast cancer screening - mammo every 1 or 2 years for women 50 - 75 yo
* ACA says women 40- 44 should get yearly mammos if they want, 45-54 yearly, 55+ q2yrs or yearly if they want - BRCA
A. Non-Ashkenazi
- 2 1st degree relatives w breast cancer, one diagnosed prior to age 50
- 3+ 1st or 2nd degree relatives w breast cancer
- 2+ 1st or 2nd degree relatives w ovarian cancer
- 1st and 2nd degree relatives w breast and ovarian cancer, or one with both cancers
- 1st degree relative w b/l breast ca
- male relative with breast ca
B. Ashkenazi Jew
- any 1st degree relative with breast or ovarian ca
- 2 2nd degree relatives on same side of family w breast or ovarian ca
[USPSTF] Grade A and B recs for: Screening 6. AAA 7. Osteoporosis 8. Hep C 9. GCC 10. Diabetes 11. HIV
Screening
6. AAA screening in men - one time U/S screening in men 65-75 yo who have ever smoked (100+ cigs)
- DEXA scan for women 65+ or <65 yo with risk factors (low body weight, prev fractures, FHx)
if T = -2.5 –> start bisphosphonates (eg alendronate)
* AAFP says men 70+ should also be screened - Hep C - screen one time HepCAb in baby boomers born bw 1945 - 1965
- GCC testing - GCC testing for chlamydia and gonorrhea in sexually active women 24 yo and younger
- Diabetes - screen blood glucose in adults 40- 75 who are overweight or have HTN (>130/85) or HLD (as part of CV risk assessment)
- HIV - one-time in 15 - 65 years old, testing for all pregnant women
* also depression screening in 12+ if there are support resources available
[USPSTF] Grade A and B recs for: 12. Aspirin preventive medications 13. HLD screening 14. Statin-preventive medications
- Aspirin preventive medications - low-dose aspirin for primary prevention of CVD and CRC in adults 50-59 yo with a >10% 10-year CV risk
- need to take aspirin for 10 years (so have life expectancy of that timeframe) and cannot have increased risk bleeding - HLD - screening nonfasting total and HDL cholesterol
- screen M > 35 yo or F > 45 yo or either M or F > 20 yo with risk factors (smokers, DM, FHx, HTN)
- if >240 or 200+ with risk factors - get fasting lipid panel - Statin-preventive medications - adults w/out hx of CVD should use low or moderate-dose statin if:
- 40-75 yo
and 1+ CVD risk factors (HLD, DM, HTN, or tobacco)
and >10% 10-year CVD risk
[USPSTF] Grade A and B recs for: 15. Screening in pregnant women 16. Immunizations 17. Tetanus booster for clean vs dirty wounds
- Pregnant women:
- Bacteriuria screening - UA and urine cx bw 12-16 wks or at 1st prenatal visit
- gestational DM screen post 24 weeks gestation
- type and screen (Rh, ABO incompatibility)
- pap smear + Rb Ab, CBC
- Hep B, HIV, GCC, syphilis (RPR) - Immunizations
- influenza yearly (need to be <50 for live nasal spray, egg allergy c/i IM inactivated)
- PCV23 for immunocompromised or chronic conditions (COPD, DM, smoking, cancer) for 19-64 yo
- at 50 yo, start giving herpes zoster vaccine (Shingrix > Zostavax)
- at 65 yo (or 5 yrs after last PCV) - PCV 13 (Prevnar), then PCV23 (Pneumovax) at least 8 weeks apart - Tetanus booster q10yrs, replace one with Tdap; also Tdap to >65 yo in contact w infant <12 mos
Wounds: need 3
A. Clean
- if 3+ doses, incl 1 in past 10 years –> nothing
- if <3 doses or >10 yrs since last dose –> tetanus toxoid vaccine
B. Dirty
- if 3+ doses, incl 1 in past 5 years –> nothing
- if 3+ doses but >5 yrs since last dose –> TTvax
- if <3 doses –> TTvax + TIG
[Pediatrics] Immunizations / Vaccinations At birth 2,4,6 mos 6 mos and yearly 12 mos Age 2 Kindergarten Age 12
At birth - Hep B; if mom HbsAg + –> Hep B and HepBIG in separate thighs; also erythromycin eye drops (prevent GC) and vitamin K IM
2,4,6 mos - Hep B, Rota, Dtap, HiB, PCV (pneumococcal), IPV (polio)
6 mos and yearly - flu (first time get 2 doses, 4 weeks apart)
*6+ mos for inactivated shot, 2+ yo for live attenuated nasal spray
12 mos - MMR (neomycin/streptomycin allergy is c/i), Varicella, HepA
Age 2 - Dtap and 2nd HepA (6 mos after 1st one)
Kindergarten (~age 4) - Dtap, last IPV, MMR, Varicella
*5 doses total of Dtap from 6 weeks to 6 years
Age 12 - Tdap booster (every 10 years), meningococcal, Gardasil (3 doses)
- Only need two doses gardasil if 11-14 but they need to be 6+ mos apart. If less then need three doses
- Need 2 doses Hep A, 3 B - pick up where you left off; if you don’t know - then redo vaccination schedule
- can’t play catchup with Rota >15 weeks after schedule
[Pediatrics] Developmental milestones - motor, language, social 1 month 2 months 4 months 6 months 9 months
Developmental milestones: 1 month A. Motor - reacts to pain B. Language - responds to noise C. Social - regards face, eye contact
2 months
A. Motor - sustains head, follows object to midline
B. Language - coos
C. Social - social smile, recognizes parents
4 months
A. Motor - rolls over, follows objects / hands to midline, sits with support
B. Language - laughs
C. Social - looks around and turns to voice, regards hand
6 months
A. Motor - rolls over both ways, sit with support or unsupported, transfers objects hand to hand
B. Language - babbles
C. Social - stranger anxiety
9 months
A. Motor - sits unsupported, pulls to stand / cruises, crawls, 3 finger pincer grasp, holds cup
B. Language - says dada and mama
C. Social - explores, waves bye
[Pediatrics] Developmental milestones - motor, language, social 12 (1 year) 24 (2 years) 36 (3 years) 60 (5 years)
12 (1 year)
A. Motor - walks, throws object, 2 finger grasp
