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Int Med A

Internal Med

QuestionAnswer
Bronchogenic carcinoma CXR Solitary nodule (coin lesion): <3cm; malig: spiculated margins, periph halo, cavitary lesions w/walls >16mm; alig, ctrl calcification usu benign; CT any suspicious nodule
Bronchogenic carcinoma Tx 1st: review prior CXR (estimate doubling time: <30 d is prob infxn, >465 d prob benign); routine screening no mort benefit); LDCT > CXR
Bronchogenic carcinoma mgmt Low prob: watchful waiting; intermediate prob: bx (bronch lower yield for <2cm, fewer comps, TTNA higher yield, more comps), poss PET or VATS; high prob: staging & resection
Carcinoid tumors Sx/Sx cough, hemoptysis, focal wheezing, recurrent pna; diarrhea, flushing
Carcinoid tumors DDx asthma; other carcinoid syndrome: IBS, Crohn, menopause
Carcinoid tumors Dx studies fiberoptic bronch: pink/purple tumor in central airway w/well vascularized stroma; CT to localize; urine 5-hydroxyindoleacetic acid, serum chromogranin A/B
Pulmonary embolism Pathophysiology thrombi from DVT, usu iliofemoral vein; causes hypotension (SBP <90 mmHg or drop in SBP of ≥40 mmHg from baseline for >15 min; may be saddle PE (at bifurcation of L/R PA)
PE Sx/Sx May be Asx; dyspnea, pleuritic pain, cough, orthopnea, calf or thigh pain/swelling, wheezing; tachypnea, tachycardia, rales; decreased breath sounds, loud P2, JVD
PE Dx studies CXR; d-dimer (high NPV); V/Q scan; CT pulmo angiography; Wells criteria
Common sequela of PE pulmonary HTN
Pulmonary hypertension pathophys diffuse narrowing of pulmo arterioles; Mean PA pressure >25 mmHg at rest, and secondary RV fail
PPH plexogenic pulmonary arteriopathy: medial hypertrophy, intimal proliferation and fibroelastosis, and necrotizing arteritis.
PAH Etio (Group 1-5 ); Idiopathic PAH (sporadic & hereditary)(young women), drugs/toxins, CTD, HIV, portal HTN, congenital heart dz
PAH Sx/Sx dyspnea, cyanosis; loud palpable P2, narrowly split or single S2; SEM or diastolic pulmonic regurg w/inspiration; RV 3rd ht sound, RV heave, JVD w/V wave; poss HM, ascites, pleural effusion
PAH DDx PE, COPD, ILD, OSA, pickwickian, CTD/scleroderma, HAPE, P vera
PAH Dx studies CXR (RVH, lg PAs), EKG (RAD, RVH, RBBB), echo, PFT, overnight oximetry, PSG, V/Q scan (confirmed by pulmo angiography)
PAH Tx underlying cause; diuretic, O2, anticoag, digoxin, exercise tx; Group 3: O2 tx, NOTT trial; Grp 4: anticoag. Meds: CCBs, prostanoids (epoprostenol), endothelin receptor antagonists, transplant
Cor pulmonale Pathophysiology Altered RV 2/2 pulmo HTN 2/2 dz; Pulmo vasoconstriction (2/2 alveolar hypoxia or blood acidosis); Anatomic reduction of pulmo vascular bed (emphysema, PE); Inc blood viscosity (polycythemia, SCD); inc pulmonary blood flow
Cor pulmonale Most frequent cause: COPD 2/2 chronic bronchitis or emphysema.
