Clinical medicine I Final Review
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| Vector same direction as the axis | + deflection
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| Vector and Axis perpendicular to each other | Straight line or equal deflections up and down
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| Vector and axis is opposite direction | - deflection
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| Length of the PR interval, QRS width, | .12-.20s, <.12
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| SA, AV, Ventricle node conduction rates | SA: 60-100, AV: 40-60, Ventricles: 20-40
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| Time from the SA node to the AV node | PR interval
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| How do we determine the axis? | look at lead I and lead aVF,
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| Determination BPM on EKG sheet | 300 150 100 75 60 52 45
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| Rhythm that is no NSR but is irregular | Sinus arrhythmia
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| Another name for Paroxysmal atrial tachycardia (PAT) | Supraventricular tachycardia (SVT)
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| Atrial rate in atrial flutter | 250-350bpm sawtooth pattern
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| MC cause of Atrial flutter | Underlying Heart dz, 30% find no cause, seen w/ dig tox, and PE
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| MC cause of Afib | Rheumatic ht dz, HTN, Ischemic ht dz, thyrotoxicosis ->predisposes for thrombus in atria
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| If SVT stimulus is near SA node, how can we tell the diff b/w SVT and sinus tach? | Rate, Sinus tach
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| Tx of SVT | vagal maneuvers, Adenosine, verapamil, break conduction through re-entry circuit
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| Three or more ectopic beats in a row w/ wide QRS | V-tach –usually underlying ht dz
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| Tx Vtach | Immediate electrical defibrillation, CPR, amiodarone, lidocaine
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| PR interval >,20 sec, in nl hearts, no tx | 1st degree heart block
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| Preogressive prolongation of PR interval until blocked non-conducted P wave | 2nd degree ht block type I (wenckebach)
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| Do distance b/w P waves change with type I 2nd degree ht block? | No, PR gets longer to no QRS complex
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| Causes of 2nd degree block type II | Acute anteroseptal MI, Cardiomyopathy
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| Nl PR interval with sudden dropped QRS complexs | 2nd degree AV block: mobitz II, (non-wenkebach)
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| Atrial and ventricular depolarizations are independent of each other | 3rd degree AV block
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| Causes of 3rd degree AV block | Acute MI, drugs (dig, BB)
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| Are premature atrial contractions problematic | no happen in all ages all ppl, frequent
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| MC cause of PVC’s | hypoxia (uncommon in absence of ht dz): stress, alcohol, caffeine
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| 3 or more PVC’s in a row | considered Vtach , problematic w/ >10/min
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| Dz orientated, ability of a test to correctly identifiy those w/ the dz (true +) | sensitivity True +/True + + false -
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| Healthy orientated, refers to true negatives | specificity
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| Main components of CBC | Hgb, Hct, WBC, MCV, platelets (also get MCH, MCHC, RBC)
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| Nl value of Hgb and Hct | 12-18gm/dl, 21-48%
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| Causes of elevated hgb | dehydration, ^altitude, smokers, Congential ht dz, polycythemia vera
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| Cuases of low hgb | ^ destruction RBC, dec production of RBC, blood loss, preggo, Vit def.
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| Nl value of WBC | 4,000-10,000 x 10^9/L
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| WBC w/ diff components | Neutrophils, lymphocytes, eosinophils, basophils, macrophages
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| MC WBC and found when | Neutrophils 50-70%, bacterial infx, inflammatory condistion
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| When do we see lymphocytes and eosinohpils | lymphocytes: viral (25-40%) E: 1-3%, allergic or fungal infx
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| When do we see basophils and monocytes | B: inflammatory states/parasitic infx, M: phagocytosis bacterial infx
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| Reasons for low WBC | Viral, overwhelming bact. Infx, hypersplenism, meds that suppress bone marrow,
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| Left shift | ^ ration of band cells (immature neutrophils): healthy immune response to infx
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| Increase and decreased of MCV | I: Vit b12, folic acid def. D: iron def. nl: 90-100femoliters
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| Nl platelet count | 150,000-400,000
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| What is found in with a urinalysis dipstick? | Specific gravity, pH, protein, glucose, ketone, leukocyte esterase, bilirubin, blood, urobilinogen, nitrates
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| Bence Jones Proteins is associated with | Multiple myeloma
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| What do RB casts and WB casts signify | R: glomerulonephritis, W: pyelonephritis