B. Language - 1-3 words, follows 1-step commands (“come”)
C. Social - separation anxiety
24 (2 years)
A. Motor - walks up and down stairs, runs, kicks ball, holds spoon
B. Language - 1/2 speech comprehensible, 2 word sentences
C. Social - parallel play
36 (3 years)
A. Motor - copies circle, rides tricycle
B. Language - 3/4 speech understandable, recognizes 3 colors
C. Social - group play, knows name age and sex
48 (4 years)
A. Motor - copies cross and square, hops on 1 foot, throws ball, goes to toilet alone, can ID 4 body parts
B. Language - speech understandable
60 (5 years)
A. Motor - copies triangle, catches ball, dresses mostly independently
B. Language - writes name
72 (6 years)
A. Motor - ties shoes, skips w alternating feet, draws person w 6 parts
B. Language - IDs left and right
[Pediatrics]
Describe causes, clinical, mgmt of wheezing in kids:
1. RSV bronchiolitis
2. Croup
- RSV bronchiolitis - MCC acute wheezing in infants <6 mos; more common in winter
A. Cause - viral, more common in winter
B. Clinical - URI prodrome (rhinorrhea, nasal congestion) –> wheezy cough, low grade fever, decreased feeding, dehydration
- respiratory distress (tachypnea with retractions and low Sa02) but NO stridor
C. Mgmt - give 02 if Sa02 < 90% + supportive care (humidified 02, fluids)
- pavalizumab vaccine if preemie <29 weeks, chronic lung disease of prematurity, or CHD
- complication is apnea esp if <2 mos - Croup (laryngotracheobronchitis)
A. Cause - parainfluenza virus, 6 mos - 3 yrs, more common in fall/winter
B. Clinical - URI prodrome (rhinorrhea, nasal congestion) –> gradual onset of low grade fever with barking cough, inspiratory stridor 2/2 laryngeal subglottic edema
- sx improve in cold air
C. Mgmt - steroids- glucocorticoids (dexamethasone), nebulized racemic epi for moderate to severe distress
[Pediatrics]
Describe causes, clinical, mgmt of wheezing in kids:
3. Epiglottitis
4. Bacterial tracheitis
- Epiglottitis
A. Cause - HiB is MCC (Even in immunized children),also GABHS; peak incidence ~3 yo
B. Clinical - bacterial infection of supraglottic tissue –> acute onset of high fever + drooling, dysphagia, distress (no prodrome of cough, rhinorrhea, congestion)
- signs of impending airway obstruction - worsening inspiratory stridor, muffled hot potato voice, tripod position of sitting, hyperextension of neck
C. Mgmt - emergency! OR for endotracheal intubation; IV Augmentin (amoxicillin + clavulanate) + ceftriaxone - Bacterial tracheitis
A. Cause - S aureus, GABHS, H flu, Moraxella
B. Clinical - sudden worsening post-URI with high fever, stridor, cough
- thick secretions –> risk of upper airway obstruction
C. Mgmt - similar to epiglottitis - OR for intubation + ceftriaxone, clinda, unasyn (amp + sul)
[Pediatrics]
Describe causes, clinical, mgmt of wheezing in kids:
5. Retropharyngeal abscess
6. Peritonsillar abscess
- Retropharyngeal abscess
A. Causes - polymicrobial –> S aureus, S pyogenes, anaerobes; direct spread of bacterial infection
B. Presentation - abrupt onset fever w sore throat, refusal of food or to turn head or extend neck (neck pain and limited mobility), posterior pharyngeal bulge, tender cervical LAD, muffled voice, stridor and wheezing
- in kids <4 yo
- prevertebral soft tissue swelling and widening of retropharyngeal space on lateral cervical X-ray
C. Tx - do CT w contrast to determine presence and size of abscess
- needle aspiration or I and D
- abx - IV clinda or 3rd gen ceph + amp, then PO abx
D. Complications - mediastinitis, upper airway obstruction - Peritonsillar abscess - MCC deep neck infection in pediatrics, most common in adolescents
A. Causes - extension of tonsillitis; polymicrobial –> GABHS, S aureus, anaerobes
B. Presentation - “hot potato” voice, uvula deviated, u/l throat and ear pain, dysphagia with drooling
- more common in young teens
- abscess on CT –> hypodensity w rim enhancement, can see extension to contiguous structures
C. Tx - needle aspiration or I and D
- abx (penicillin or unasyn or clinda) for 14 days
- tonsillectomy if recurrent (>5x/year for 2 yrs or >3x/year for 3 yrs)
D. Complications - airway obstruction, cellulitis, nec fasc
[Pediatrics] Describe DDx for causes of limp in: 1. Infants and toddlers 2. Young children 3. Adolescents
- Infants and toddlers
A. Septic arthritis - Kocher criteria –> systemic sx (fever >101.4F), no weight bearing, ESR >40, WBC>12K
- hip kept flexed and abducted, externally rotated; pain with internal abduction
- GABHS and S aureus in <4 mos, S aureus and Strep pyogenes in >4 mos
- tx - joint aspiration, abx + I&D
B. Fractures - stress or traumatic, do plain films
- toddler’s fracture = spiral fracture of tibia in <2 yo, tenderness over site
C. DDH - painless limp, toe-walking on affected side; dx - U/s if <6mos, XRay if >6 mos; tx - Pavlik harness - Young children - workup includes X-rays and CBC/CRP/ESR if there are systemic signs (fever); do U/S to r/o joint effusion; all nl –> do MRI and bone scan
A. Transient synovitis - post-viral hip pain leading to limp and refusal to bear weight and decreased ROM; low-grade fever and normal or slightly elevated ESR CRP WBC
B. Legg-Calve-Perthes - idiopathic avascular necrosis of femoral head, MC in ages 4-8 yo, M>F
- gradual onset hip, thigh, or knee pain with antalgic limp, TTP, and proximal thigh muscle atrophy
- cast leg to maintain femoral head in acetabulum - Adolescents