Cor pulmonale Sx/Sx Fatigue, lethargy, exertional syncope / angina; cough, wheeze, hemoptysis, hoarse (recurrent laryngeal n.); anorexia, RUQ pain (2/2 passive hepatic congestion 2/2 RV fail); loud P2, parasternal lift, tricuspid regurg, JVD, edema, HM, ascites
Cor pulmonale Dx studies polycythemia, CXR (lg pulmo arts), EKG (RAD, RVH, big P wave in II), echo, PFT, R ht cath, radionuclide ventriculography, lung bx
Cor pulmonale Tx O2, salt & fluid restriction, diuretics
Bronchiectasis Pathophysiology local parenchymal collapse; irreversible dilation of part of bronchial tree 2/2 mx & elastic tissue destruction
Bronchiectasis requires (1) an infectious insult and (2) impaired drainage, airway obstruction, or a defect in host defense -> transmural inflam, edema, cratering, airway neovasc -> permanent abnl bronchi dilatation / destn
Bronchiectasis Etio obstruction (FBO), defective host defenses, CF, Young syndrome, rheumatic & systemic dz, dyskinetic cilia, pulmonary infxn, allergic bronchopulmonary aspergillosis (ABPA), smoking
Bronchiectasis Sx/Sx cough, daily mucopurulent sputum; dyspnea, wheezing, recurrent pleuritic CP, rhinosinusitis, hemoptysis, crackles, urinary incontinence; digital clubbing uncommon
Bronchiectasis Dx studies CBC, Ig quant, sputum C&S, serum alpha-1 antitrypsin (S or Z alleles and MM phenotype = alpha-1 antitrypsin def↓); PFTs
Bronchiectasis CXR: obscured hemidiaphragm, thin-walled shadows, linear atelectasis, dilated/thickened airways (ie, tram or parallel lines, ring shadows on cross section), irregular ovoid peripheral opacities (= mucopurulent plugs)
Bronchiectasis Hi-res chest CT: thick dilated airways +poss air-fluid levelsl tree-in-bud pattern.
Bronchiectasis tx treat exacerbations: resp FQ +/- tobra; prevention: Ppx Abx (daily cipro or macrolide; 3 problematic orgs: PA, MAC, Aspergillus spp). Bronchial hygeine, hydration & mucus clearance; chest PT; surgery.
COPD RF smoking, BMI<21, HIV, increased airway bacterial load, high CRP, decreased exercise capacity, male
COPD Sx/Sx hyperinflation, decreased breath sounds, wheezes, crackles at lung bases, and/or distant heart sounds; diaphragm depressed /ltd motion; inc AP diameter of chest
End stage COPD s/s Hoover sx (paradoxical retraction of lower interspaces during inspiration), tripod, accessory resp mx use, cyanosis, asterixis due to severe hypercapnia, enlarged, tender liver due to right HF
Chronic bronchitis prod cough for 3 mos in 2 successive yrs
COPD Dx studies GOLD criteria (I-IV: 30-50-80%); BODE index (BMI, FEV1/ obstruction, dyspnea, exercise capacity)
COPD Tx SABA (& anticholinergics); LABA (salmeterol/Serevent, formoterol/Foradil); ICS (fluticasone/Flonase/Flovent, budesonide); Refractory: triple inhaler tx; systemic steroids; poss surgery for emphysema
Most common type of ILD Idiopathic pulmonary fibrosis (epi >40 yo)
IPF RF smoking, infection, environmental pollutants, chronic aspiration, and drugs
IPF DDx other lung dz: drug-related, environmental, infxn, ARDS, amyloid, sarcoid, goodpasture, Wegener, pulmo edema (DDx for ILD: CHF, asthma, COPD)
IPF Dx studies PFT = restrictive LD; CXR, hi-res CT (diffuse patchy fibrosis w/honeycombing), may req surg bx
Hyperthyroid Sx/Sx sweating, heat intolerance, moist skin, fine thinning hair; stare/lid lag; poss cardiac (A-fib or atrial tachy); bone changes (high serum Ca, low PTH, clubbing); irritability; wt loss, loose stool, SOB; fine resting tremor, hyperreflexia
Graves S/S: ophthalmopathy (exophthalmos, eye mx impairment, periorbital edema) & pretibial myxedema (nonpitting scaly thickening, orange-peel)
Hyperthyroid Dx studies low lipids, high glucose, high alk phos, n/n anemia, poss prothrombotic
Hyperthyroid Tx Graves: beta blocker for sxs; thionamides (methimazole, PTU); ablation (radioiodine or surgery)
Hypothyroid Dx studies Primary (95%): high TSH (>5 mU/L), low FT4 (subclinical: high TSH, normal FT4); Central/Secondary: normal TSH, low FT4
Thyroiditis With thyroid pain/TTP Subacute (granulomatous / de Quervain), infxs, radiation-induced, or trauma-induced thyroiditis; 2/2 viral infxn or postviral inflam process, often h/o URI (eg, coxsackie) & assoc w/HLA-B35.