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| Nl values of AST and ALT | AST: 10-40IU/L: elevated w/ liver, muscle, cardiac injury ALT: 5-35IU/L ^w/ liver injury (more sensitive)
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| Marker of liver fxn | albumin
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| Coagulation studies | Prothrobin time PT, Partial thromboplastin time aPTT
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| Pancrease studies | Amylase 12-60 U/L, elevates first. Lipase: 20-200U/L remains elevated longer
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| Na+ elevation causes | V/D endocrine K+ dec w/ V/D
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| Nl blood fasting glucose, A1C | 60-126, <5%
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| Nl BUN, creatinine | 6-20 mg/dL C: .6-1.3 (elevated: impaired renal fxn)
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| Increases w/ congestive heart failure | BNP brain natriuretic peptide: produces by ventricles
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| Grades of Heart murmurs | 1-6, 1 hard to hear w/ stethoscope, 4-6loud with palpable thrills
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| Where are most murmurs located? | 95% L sided 50%mitral 45% aortic
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| Sxs frequently seen w/ murmurs | Decreased exercise tolerance, fatigue, syncope, CP, dyspnea, BP^ delayed upstroke or bounding
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| Crescendo-decrescendo murmurs | Systolic, Aortic& Pulmonic stenosis, hypertrophic cardiomyopathy
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| Holosystolic murmurs | Systolic: Mitral & tricuspid regurg, VSD
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| Decrescendo, pistol shot sound murmur | Aortic regurgitation (diastolic)
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| Mid-diastolic murmur | Pulmonic regurg, (diastolic)
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| Low pitched ruble, opening snap murmur | Mitral stenosis (diastolic)
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| Low pitched ruble w/ RV heave | Tricuspid stenosis (diastolic)
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| MC of all valvular ht dz | Aortic stenosis: d/t athreloclerosis, bicuspid valve in the young, Rheumatic ht dz
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| Aortic Stenosis Complications | Angina, Syncope, CHF
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| Palpable S4 heard with heave | aortic stenosis, ECG makes dx
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| Mitral stenosis is a complication of? Sxs? | Rheumatic fever, sxs: exercise intolerance, CHF, Horseness, Afib
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| Crisp systolic click and late systolic murmur | MVP
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| Causes of MVP | Congenital, Autosomal dominant, Connective tissue disorders
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| What increases/decreases the length of a MVP murmur | Standing: valsalva, brings the click closer to S1, squatting: relax, click closer to s2
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| Primary and secondary causes of Mitral regurg | 1: MVP, leaflet defects, 2: LV dilation, Endocardial cushions d/t ischemic ht dz
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| When are prophylactic Abx recommended? | With prosthetic ht valve, hx endocarditis, Cong HD,
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| Types of prosthetic heart valves and uses | Bioprosthetic: mitral, reoperation common, Mecahnical: bleeding common: aortic valve Tissue: recommended w/ life expectancy <15 yrs
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| RF of PVD | age, smoking, obesity, sedentary, hyperlipidemia, HTN, DM
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| PVD Chart | Refer to it :D
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| Significant about sxs of PAD | reproducible pain w/ cramping and tightness
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| Gold std for Temporal arteritis | temporal artery bx: shows giant cells infiltrating the tissue
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| Ankle brachial test | assessing for PAD, take the systolic pressure in legs/ SP in arms Nl: .9-1.2 if > than that: hardening of arteries, .8-.9mild, .5-.8 mod <.5 severe
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| Diff b/w raynauds dz and phenomenon | D: young, no other factors, both hands, -Allen’s P: secondary to HTN, unilateral, + Allen’s
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| Inflammatory changes in sm/med sized arteries and veins in extremities | Buerger’s Dz (Thromoangitis Obliterans)
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| Sxs Buerger’s dz | Male, 20-40 smokers, severe pain w/o physical findings, Clinically dx, w/ angiogram for integrity of arteries
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| Tx Buerger’s dz | Avoid vasoconstriction, proper fitting shoes, elevate foot of bed
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| Etiology of thrombus formation | Virchow’s Triad: Stasis, Intimal Injury, Hypercoagulability
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| Prolonged venous thrombosis | Chronic Venous Insufficiency or Venous Stasis
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| Diagnostic test for DVT, | Homan’s test, Wells Score
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| Wells score results | >3 75% DVT, 1-2, 17%, <1 3%
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| Tx for Superficial venous thrombosis, DVT | SVT: warm compression, NSAIDs for pain and inflammation, DVT, anticoag, compression socks, may need surgery
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| Leading cause of death for men and women of all races and ethnicities | Coronary Heart Disease