A. SCFE - overweight boys with pain in hip, thigh, or knee and antalgic limp
- hip flexed and externally rotated
- tx - surgically pinning of femoral head in place to avoid avascular necrosis
B. Osgood-Schlatter - overuse injury with repeated jumping, in male athletes ~13 yo
- painful bump below knee where patellar tendon attaches to tibia
C. Gonoccocal arthritis - purulent arthritis or triad of polyarthralgias, tenosynovitis, and dermatitis (pustules)
[Pulm] COPD Pathophys, CXR and clinical findings: 1. emphysema vs 2. chronic bronchitis
COPD - fixed airway obstruction that is irreversible and progressive
1. Emphysema - “pink puffers”
A. Pathophys - destruction of alveolar walls (smoking, antitrypsin deficiency) –> enlargement of alveoli and respiratory bronchioles –> ↑ compliance and ↓ recoil –> SOB, exhalation through pursed lips to ↑ airway pressure and prevent collapse, skinny bc of ↑ respiratory effort
B. CXR - ↑ AP diameter and flattened diaphragm (barrel chest), ↑ lung field lucency and hyperinflation –> distant heart sounds
- Chronic bronchitis - “blue bloater”
A. Pathophys - hyperplasia of mucous-secreting glands in bronchi (smoking, occupational exposure) –> Reid index >50%, ciliary dysfunction, poor mucous clearance –> productive white thick cough >3 months of year for >2 years
- wheezing, cyanosis (hypoxemia 2/2 shunting), C02 retention, 2 polycythemia
- over time - DOE, pulm HTN, cor pulmonale (RHF 2/2 ↑ pressures in pulm circulation)
B. CXR - bronchial wall thickening, cardiomegaly
[Pulm] COPD 3. Mgmt of COPD A. Stage I B. Stage II C. Stage III D. Stage IV
- Acute exacerbation
A. Causes
B. Clinical presentation
C. Mgmt
- Mgmt of COPD - FEV1/FVC <70%; decline in lung function is irreversible
A. Stage I - FEV1 > 80% –> inhaled SABA (albuterol) prn, inhaled ipratropium BID
B. Stage II - FEV1 50-80% –> add inhaled LABA (salmeterol) BID
C. Stage III - FEV1 30-50% –> add inhaled steroids (fluticasone, triamcinolone) BID to reduce frequency of exacerbations *increase risk bruising, candida, PNA
D. Stage IV - FEV1 <30% –> 02 therapy if evidence of hypoxemia (Sa02 <88%, Pa02 <60mmHg) *only intervention that decreases mortality other than smoking cessation; must be used at least 15 hrs / day - Acute COPD exacerbation
A. Causes - viral or bacterial infection, air pollutants
B. Clinical presentation - cough and change in sputum color (white to green), wheezing, tachypnea, mild respiratory distress (use of accessory muscles), cyanosis
C. Mgmt - short-acting bronchodilator (SABA and anticholinergic), systemic steroids (IV or PO prednisone) for 5-7 days, and oral abx (doxy, ammo, TMP-SMX)
- sputum cx (MCC S pneumo, H flu, and M catarrhalis - and Pseudomonas) and abx (azithro, cipro, augmentin)
- hospitalize if severe sx, nonresponders, AMS, etc
[Pulm] Causes, clinical, and mgmt of URIs: 1. Cough 2. Acute bronchitis 3. Cold
I. Cough
A. Causes - URI, pulm disease (PNA, COPD, Asthma, Cancer, TB), CHF w pulm edema, smoking, postnasal drip, sinusitis, GERD, ACEIs
B. Clinical - acute (<3 weeks) vs chronic (>3, MCC are postnasal drip, GERD, and asthma)
C. Mgmt - treat underlying cause, antitussives eg codeine dextromethorphan
II. Acute bronchitis - inflammation of the tracheobronchial tree (vs PNA which is infection of distal bronchioles and alveoli) –> mucus oversecretion
A. Causes
- MCC is viral; dx of exclusion - r/o PNA, asthma, GERD
- bacterial - higher fever and productive cough (Myco, Chlamydia, B pertussis) esp in young adults
B. Clinical - persistent cough w sputum lasting 1-2 weeks +/- mild fever / malaise, rhinorrhea, nasal congestion
C. Mgmt - self-limited illness - no abx! regardless of duration
- antitussive, albuterol bronchodilator, analgesics
- if persistent cough, likely due to hyperresponsive airways –> inhaled steroids or oral steroid taper
- CXR to r/o PNA if: fever >100.0°F, bloody sputum, or signs of consolidation on PE, tachypnea/cardia
III. Cold - most common URI
A. Cause - viral MCC rhinovirus also adeno, corona, parainfluenza,
B. Clinical - rhinorrhea, sore throat, nonproductive cough, nasal congestion
C. Mgmt - hydration, rest, analgesia, antitussive, nasal decongestant spray, 1st gen antihistamines
[Pulm]
Causes, clinical, and mgmt of URIs:
4. Sinusitis - acute vs chronic
IV. Sinusitis - inflammation of the mucosa of the paranasal sinuses (MC maxillary) and nasal mucosa
A. Causes - allergic rhinitis, viral URIs, nasal obstruction r/t polyps, deviated septum, foreign body
- viral (NCC) - copious b/l clear rhinorrhea; if it lasts > 10 days, fever, worsening sx, or b/l purulent discharge –> think bacterial
- bacterial - S pneumo MCC, H flu –> consider if >7-10 days symptoms (since most viral etiologies resolve by then); anaerobes (more likely chronic)
B. Clinical - acute vs chronic
i. acute - purulent rhinorrhea, cough, stuffiness, sinus or thooth pain or pressure (in maxillary - over the cheeks), fever, worsening of sx after initial improvement
ii. chronic - >2 months with nasal congestion, nasal d/c, facial fullness/discomfort (not really pain), HA
C. Mgmt
i. acute - saline nasal spray, peudoephedrine decongestant (no more than 3-5 days), abx (augmentin, 2nd gen cephs eg cefuroxime), antihistamine if pt has allergies; no CT or MRI necessary
ii. chronic - augmentin, clinda, or moxi + intranasal steroid, endoscopic drainage if needed
[Pulm]
Causes, clinical, and mgmt of URIs:
5. Pharyngitis incl Centor criteria
V. Pharyngitis