Thyroiditis Without thyroid pain/TTP [variant of hashimoto]: painless (silent) thyroiditis; postpartum, drugs (interferon, IL-2, lithium); fibrous (Riedel)
Thyroiditis Sx/Sx painful: hyper (neck pain, tender diffuse goiter, high T4 and/or T3).then hypo, then recovery; infxs: abrupt neck pain/TTP, f/c, unilateral fluctuant neck mass
Thyroiditis Tx Painful: anti-inflammatory (prednisone, ibuprofen); painless: poss beta for sxs; if TSH>10 during hypo phase, T4 replacement; Infxs: drain, Abx; Riedel: prednisone for sxs
Thyroid neoplasm classification Papillary (75%): MAPK pathway gene mutations; Follicular (ca of thy epithelium; MIFC & WIFC growth patterns; RAS & PPAR-gamma mutations); Anaplastic (5%, undifferentiated, very aggressive) cancer
Thyroid neoplasm Sx/Sx anaplastic: rapidly enlarging mass, bilateral asymmetric thy enlargement (poss dyspnea, dysphagia, hoarse, cough); anorexia, weight loss, fatigue, FUO
Thyroid neoplasm Dx studies thy labs; U/S & FNA (FNA bx dx papillary but not follicular, which req path dx); For recurrence; U/S most sensitive
Thyroid neoplasm Tx Surgery (primary tx for differentiated thy ca): usu uni lobectomy; RI tx; levothyroxine tx (T4 replacement & prevent TSH stim of thy); external beam RT for ca w/mets; For anaplastic: local resection if poss, aduvant tx (rad, CT: doxorubicin/cisplatin)
Cushing syndrome Pathophysiology ACTH dependent (85%): pit adenoma or corticotroph hyperplasia/ ectopic ACTH secretion; ACTH independent(15%): iatrogenic/factitious (most common); adrenocortical adenomas / carcinomas
Cushing Etiology PG 3rd tri, stress, gym rats, depression, EtOH/withdrawal, anorexia, panic dz
Cushing Sx/Sx Centripetal obesity, facial plethora, glucose intolerance, HTN, weakness, proximal myopathy/mx wasting; moon face, buffalo hump, purple striae, hirsutism; osteoporosis; poor wound healing; psych changes
Cushing DDx obesity, metabolic syndrome; EtOH, GHB, depression
Cushing Dx studies firstline: late night salivary cortisol (>0.25 abnl), urinary cortisol, LD dex suppression test (abnormal is >1.9 mcg/dL); midnight serum cortisol >7.5 mcg/dL; also 24 hr urinary cortisol; high wbc, low lymphs, low K+
Cushing Tx transsphenoidal resection of pit adenoma, then 1-3 yrs steroid replacement tx. Alt: gamma knife rad tx (23% cure rate)
Cataracts Pathophysiology opacity of lens causes blindness; prob assoc w/photo-oxidative insult to stratified epi cells in matrix that have high cytoplasmic protein (crystallin) content
Cataracts RFs >60 yo, smoking, EtOH, sunlight exposure, low education, malnutrition, physical inactivity, metabolic syndrome, DM, systemic corticosteroid use
Cataracts Sx/Sx painless, progressive decline in vision; 3 components: nuclear sclerosis, cortical spoking, posterior subcapsular haze
Nuclear cataract characteristics progresses very slowly, usu affects distant vision
Posterior subcapsular cataract causes: disabling glare in bright light
Cataracts Dx studies nondilated fundus exam: lens opacity, poss darkened red reflex, opacities within red reflex, or obscuration of ocular fundus detail. Slit lamp exam: opaque nucleus; “mature cataract” = when red reflex has been lost
Cataracts Tx prevention (diet: lutein & zeaxanthin; vitamins: beta-carotene, C, E; stop smoking); outpatient microsurgery; Post-op: steroid eye drops, NSAID eye drops (ketorolac)
Macular degeneration Pathophysiology degenerative dz of central portion of retina (macula) that results primarily in loss of central vision; dry (atrophic) or wet (neovascular or exudative)
Macular degeneration Poss etio Dry: RPE ischemia or apoptosis; Wet: choroidal neovascularization
Macular degeneration Sx/Sx early is Asx; Dry: gradual vision loss in one or both; Wet: acute visual distortion, usu unilateral
Macular degeneration Dx studies Amsler grid: Wet = distortion of straight lines. Dilated eye exam: Dry = visible drusen; subretinal drusen; retinal pigment epithelium (RPE) atrophy, sub-RPE clumping.