A. Causes - MCC is viruses (EBV, HSV, rhino, parainfluenza, adeno), GABHS, GCC, Candida
B. Clinical
- viral more likely to have cough, coryza, rhinorrhea
- Centor criteria for GABHS - 1 point for each:
Cough absent
Exudate on tonsils
Nodes (tender anterior cervical LAD)
Temperature >100.4F
OR - young <14 add one point, OR old >45 subtract 1 point
C. Mgmt
<1 - reassurance that it is viral, analgesia, salt water gargle, lozenges
2-3 - rapid strep, then throat culture
>4 - no rapid strep necessary, empiric tx - PCN, ammo, or erythro to prevent ARF (will not present PSGN)
tender cervical LAD and splenomegaly - do monospot for CMV
[Pulm] PNA A. Causes i. CAP ii. HAP iii. HCAP
B. Clinical
Pneumonia (PNA) - infection of lung parenchyma (LRTI)
A. Causes -
i. CAP
- bacterial typicals (- S pneumo, H flu, Moraxella) - more common in young/old; atypicals (Myco, Chlamydia, Legionella) - more common in adolescents / young adults
- viral - influenza, adeno, RSV, parainfluenza
ii. HAP - at least 48 hours post admission to hospital; Klebsiella, Pseudomonas, Actinebacter, S aureus
iii. HCAP - within 90 days of hospital, nursing home, dialysis - same bugs as HAP
B. Clinical - f/c, productive cough with green sputum, dyspnea, pleuritic chest pain; can present as AMS in elderly
- abrupt onset - more common in bacterial (staph or strep)
- diarrhea, LFTs, hyponatremia - Legionella
- postflu PNA - Staph
- PE - dullness to percussion or egophony, decreased breath sounds, rhonchi or rales; reduced Sa02, tachypnea, tachycardia, hypotension
[Pulm] PNA C. DIagnosis D. Mgmt E. Complications
C. Diagnosis - need fever and infiltrate on CXR to dx (lobar in typicals, b/l and diffuse in atypicals)
- if fever and cough but no infiltrate (negative CXR) –> bronchitis
- if fever and cough and cavitation on CXR –> abscess, do CT to look for fungus, TB
D. Mgmt - determining whether to hospitalize: admit if 2-5 on CURB65 (Confusion, Urea>7, RR>30, BP<90/60, age >65)
- CXR, sputum Gram stain and Culture, blood cultures + CBC / CMP
- infants and school-age kids - MCC is S pneumo –> give ammo
- adolescents + adults –> give azithro + doxy
- chronic comorbidities (DM, CAD, COPD) –> levofloxacin or azithro + augmentin (or cefuroxime or other beta lactam)
- HAP or HCAP - vanc + zosyn (pip/taz)
E. Complications - bacteremia, sepsis, pleural effusion, empyema
[Pulm] Asthma 1. Risk factors 2. Pathophys A. Acute response B. Late phase C. Diagnosis
3. MOA and adverse effects of alcohol pharmacotherapy A. SABA B. LABA C. Corticosteroids D. Montelukast
Asthma - median age of onset 4 yrs
- Risk factors - atopy (hx atopic dermatitis, nasal polyps), family hx
- early respiratory infections eg RSV bronchiolitis - Pathophys - airway inflammation
A. Acute response - IgE response to environmental triggers in lower airways –> mast cell activation –> vasodilation, vascular permeability, smooth muscle bronchoconstriction, mucous secretion –> cough, wheezing
B. Late phase reaction - infiltration of CD4+ T cells into airway parenchyma, inflammatory response comes on after 2-4 hours and persists for weeks
C. Diagnosis - do spirometry (PFTs) –> if pt has normal spirometry, methacholine challenge is gold standard - MOA of alcohol pharmacotherapy
A. SABA (albuterol) - agonizes B2R on bronchial smooth muscle cells –> Reverses bronchoconstriction
- side effects - tachycardia, HA, dizziness
B. LABA (salmeterol) - same MOA; rarely used and never alone bc a/w increased mortality
C. Corticosteroids (prednisone, prednisolone) - block late phase reaction and reduce hyperresponsive airways
D. Montelukast (LRAs) - blocks leukotriene receptors (which increase bronchial tone), good for aspirin- or exercise-induced asthma, or in pts intolerant of ICS; takes 2-4 weeks for effects
*use peak expiratory flow (PEF) to monitor asthma, 80-100% of personal best is good range, <50% needs hospitalization
[Pulm] Asthma Differentiate different types by symptoms, lung function, and management: 1. Intermittent 2. Mild persistent 3. Moderate persistent
1. Intermittent A. Symptoms - daytime sx and SABA use <=2x week - nighttime awakenings <=2x/month - 0-1 exacerbations yearly requiring systemic steroids B. Lung function - normal PFTs bw exacerbations - FEV1/FVC > 85% C. Mgmt - SABA (albuterol) prn
Persistent - >= 2 exacerbations yearly requiring steroids
- Mild persistent
A. Symptoms
- daytime sx and SABA use >2x week
- nighttime awakenings 3-4x / month
B. Lung function - FEV1 > 80%, FEV1/FVC > 80%
C. Mgmt - SABA prn + low-dose inhaled corticosteroid (ICS) - Moderate persistent
A. Symptoms
- daytime sx and SABA use daily
- nighttime awakenings >1x week
B. Lung function - FEV1 = 60-80%, FEV1/FVC = 75%
C. Mgmt - SABA prn + ICS + LABA (salmeterol)
[Pulm] Asthma Differentiate different types by symptoms, lung function, and management: 4. Severe persistent 5. Asthma exacerbation
- Severe persistent
A. Symptoms
- daytime sx and SABA use multiple times / day
- nighttime awakenings nightly
B. Lung function - FEV1 < 60%, FEV1/FVC <75%
C. Mgmt - SABA prn + medium-dose ICS + LABA + oral steroids / montelukast - Asthma exacerbation
A. Symptoms - tachypnea, pulsus paradoxus (weak with inspiration), inspiratory wheezing, absent expiratory breath sounds
- signs of impending respiratory collapse - drowsiness, delayed capillary refill, use of accessory muscles
B. Lung function - worsening bronchoconstriction + airway inflammation + mucus plugging