Mac degeneration: Dilated eye exam: Wet = subretinal fluid +/- hemo (growth of abnormal vessels into subretinal space)
Mac degeneration Tx Dry: progresses slowly; no proven tx (try antioxidants & zinc). Wet: VEGF inhibs; thermal laser photocoagulation, photodynamic tx, surgery
Sialadenitis Pathophysiology inspissated mucous plug -> ductal obstruction -> salivary stasis -> secondary infxn (SA) -> poss suppurative sialadenitis (life threatening); Acute bac usu parotid or submandibular
Sialadenitis Sx/Sx swelling, pain w/meals, TTP & erythema of duct opening, purulence
Sialadenitis DDx tumor, mumps, TB, sarcoidosis, dental abscess, Ludwig angina, angioedema
Sialadenitis Dx studies u/s or CT
Sialadenitis Tx IV nafcillin (1gm q6h), switch to PO for total 10 days (Alt: Unasyn, Aug, Keflex, Clinda); hydration, warm compress, sialogogues (lemon drops), gland massage
Esophagitis Pathophysiology prolonged esophageal acid clearance
Esophagitis Etio Transient LES relaxations; Hypotensive LES; hiatal hernia, obesity; PG; eosinophilic esophagitis (allergic)
Esophagitis Tx eosinophilic: acid suppression, esoph dilation, elimination diets, steroids
Esophageal motility disorders etiology diffuse esophageal spasm (DES), nutcracker, hypertensive LES (hypercontractile; resting, midrespiratory pressure >45 mmHg)
Nutcracker esophagus = high amplitude peristaltic contractions in the distal 10 cm of the esophagus
Achalasia = loss of peristalsis in the distal esophagus & failure of LES relaxation, due to degeneration of neurons in the esophageal wall
Achalasia Sx/Sx heartburn, dysphagia, CP; achalasia: dysphagia, wt loss, regurg, CP
Achalasia Dx studies Ba esophagram/xray: birds beak; manometry: high resting LES pressure, incomplete LES relaxation, aperistalsis; endoscopy: dilated esoph
DES Dx studies excess numbers of simultaneous contractions in the distal esophagus; xray: rosary bead or corkscrew esoph
Achalasia: Tx Non-achalasia: diltiazem, trazodone, or botox; dilation w/tapered dilator (bougienage); myotomy
Aortic insufficiency Sx/Sx Asx for decades; wide pulse pressure; S3; water hammer pulse, Corrigan pulse (pulse collapse in carotid);
Aortic insufficiency Signs: deMusset' (head bob), Duroziez (bruit when femoral art is partially compressed), Quincke (capillary pulsations in fingertips); murmur (mild: soft diastolic blowing), apical impulse laterally displaced
Aortic insufficiency Tx serial monitoring; ACEI, CCB; surgery/valve replacement if EF <55%
PUD Pathophysiology extend thru mx mucosa layer; epi: 500k/yr
PUD Etio NSAID, HP, hypersecretion (Z-E syndrome)
PUD DDx GERD, biliary, panc, gastric volvulus, Ao aneurysm
PUD Dx studies upper endo w/gastric bx for HP; urea breath test; serum IgG; fecal Ag
PUD Tx Triple tx: PPI + Amox + clarithro; Quadruple tx: PPI + bismuth + Flagyl + tetracycline
Acute Pancreatitis Etiology EtOH 35%, genetic, obstructive (bil sludge/stones 45%, tumors), SLE, idiopathic 10-30%
Acute Pancreatitis Sx/Sx abd pain, rad to back, worse supine, n/v/f, poss ileus, Cullen sx, Gray Turner sx
Acute Pancreatitis Dx studies lipase more specific than amylase: 3xULN; EGD, ERCP, CT
Ranson’s criteria for acute panc; GALAW (glu, age>55, LDH >2nl, ALT>6nl, WBC>16k
Chronic panc: Etiology EtOH, genetic, obstructive (bil sludge/stones, tumors), SLE, 10-30% idiopathic
Chronic panc Sx/Sx abd pain, rad to back, worse supine, n/v/f, poss steatorrhea, wt loss; late: DM2