C. Mgmt - low PC02 (due to hyperventilation) –> inhaled albuterol (B2 agonist) and PO/IV steroids (prednisone) and 02 + IVF
*wheezing increases as airways respond to tx and open up
- intubate if PC02 normalizes (impending resp failure)
- complications – > allergic bronchopulmonary aspergillus
[CV]
CHF
1. Pathophys
2. CXR findings
CHF
- Pathophys - MCC are CAD (2/3) and also HTN, MI, valvular disease, chagas; systolic vs diastolic dysfunction; R vs L HF
- systolic (HFrEF) - dilated ventricle with impaired contractility
- diastolic (HFpEF) - normal LVEF but impaired ventricular relaxation and filling –> LVH, S4
- end result, impairment of ventricle’s ability to fill with or eject blood –> inadequate circulation of blood to meet metabolic needs –> fatigue, fluid retention, overloading of fluid in lungs, low Sa02
- fluid overload –> dyspnea and anxiety –> increased SNS release of catecholamines –> tachycardia, increased PVR –> worsening of symptoms - CXR
- cardiomegaly 2/2 systolic dysfunction
- central vascular congestion (hilar fullness)
- cephalization of pulmonar vessels (can be seen extending from hilum in upper lung fields) 2/2 increased preload
- Kerly B lines (linear densities in periphery of lung fields, represent interstitial fluid in lung tissue) - seen in progressed HF
- pleural effusions (blunting of costophrenic angles)
[CV] CHF 3. Clinical - common signs and sx A. LHF B. RHF
- Mgmt
CHF
- Clinical - RHF vs LHF signs and symptoms
- common symptoms - fatigue, weakness, HA, PND, S3 (volume overload in dilated LV 2/2 rapid ventricular filling OR poor functioning)
- common signs - PMI displaced towards axillary line, tachycardia, cyanosis, oliguria / nocturia, peripheral pitting edema
A. Left HF - increased pressure in pulmonary veins –> pulm congestion and edema
- Symptoms - DOE, SOB, orthopnea, wheezing, tachypnea, cough
- Signs - crackles, Cheyne-Stokes respirations, pleural effusion
B. Right HF - MCC is LHF –> RV systolic dysfunction w dilation and tricuspid regurg –> increased pressure in systemic veins
- Symptoms - n/v, abd distension, RUQ pain, decreased appetite
- Signs - JVD, peripheral edema, jaundice, hepatomegaly or ascites (shifting dullness) or hepatojugular reflex (JVD when you press on liver)
- Mgmt - evaluate via echo, MCC hospitalization in >65 yo
- morphine - anxiolytic AND vasodilator
- furosemide - loop diuretic AND immediate vasodilator of bronchial vasculature
- also ACEI/ARB, BB to decreased preload/afterload and reduce cardiac remodeling
[CV]
Acute decompensated CHF
1. DDx
2. Mgmt of CHF exacerbation
Acute decompensated CHF
- DDx:
- MC triggers are infection and anemia
- MI
- arrhythmias eg afib
- diastolic dysfunction 2/2 uncontrolled HTN –> HFpEF
- ischemic cardiomyopathy
- non-ischemic (dilated, hypertrophic, restrictive, RV dysplasia)
- PE
- hypothyroid or hyperthyroid
- valvular disease - Mgmt of CHF exacerbation - goal is to stabilize cardiopulm system
- reduce preload by sitting patient up, maintain airway and give high-flow 02, and sublingual nitroglycerin (reduces myocardial 02 demand); consider CPAP if still hypoxic
- loops for volume overload
- IV morphine –> analgesic, anxiolytic, and venodilator
- dobutamine or milrinone if HFrEF
- dopamine vasopressor if hypotensive
* avoid NSAIDs - can worsen fluid retention and decrease efficacy of diuretics, ACEIs; avoid BBs - can worsen sx (negative chronotrope, inotrope)
[CV]
CHF management
1. HFrEF
2. HFpEF
- Mgmt of systolic heart failure (HFrEF)
- ACEI or ARB - 1st line; dose-dependent, reduce preload/afterload, improve CO w/out increasing HR, inhibit RAAS and improve myocardial compliance; c/i in pregnancy, b/l renal artery stenosis (bc they dilate efferent arterioles and increase Cr), hypotension, hyperkalemia
- loop diuretics eg Lasix (not for use in HFpEF since diuresis decreases LV filling and worsens HF)
- BBs eg metoprolol, carvedilol - reduce mortality in symptomatic pts when combined w ACEI/ARB; c/i in bradycardia, hypotension, PVD, and bronchospasm
- aldosterone antagonists eg spironolactone, eplerenone - reduce mortality in advanced HF
- digoxin - indicated to reduce hospital stay for uncontrolled HF; no mortality benefit and narrow TI (also increased risk toxicity w renal insufficiency)
* CCBs increase mortality except for amlodipine (treats HTN)
- cardiac resynchronization therapy (pacemaker) - for EF <35%, classes III-IV, QRS >120ms –> prevents cardiac death 2/2 ventricular arrhythmias - Mgmt of diastolic heart failure (HFpEF) - goal is to slow HR, increase filling time; avoid reducing preload and excessive diuresis
- BB eg metoprolol
- CCB eg diltiazem, verapamil - lower HR –> more ventricular filling time –> improved CO
[CV] Cardiovascular diseases - general risk factors I. HTN 1. Causes 2. Risk factors 3. Diagnosis
Cardiovascular diseases: risk factors –> HLD, DM, smoking, HTN, obesity, age > 60, M>F until age 60, and FHx
I. HTN 1. Causes A. Essential (95% cases) B. Secondary - HHHARP CO Hypercalcemia Hyperthyroid Hyperaldosteronism (dx - PRA) Aortic coarct Renovascular HTN - if good control w renal artery stenosis, no testing other than monitoring renal fx; a/w incr in Cr post ACEI/ARB Pheo - pain (HA), pressure (HTN), perspiration, pallor Cushing (dx - dexa suppression test) OSA * also meds - sudafed (pseudophedrine, MAOIs, steroids, cocaine, OCPs)
- Risk factors - age, gender, race (blacks > whites), obesity, FHx, sodium and alcohol intake
- Diagnosis - 2+ readings over 4+ week span greater than 140/90
- get CMP, fasting glucose, lipid panel, UA, and EKG to assess overall CV risk and assess for end-organ damage
[CV] Cardiovascular diseases I. HTN 4. Clinical effect by system 5. Define HTN urgency/emergency and mgmt
- Clinical effect on systems:
A. cardiac - increased SVR (aferload) –> LVH –> decreased LV function –> HF
- accelerates atherosclerosis –> CAD (eg MI), PVD
- aortic dissection
B. neuro - stroke / TIA (most important risk factor for stroke), intracerebral hemorrhage, HTN encephalopathy
C. renal - CKD
D. eyes - retinopathy –> AV nicking, cotton-wool spots, papilledema, hemorrhage and exudates - HTN urgency / emergency: >180 / 120, emergency has end-organ damage (HA, AMS, n/v, syncope, CP, dyspnea, decreased UO)
- lower MAP by 25% in 1st 6 hours
- IV labetelol, nitroprusside, fenoldapam, nicardipine
[CV] Cardiovascular diseases I. HTN 6. Mgmt - goals in blacks, nonblacks, by age, comorbidities (CKD, CAD, DM, CHF, stroke)
- Mgmt - Goals: 150/90 in pts 60+ with no comorbidities (only HTN), 140/90 in <60 w no comorbidities, also with DM or CKD at any age
- lifestyle changes (weight loss via diet/exercise, cut alcohol)
- black - CCB or thiazide, unless they have CKD –> ACEI/ARB
- nonblack <60 yo - ACEI/ARB, thiazides, CCBs
- nonblack >60 yo - CCB, thiazides, ACEI/ARB
- CKD - ACEI/ARB except for stage IV (bc Cr increase can push into stage V –> use hydralazine instead)
- CAD - BB + ACEI/ARB, then CCB
- DM w/out CKD - ACEI/ARB unless black - give CCB or thiazide
- CHF - BB + ACEI, then loops, then spironolactone or combo of vasodilator hydralazine and venodilator isosorbide dinitrate (BiDil)
- stroke - ACEI/ARB + thiazide
[CV] Cardiovascular diseases I. HTN 7. Med side effects A. ACEI/ARB B. Thiazide C. CCB D. BBs E. Clonidine
- Med side effects
A. ACEI/ARB - renoprotective, decreased risk new-onset DM; increase in Cr and K, teratogens; ACEI can cause dry cough, angioedema
B. Thiazides - work synergistically w ACEI but can raise blood sugar; decrease serumK and urineCa; K-wasting, do not work well in CKD (GFR <30), can cause ED
C. CCB (dihydropyridine “-dipines”) - vasodilation of arterial vasculature –> peripheral edema, hypotension
D. BBs (metoprolol, carvedilol, labetelol) - negative inotrope / chronotrope, decrease CO (=SV x HR), decrease renin release
- good for migraines, anxiety, tremor
- can cause bradycardia, bronchospasm (c/i in asthma), depression, ED
- masks hypoglycemic sx in diabetics on insulin
- NOT a 1st line HTN drug* but good for CHF and CAD
E. Clonidine - rebound HTN w missed doses
[CV] Cardiovascular diseases II. HLD 1. Causes A. Primary B. Secondary 2. Risk factors 3. Diagnosis 4. Clinical
II. HLD
1. Causes
A. Primary - familial (Type I exogenous hyperlipidemia - chylomicrons, II hypercholesterolemia- LDL, III dysbetalipoproteinemia - IDL, IV endogenous hyperlipidemia - VLD, V hypertriglyceridemia - VLDL, which distribute TGs, + chylomicrons)
B. Secondary - endocrine (DM, Cushing, hypothyroid), renal (nephrotic syndrome), cirrhosis, meds (estrogen, thiazides, BBs, steroids), pregnancy
- Risk factors - diet, age, obesity, sedentary, FHx, M>F
- Diagnosis - want total cholesterol <200, LDL < 130, TGs < 125
- LDL = total cholesterol - HDL - TG/5
- get TSH, LFTs, BUN/Cr, and glucose levels to exclude secondary causes (hypothyroid, liver disease, nephrotic, and DM, respectively) - Clinical - usually asx or xanthelesma (eyelids), xanthoma (on tendons), pancreatitis
[CV] Cardiovascular diseases II. HLD 5. Mgmt incl MOA, indications, and side effects of meds: A. Statins B. Niacin C. Cholestyramine D. Gemfibrozil E. Ezetimibe
- Mgmt - target LDL is <130 UNLESS pt has established coronary heart disease or DM – target <100
- diet - lower fat intake; aerobic exercise and weight loss and smoking –> increase HDL
- medications:
A. statins - inhibit HMG CoA reductase, lower LDL, reduce mortality; monitor LFTs, can cause myopathy and increase in CPK; teratogen - ACC/AHC says start high intensity statin (atorvastatin, rosuvastatin) if:
*anyone with LDL > 190
*<75yo w clinical CVD (eg prior MI, ischemic stroke, HF, arrhythmia, valvular disease)
*40-75 w DM and LDL >70
*40-75 w 10-year CVD risk >7.5% and LDL >70 - USPSTF says medium intensity statin if 40-75 yo and 1+ CVD risk factor (DM, HTN, HLD, smoking) and >10% 10-year CVD risk
B. Niacin - best at increasing HDL, moderately lowers TGs; do not use in diabetics bc worsens glycemic control; causes flushing (take NSAIDs) and hyperuricemia, check LFTs and CPK
C. Cholestyramine - bile-acid binding resin (liver must use cholesterol to make more); use w statins or niacin to lower LDL; does increase TGs and causes constipation and bloating, decreased absorption of ADEK
D. Gemfibrozil - fenofibrate, lowers TGs by changing hepatic metabolism of lipoprotein (increasing LPL), 2nd best at increasing HDL; can cause cholesterol gallstones, myopathy
E. Ezetimibe - inhibits absorption of cholesterol in small intestine; 2nd line for decrease in LDL (after statins); can cause increase LFTs and diarrhea
[CV] Cardiovascular diseases III. ACS 1. Compare stable, unstable angina vs NSTEMI, STEMI 2. Diamond criteria 3. Workup for CP
ACS
1A. Stable angina - managed outpatient
B. Unstable angina - no heart damage, but demand ischemia 2/2 90% occlusion –> urgent cath
C. NSTEMI - heart damage due to demand ischemia 2/2 90% occlusion –> urgent cath