Chronic panc Dx studies gold std: secretin stim test; 72hr fecal fat (not sens/spec); serum trypsinogen; plain film KUB, ERCP, EUS, MRCP
Chronic panc Tx panc enzyme preps (pancreatin); EtOH abstinence, pain meds
BPH Pathophysiology dev in periurethral or transitional zone; BPH req older age and functioning Leydig cells. Poss: androgen, estrogen, stromal GF dysregulation, decreased cell death, inc stem cells, genetics
BPH Sx/Sx AUA sx score (0-35, severe >20), IPSS; LUTS (irritative & obstructive sxs). DRE: firm smoothly enlarged, non-nodular
BPH DDx overactive bladder, interstitial cystitis, prostatitis, prostate or bladder ca, UTI, neurogenic bladder, urethral stricture
BPH Tx AUA score 0-7 (mild): watchful waiting; mod/severe: alpha blockers (terazosin, tamsulosin); 5alpha-reductase inhibs (finasteride, dutasteride); TURP; TUNA
Acute renal failure Pathophysiology multiple: pre, infra (vascular, glom, interstitial, tubular [ischemic, nephrotoxic, sepsis), postrenal
ARF Etio contrast, aminoglycoside, NSAIDs, COX-2, cisplatin
ARF Sx/Sx poss edema, rash, purpura; ATN: wt loss; inc K+, dec Ca+
ARF DDx CKD (anemia more likely); ATN: high U-Na, FeNa; lowU-Cr, UrOsmo; Prerenal Azo: low U-Na, FeNa; high U-Cr, UrOsmo
ARF Dx studies FENa <1: prerenal azo; FENa >1: ATN; Inc Cr >0.3 or oliguria <0.5 mL/kg/hr
ATN on micro brown gran cast/tubular epi
RBC Casts: Glomerulonephritis
WBC casts AIN, pyelo
Epithelial casts ATN, AIN (also see eosino casts), GN
Granular casts parenchymal
Waxy casts advanced RF
Fatty casts proteinuria
ARF dx studies Renal US; IVP; CT; MRI
CKD etiology DM (40%), HTN (33%)
Glomerulonephritis Etio PSGS, Hep, Wegener, Goodpasture, Churg Strauss
Glomerulonephritis Dx studies bx & stain (immunofluorescent)
Glomerulonephritis Tx cyclophosphamide, prednisone
Nephritic syndrome AKI, HTN, urinary sediment (RBC, RBC casts)
Nephritic syndrome DDx PSG, SLE, SBE, IgA nephropathy, HSP, Wegener
Nephrotic syndrome Etiology DM2, multi myeloma, amyloid, MCD; Hep C (membranoproliferative); HIV (FSGS)
Nephrotic syndrome Dx studies proteinuria (>3.5 g pro/24hr), albumin <3g/dL, edema, hyperlipidemia; poss hypercoag
Respiratory acidosis Etio impairment in rate of alveolar ventilation; acute medullary resp ctr depression (narcotic OD), resp mx paralysis, airway obstruction; chronic: emphysema, pickwickian
Resp acidosis Sx/Sx somnolence, confusion, narcosis, asterixis; fundi: dilated, tortuous vessels, possible papilledema
Resp acidosis DDx COPD, airway obstruction, CNS depression (opioids), neuromx (GBS, MG, botulism), myxedema
Resp acidosis Dx studies ABG (inc bicarb, dec pH)
Resp alkalosis (hypocapnia) Patho/etio hyperventilation reduces PCO2, inc pH; No. 1 is hyperventilation syndrome (including anxiety); also GNR septicemia/fever, cirrhosis, PE, CHF, ILD, pna, pulmo edema, HAPE, CVA, anemia, PG (2/2 progesterone stim of resp ctr), acute salicylism
Resp alkalosis Sx/Sx lightheadedness, anxiety, perioral numbness, paresthesias
Resp alkalosis DDx PE, pulmo edema, PTX, ARDS, pulmo art HTN, asthma, interstitial pulmo fibrosis
Resp alkalosis Dx studies ABG (inc pH, low PCO2, low bicarb in chronic)
NAGMA = extrarenal bicarb loss (diarrhea, renal bicarb excretion); renal tubular acidosis; CAIs, primary hyperPTHism, Addison dz
AGMA: MUDPILES methanol, uremia, DKA, propylene glycol, isoniazid, lactic acidosis [shock, septicemia, hypoxemia], ethylene glycol, salicylates
AGMA: CUTE DIMPLES C for Cyanide & T for Toluene plus MUDPILES