D. STEMI - heart damage due to supply ischemia 2/2 100% occlusion –> emergent cath (door to balloon 90 min)
- Diamond criteria for typical angina:
i. substernal or L sided CP
ii. CP worsened with exertion, relieved with rest
iii. CP relieved with nitroglycerin - Work-up:
- first, rule out NSTEMI, STEMI
- next, determine if pain is due to coronary ischemia via stress test –> pharm (dobutamine) vs exercise, EKG (look for changes) vs echo (look for stunned myocardium during exertion) vs nuclear (use if prev bypass or HF)
- <3 vessels –> Stent; 3+ vessels –> CABG
* MCC CP in O/P - MSK (eg costochondritis), then GI (eg GERD, PUD, pancreatitis)
[CV]
Cardiovascular diseases
III. ACS
4. Medication mgmt
- Medications for ACS: MONABASHC
Morphine - reduces 02 consumption; a/w increased mortality if used
O2 - give to all to increase 02 carrying capacity
Nitro - subL q5min for 3 doses; treats anginal sx; c/I in right MI (II III avF), hypotension, PDE5 use
Aspirin - give chewable (not enteric) ASAP with chest pain
BBs - give right after aspirin, bc MCC death in first 24hrs after MI is ventricular arrhythmias, also prevent ventricular remodeling
ACEI
Statin
Heparin (therapeutic) - give if NSTEMI/STEMI
Clopidogrel - give load if NSTEMI/STEMI
*give aspirin, BB, ACEI, statin to every patient with ACS
*aspirin and IV nitroglycerin reduce risk of subsequent MI
*CCBs c/i - increase mortality
[CV}
LE edema - cause, clinical, mgmt + compare to PAD
LE edema
A. Cause - MCC is chronic venous insufficiency, also pulm HTN (2/2 OSA) and CHF, DVT, idiopathic esp in younger women, meds (NSAIDs, CCBs, OCPs)
B. Clinical
- CVI - brawny indurated pitting LE edema, stasis dermatitis, large shallow ulcers with irregular edges on medial malleolus; can be u/l or b/l
- lymphedema - 2/2 malignancy (prostate, ovarian, lymphoma), radiation, surgery - nonpitting, varicocities, inability to pinch fold of skin, warty texture
- DVT - u/l leg swelling, tenderness, and pitting edema
- CHF - generalized edema, also seen with renal and hepatic failure
C. Mgmt - first determine u/l vs b/l
- u/l –> get doppler U/S to r/o DVT; erythema –> give abx for cellulitis
- b/l with JVD/crackles/DOE –> get CXR and echo; with ascites –> get LFTs and give spironolactone; otherwise, check U/A for AKI (ATN, nephritic/nephrotic syndrome)
- leg elevation and compression stockings, low sodium diet, decreased fluid intake; diuretics - spironolactone, thiazides
- do not give diuretics for lymphedema, consider abx ppx for cellulitis and pneumatic compression, lymph drainage
- do not biopsy CVI ulcers
D. Compare to PAD –> shiny hairless skin, dependent rubor; intermittent claudication, no edema, weak pulses; round smooth deep ulcers on toes; do venous and arterial Doppler U/S and calculate ABI (lower = more severe)
>1.3 - incompressible vessels eg DM, elderly
1 to 1.3 - normal
.91 - .99 - borderline
<0.4 - severe
[CV}
Palpitations - cause, workup, mgmt
Palpitations
A. Cause -
- MCC is dysrhythmias eg benign disturbances (PAC, isolated PVC, sinus tachy or brady), WPW, sick sinus (tachy-brady), PSVT (AVNRT), VT, Long QT (>440 in M and >460 in F), Brugada (Asian males), afib
- psychiatric - anxiety or panic d/o, stress
- structural heart problems eg MVP, CHF, cardiomyopathy, ASD/VSD - HOCM MCC SCD in adolescents
- noncardiac - anemia, thyroid (hypo or hyper), pheo, hypovolemia, vasovagal syncope
- drugs - caffeine, alcohol, cocaine, decongestants (pseudoephedrine), digoxin, albuterol, theophylline
B. Workup
- EKG for all patients
- CBC, CMP, TSH, urine collection of HMA and VMA (if suspecting pheo)
- can do Holter monitor, echo, exercise stress test (avoid if suspecting HOCM)
C. Mgmt
- BB and CCBs
- SVT - vagal stimulation via valsalva, carotid massage; IV adenosine; if unstable – cardioversion via defibrillation
- afib - anticoagulate, TEE then cardioversion or rate/rhythm control (amiodarone, sotalol, 1C flecainide *c/i with structural heart disease)
- vtach - defibrillation, then amiodarone or lidocaine then AICD
[CV]
Diseases of aorta - causes, clinical, mgmt
1. AAA
2. Dissection
Aorta diseases
1. AAA
A. Cause - atherosclerosis, screen for smokers via abd US in M 65-75 yo who have ever smoked
B. Clinical - pulsatile, asx abd mass; if rupture –> hypotension and back pain
D. Mgmt - aortic diameter >3.5 cm - AAA, observe q1yr with US or CTa
- >4.5 cm - observe q6mos
- >5.5 cm or >0.5cm growth in 6 months - surgery
- Dissection
A. Cause - HTN, Marfan, syphilis (aortitis 2/2 vaso vasorum destruction)
B. Clinical - tearing chest pain radiating to back, asymmetric BP in arms, widened mediastinum on CXR
C. Clinical - dx via CTa
- Stanford type A (ascending aorta) –> sx
- Stanford type B (descending aorta) –> meds (IV labetolol) to control HTN
[Endocrine] 1. Diabetes A. Diagnosis B. Mgmt goals C. Meds incl MOA, side effects - metformin - sulfas - glitazones - AGIs - GLPa agonists - DPP4 inhibitors - SGLT2s - amylin analogs
- Diabetes
A. Diagnosis
- HbA1c > 6.5%
- 2x fasting plasma glucose ≥ 126 mg/dl (7.0 mmol/l)
- plasma glucose ≥ 200 mg/dL (11.1 mmol/l) two hours after a 75 g glucose load (OGTT)
- symptoms (such as polyuria, polydipsia, unexplained weight loss) and a random plasma glucose ≥ 200 mg/dL (11.1 mmol/l)
B. Mgmt goals
- HbA1c < 7.0%
- LDL < 100
- BP < 140/90 or <130 systolic
C. Meds
i. Metformin (biguanide) - 1st line for DM2 –> decreased mortality, insulin levels, LDL + weight loss