Metab acidosis Sx/Sx CP, palpitations, HA, AMS (anxiety), decreased visual acuity, n/v/abd pain, wt loss, mx weakness, bone pain; Kussmaul (profound DKA), lethargy, stupor, coma, seizures; V-tach, hypotension
Metab acidosis Tx IV bicarb if pH<7.1 and hemo unstable; tx underlying disorder
Metabolic alkalosis: chloride-responsive (low urine Cl): due to: diuretic tx (contraction alkalosis) or loss of gastric secretions (2/2 vomiting or NG tube)
Metabolic alkalosis: chloride-resistant (high urine Cl): etio Bartter or Gitelman syndrome; hyperaldosteronism; bicarb intake in CKD
Metabolic alkalosis: Dx studies if hypertensive, w/u for hypercorticism (Cushing, or 2/2 renal art stenosis)
Metabolic alkalosis: Tx: Chloride-responsive: correct ECF volume deficit with isotonic saline; d/c diuretics; add H2 blocker or PPI; IV acetazolamide if CV or pulmo dz
Metabolic alkalosis: Tx: Chloride-resistant: surgical resection of mineralcorticoid-producing tumor; ACEI or spironolactone to block aldosterone effect
Which condition: low pH (<7.4), normal-high bicarb (26), high pCO2 (60-100) = Acute respiratory acidosis
Which condition: high pH (>7.4), normal-low bicarb (16-20), low pCO2 (12-35) = Acute respiratory alkalosis
Which condition: low pH (<7.4), low bicarb (4-10), low pCO2 (15-30) = metabolic acidosis (with expected resp compensation if bicarb is 8-10)
Which condition: normal-high pH, low-normal bicarb (8-20), low pCO2 (12-30) = Chronic respiratory alkalosis
Which condition: low pH, high bicarb (28-48), high pCO2 (50-110) = Chronic respiratory acidosis
Which condition: high pH, high bicarb (28-52), high pCO2 (40-70) = metabolic alkalosis (pCO2 lower = 40-50, if W/O expected resp compensation)
Cardiomyopathy types HCM (auto dom), DCM, restrictive (2/2 amyloid)
Cardiomyopathy EKG/CXR CXR cardiomeg, effusions; EKG: ST/TW changes
Giant cell arteritis DDx PMR, Takayasu, RA, amyloid, SLE, polymyositis
Giant cell arteritis S/S / Dx test low fever, temporal TTP, pale fundi, Ao regurg murmur; CRP, ESR, anemia
Giant cell arteritis tx HD csteroids
Giant cell arteritis physiology immune-mediated, large arts (subclavian, axillary, Ao); M>F; w/polymyalgia rheum
PVC: tx beta, amiodarone, poss ablation
Tachyarrhythmia pathophys narrow complex (QRS <.12) or wide (usu VT); either by abnormal impulse formation (enhanced automaticity) or abnormal impulse propagation (reentry)
Most common cause of Tachyarrhythmia (reentry; >1 pathway; most common cause of tachy)
SVT RFs hyperthyroid, HTN, MV dz; VT: prior MI, ischemia, long QT, antiarrhythmics, low Mg
AVRT/AVNRT tx nodal blockers
Arterial occlusive dz RF M>F; 20-30% of >70 yo; Smoking, dyslipidemia, HTN, homocysteinemia, DM, metabolic syndrome; <50 yo w/DM + 1 other RF; 50 - 69 yo with h/o smoking or DM; ≥70 yo
Arterial occlusive dz Pathophysiology flow limiting stenoses occur segmentally
Arterial occlusive dz Sx/Sx exertional intermittent claudication; dec periph pulses, bruits, hair loss, thin shiny skin, mx atrophy
Arterial occlusive dz 2 systems of classification Fontaine and Rutherford: based on sx severity and presence of ulcer or gangrene
Leriche syndrome = aortoiliac dz (arterial occlusive dz of buttock and hip)
Buerger test foot pallor with elevation of leg and, in the dependent position, a dusky red flush spreading proximally from the toes
Arterial occlusive dz DDx DVT, musculoskeletal d/o, peripheral neuropathy, lumbar degenerative spinal canal stenosis (not relieved w/rest) (pseudoclaudication)