- MOA - decreases hepatic gluconeogenesis, increases peripheral tissue sensitivity
- side effects - GI (n/v, diarrhea), lactic acidosis - c/i with renal (Cr>1.4) or hepatic insufficiency, CHF
ii. Sulfonylureas eg glyburide, chlorpropamide and meglitinides
- MOA - insulin secretagogues –> fast acting but cause hypoglycemia, weight gain
iii. Glitazones /TZDs eg rosiglitazone
- MOA - increase insulin sensitivity in peripheral tissue (muscle and fat) –> can be used in CKD but cause weight gain, fluid retention, bone fracture
iv. alpha-glucosidase inhibitors eg acarbose
- MOA - delay carb absorption in small intestine –> weight neutral, GI side effects (flatulence)
v. GLP-1 agonists eg exanatide
- MOA - stimulate insulin release, suppress glucagon, can be used as adjuncts - early satiety, weight loss but n/v, pancreatitis; c/i in DM gastroparesis
vi. DPP4 inhibitors eg sitagliptin
- MOA - allow for GLP1 activation –> insulin release, can be used as adjuncts - weight neutral, upper respiratory sx
vii. SGLT2 inhibitors eg “flozins” - can cause UTIs, yeast infections
viii. amylin analogs eg pramlintide - delay gastric emptying, inhibit glucagon; can cause hypoglycemia
[Endocrine]
2. Gout - causes, clinical, workup, mgmt
Gout:
A. Causes - diet high in purines (red meat, nuts, seafood), alcohol (beer, wine), meds (chemo agents, thiazides / loop diuretics)
B. Clinical - edema, erythema, warmth, effusion of joint; first flare can be confused for cellulitis
4 stages: asymptomatic deposition of crystals –> Acute gout flares –> intercritical segments –> chronic gout (tophi)
C. Workup -MCC acute monoarthritis are infection, crystals, and trauma –> joint aspiration to r/o septic arthritis (>50K WBC with >75% neutrophils); may need X-ray to r/o trauma
- MSU crystals - needle-shaped, negative birefringence
- calcium pyrophosphate - rhomboid, weakly positive birefringence –> pseudogout dx
D. Mgmt
i. acute flare - NSAIDs, colchicine, glucocorticoids eg prednisone (usually 2nd line but use if pt has CKD and NSAIDs are c/i)
ii. maintenance - 24 hr urine collection for uric acid to determine mgmt (don’t start these during acute flare)
- <600 mg –> undersecreter –> give probenicid
- if >600 mg –> overproducer –> give allopurinol
* serum uric acid level may be normal or low in acute flare but useful to monitor bw attacks
[Endocrine] 3. Anemia - workup, types, mgmt I. Microcytic II. Normocytic III. Macrocytic
Anemia: <12 in F and <14 in M –> sx based on acuity, Hb level, and cardiac reserve; Hb 10 - 13 asymptomatic –> Hb <10 leads to fatigue, pallor –> lower can lead to DOE, weakness, presyncope –> MI, TIA, high output HF
Workup: get Hb levels, then MCV
I. Microcytic - due to decreased production, TAILS - get iron studies – ferritin (most important), serum iron, TIBC, % sat
A. Thalassemia - nl iron studies, get Hb electrophoresis - alpha thal is nl and beta thal has ↑HbF, HbA2
- minor - asx (1beta) or mild (2alpha)
- major (3alpha, 2beta) - transfusion + deferoxamine iron chelator
B. ACD - ↑ ferritin, ↓ serum iron, ↓ TIBC
- tx - treat underlying condition w DMARDs, NSAIDs, EPO if severe
C. IDA - ↓ ferritin, ↓ serum iron, ↑ TIBC
- seen in older males with CRC or females with metromenorrhagia –> glossitis, dysphagia
- tx - iron, stool softener (causes constipation) –> should see 0.2g/dL/day increase in Hb
D. Lead/sideroblastic - reversible (alcohol, lead, INH, ↓B6) vs irreversible (myelodysplastic)
II. Normocytic - get retics:
>2% (increased turnover) –> then get LDH, Tbili, hapto
A. Hemolysis - ↑ LDH, ↑ Tbili, ↓ haptoglobin –> then get blood smear to differentiate different types eg sickle cell, G6PD, PNH, AHA, hereditary spherocytosis
B. Hemorrhage - nl LDH, Tbili, hapto
<2% (decreased production) –> get blood smear
C. CKD - nl blood smear
D. Cancer - abnl blood smear eg leukemia, myelodysplastic syndrome
III. Macrocytic - due to decreased production - get smear
- Megaloblastic anemia - 5+ lobed neutrophils (2/2 impaired DNA synthesis)
A. Folate deficiency - develops in months
B. B12 deficiency - develops in years, due to pernicious anemia (no IF), diet, malabsorption (Crohn’s, SIBO, post-gastrectomy or ileal resection)
- subacute combined degeneration –> decreased vibratory and positional sense, do Schilling test
- non-megaloblastic anemia
C. Cirrhosis
D. Alcohol, drugs
[Endocrine]
4. Thyroid
Hypothyroid - cause, diagnosis, clinical, mgmt
Hypothyroid:
A. Cause - MCC Hashimoto (anti-TPO Ab), post-Graves thyroid ablation, thyroiditis, secondary –> hypothalamic/pituitary dysfunction (2/2 pituitary adenoma removal or intracranial radiation)
B. Diagnosis
- primary - high TSH, low fT4; no other imaging needed
- secondary - low TSH, low fT4 –> TRH test, suspect pituitary cause if no increase in TSH
- subclinical hypothyroid - high TSH, normal fT4
- with nl fT4 the TSH level must be >10 µU/mL for a diagnosis of hypothyroidism
- euthyroid sick syndrome - low TSH, low fT4 - due to nonthyroidal systemic illness
C. Clinical - decreased BMR
- cold intolerance
- bradycardia, hypotension, DOE
- fatigue, lethargy, depression
- weight gain
- constipation
- pedal nonpitting edema
- heavy periods
- decreased DTRs w prolonged relaxation phase
- dry skin, coarse brittle thinning hair
- hypercholesterolemia
- proximal muscle weakness w increased CK (normal CK in hyperthyroid)
D. Mgmt - levothyroxine, needs increased during pregnancy although free levels the same