Arterial occlusive dz: Dx studies ABI <0.9 (nl = 0.9-1.3); duplex u/s & waveform studies (esp if false normal d/t DM or renal calcification); CTA or MRA; gold std: cath angio (only for pts getting revascularization)
Arterial occlusive dz Tx RF mods: smoking, DM, HTN, HLD; surg (aorto-fem, fem-fem, fem-pop), angioplasty & stenting; cilostazol (PDE5 inhib)
Venous insufficiency RFs: age, FH, ligamentous laxity (eg, hernia, flat feet), prolonged standing, inc BMI, SMK, sedentary, LE trauma, prior DVT, AV shunt, PG, high estrogen
Venous insufficiency Patho reflux (incompetent venous valves), obstruction, venous pump dysfn
Venous insufficiency Dx studies venous u/s; ABI; venography
Venous insufficiency Tx Conservative: leg elevation, exercise, and compression therapy; derm agents; ulcer mgmt. If refractory >6 mos: ablation tx (chem, thermal, mechanical)
Venous insufficiency Mgmt guided by CEAP (clinical, etiologic, anatomic, pathophysiologic) categories
AV block Pathophysiology: 1st degree: AV node most common site; AV impulse is delayed  PR >.20
AV block Pathophysiology: Wenckebach: 2/2 normal pt w/heightened vagal tone, or drugs (digitalis, CCB, beta)
AV block Pathophysiology: 2nd degree Mobitz type II: usu 2/2 His bundle block
AV block Pathophysiology: 3rd degree: 2/2 lesion distal to His bundle; bilateral BBB
AV block Sx/Sx: 3rd degree: wide QRS & V rate <50; wide pulse pressure, cannon venous neck pulses; syncope
AV block Tx Mobitz II or 3d degree: need ventricular pacing
Venous thrombosis Epi 1 in 1000?; M>F, AA>W
Venous thrombosis RF inherited (Factor V Leiden, Pro S or C def), surgery, bedrest/immobility, PG, OCP; malig
Venous thrombosis Sx/Sx DVT & PE; palpable cord (= thrombosed vein), calf or thigh pain, unilateral edema / difference in calf diameters, warmth, tenderness, erythema, superficial venous dilation; Homan sign
Venous thrombosis DDx Mx strain/injury; lymphangitis / lymph obstruction; venous insuff; Baker cyst; Cellulitis
Venous thrombosis Dx studies venous u/s (noncompressible veins); contrast venography; impedance plethysmography
Venous thrombosis Tx – anticoag (not tx but secondary prevention); heparin (monitor aPTT) followed by warfarin x6 mos (PT 2-3); poss thrombolytics (streptokinase, urokinase, tPA)
Most common cause of LV OT obstruction Aortic stenosis (pathogenesis assoc with genetics (NOTCH1) and atherosclerosis)
Aortic stenosis 2 types Subvalvular (d/t: thin membrane (most common), thick fibromx ridge, diffuse tunnel-like obstruction, HOCM); Supravalvular (hourglass deformity (60-75%) or more diffuse narrowing along ascending Ao)
Aortic stenosis Etio US: lipid accumulation, inflammation, CALCIFICATION ; Elsewhere: rheumatic valve dz (fusion of the commissures between the leaflets, with a small central orifice)
Aortic stenosis Sx/Sx: triad w/exertion: HF, syncope, angina; Other: DOE (diastolic ventric dysfn); A-fib, V-arrhythmia, IE, Pulsus parvus et tardus;
Ao stenosis murmur harsh midsystolic crescendo-decrescendo SEM best at RUSB 2nd R intercostal, radiates to b/l carotids. Louder w/squatting, quieter w/standing or Valsalva; sit patient forward, exhalation
Ao stenosis: echo valve opening <3cm2; antegrade velocity across valve >2.6m/sec; progressive concentric hypertrophy
Ao stenosis Tx prevention of dz progression (statin, ?ACEI, HTN tx, IE Ppx); valve replacement (esp concurrently w/CABG); Survival = 2-3 yrs w/o valve replacement
Mitral stenosis Pathophysiology usu rheumatic; symmetric oval orifice & doming of the leaflets in diastole (2/2 fusion of leaflet tips); leaflet thickening / calc 2/2 chronic turbulent flow thru deformed valve -> leaflet fusion & thickening -> obstructed LA-to-LV blood flow
Mitral stenosis Sx/Sx poss A-fib / pulmo HTN; dyspnea, hemoptysis, orthopnea, PND, CP, VTE, IE, R ht fail, hoarse
Mitral stenosis murmur: low-pitched, decrescendo, holodiastolic rumble best at apex (auscult w/bell) in LLD, loud opening snap after S2, all louder with expiration (vs tricuspid stenosis)
Mitral stenosis EKG P-mitrale: broad notched P wave
Mitral stenosis Tx exercise; loop diuretic if pulmo art congestion; digoxin, beta; VTE ppx, IE ppx
Mitral insufficiency Pathophysiology increases preload but reduces afterload; Stages of MR: compensated, transitional, decompensated (EF decreases); Etio – MVP (most common), IE, trauma; MVP can lead to flail MV regurg
Mitral insufficiency Sx/Sx Asx for yrs; poss L ht fail; exercise intolerance, dyspnea
Mitral insufficiency murmur quiet S1, split S2, S3 gallop; murmur holosystolic, best over apex, radiating to axilla / back, blowing and high pitched
Mitral insufficiency Tx serial monitoring; tx A-fib or LA enlargement (poss vasodilators); surg if LV EF<60% or echo LV end sys diameter >4cm
Bacterial endocarditis Pathophys SA, Viridans strep & Strep bovis; Enterococci; HACEK group; Rheumatic; bicuspid
Bacterial endocarditis general Sx/Sx Fever; regurgitant murmurs/sx of HF; small and large emboli in fundi, conjunctivae, skin, digits: petechiae, splinter hemorrhages (nonblanching, linear reddish-brown lesions found under the nail bed)
Janeway lesions macular, blanching, nonpainful, erythematous lesions on the palms and soles
Osler nodes painful, violaceous nodules found in the pulp of fingers and toes, usu in subacute IE
Roth spots exudative, edematous hemorrhagic lesions of the retina
Bacterial endocarditis Sx/Sx (SA) SA: more rapidly progressive & destructive infxn (acute febrile illness, early embolization, valvular regurg, myocardial abscess).
Bacterial endocarditis Dx studies 3 sets blood cx; CXR, EKG; TTE & TEE: evidence of vegetation; high ESR/CRP, normo/normo anemia
Bacterial endocarditis Tx Vanc 1 gm q12h IV + ceftriaxone 2gm q24h (vs staph/strep/enterococci)
Acute rheumatic fever Pathophysiology post-GABHS infxn; strep strains with M protein (shares epitope w/myosin, thus may cause anti-myosin Ab rxn); perivascular granulomatous rxn w/vasculitis; peak 5-15 yo
rheumatic fever Sequelae include: arthritis, carditis (pericarditis, cardiomeg, CHF), chorea, subcutaneous nodules, erythema marginatum
rheumatic fever DDx RA, osteomyelitis, IE, chronic meningococcemia, SLE, Lyme, SCD
Jones criteria = 1 major [carditis (pericarditis, cardiomegaly, CHF), erythema marginatum, sydenham chorea (usu face, tongue, UE), polyarthritis) & 2 minor (fever, polyarthralgia, long PR, high ESR / CRP)
rheumatic fever: non-Jones high ASO & anti-DNAse B to dx recent infxn
rheumatic fever Tx bedrest, salicylates, PCN, csteroids for joint sxs
Aortic insufficiency Sx/Sx Asx for decades; wide pulse pressure; S3; water hammer pulse, Corrigan pulse (pulse collapse in carotid);
Aortic insufficiency Signs: deMusset' (head bob), Duroziez (bruit when femoral art is partially compressed), Quincke (capillary pulsations in fingertips); murmur (mild: soft diastolic blowing), apical impulse laterally displaced
Aortic insufficiency Tx serial monitoring; ACEI, CCB; surgery/valve replacement if EF <55%
Created by: Abarnard
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