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| Types of cholesterol | LDL: bad HDL: good, removes excejss cholesterol from tissues, Chylomicrons and VLDL: transport exogenous lipids, TG’s Main storage for fat
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| Patho of Atherogenisis | ^LDL->oxidized, Macrophages ingest ox. LDL—Foam cells, collegen over it:fibroud plaque: ruptures:platelet aggregation:thrombus
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| Unmodifiable RF for atherosclerosis | Fhx, Dm, Age, also maybe CRP, impaired fasting glucose
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| Modifiable RF for atherosclerosis | Smoking, HTN, low HDL, lifestyle: obesity, physical inactivity, atherogenic diet
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| What cause secondary hyperlipidemia | DM, Hypothroidism, obstructive liver dz, chronic renal failure, drugs ^LDL and dec. HDL
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| Metabolic Syndrome sxs | >3 of following TG’s >150, HDL <40, BP: >130/85, Fasting BGC>110, Waiste obesity
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| When do we check for lipoprotein disorders | parts of cholesterol are way high for the pt’s habitus, age, wt, etc
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| Routine lipid screening recommendations | 20yo every 5 years, FLP
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| CHD Risk equivalents | DM, PAD, AAA, symptomatic carotid A. dz, Multple RF’s confer a 10-yr risk of CHD >20%
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| Major CHD RF’s | Current cigarette smoking, HTN or on antiHTN med, Low HDL <40, FMhx CHD death/MI M<55 F<65, pt age M>45, F>55, Subtrat one RF for HDL >60
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| CHD risk or equivalents LDL goal | <100, Drug therapy of >100 or considered <100
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| Moderate high risk, 10-yr 10-20%(>2RF’s) | LDL <130, consider drugs 100-130
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| Miderate Risk , 10 yr <10% | LDL: <130, Drugs >160
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| 0-1RF Lower risk | LDL < 160, Consider Drug >190
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| TLC’s | Healthy diet, wt reduction, increased Physical activity
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| Complications of untreated hyperlipidemia | cardiovascular, cerebrovascular, peripheral vascular dz
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| Comorbitities to HTN | CAD, L ventricular hypertrophy, Ischemic stroke, chronic kidney dz, DM, PAD
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| Phase of cardiac cycle in which venctricles contract | systole
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| Phase of cardiac cycle in which ventricles relax | diastole
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| Understand wiggers diagram | wiggers diagram
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| Maximuc atrial pressure during ventricle contraction | systolic pressure
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| Point of lowest arterial pressure, pressure which L ventricle must overcome to open aortic valve | Diastolic pressure
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| Cardiac output | HR x SV
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| Nl BP | systolic < 120, Diastolic < 80
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| Prehypertension | systolic 120-139, Diastolic, 80-89
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| HTN stage 1 and 2 | 1: S: 140-159 D: 90-99 2: S: >160 D: >100
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| Measurement needed to classify HTN | two or more readings at 2 or more visits after initial screen
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| Uncomplicated and Comorbities HTN goal | U: 140/90,C: 130/80
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| Some secondary causes of HTN | Pheochromcytoma, Cushing’s, 1 aldosteronism, congenital adrenal hyperplasia, Hyperparathyroidism, Hyper,Hypothyroidism
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| Causes of 2 HTN: Renal, Mechanical, Medication-induced, “white-coat” |
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| Malignant HTN classifications | SBP ≥ 180, DBP ≥ 120
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| Longstanding HTN can lead to what? | encephalopathy, seizures/ and or coma if not treated
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| Modifiable RF’s for HTN | smoking, ETOH intake, physical inactivity, Renal Dz, Obesity, Dyslidemia, DM
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| Unmodifiable RF’s for HTN | age, genetics, race
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| Metabolic syndrome | THBFW, TG’s ≥150, HDL < 40 B: BP ≥ 130/85 F: Fasting BG: >110 Waist: >40M >35F
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| Sxs of HTN | usually asymptomatic, but Neuro: occipital HA early morning, Dizzi, palpitations, fatigue, impotence, Vascular: Epistaxis, hematuria, metorrhagia, blurred vision, CP
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| Labs for HTN workup | find underlying causes, CBC, K+ BUN/Creatinint, Ca+, phosphate, FBG, Lipid profile, TSH, UA, CXR, EKG
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| What are end organ damage evidence of HTN | Brain: stroke, TIA, Eye: Retinopathy
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| Papilledema, A/V nicking, Heemorrhage, Exudates, Cotton Wool spots | Signs of retinopathy of HTN
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| When can S4, cardiomegaly on CXR, and EKG changes all be seen together | longstanding HTN
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| Lifestyle modifications for HTN | Lower BP, Wt reduction, Diet, Exercise, Reduce ETOH to 1-2/day
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| Causes of orthostatic BP drop | MS, Parkinson’s, peripheral neuropath (DM), Gullain-barre’ syndrome, raynaud’s, Reflux sympathetic dystrophy, Drugs, Physical deconditioning, Dec. BV,
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| Dx of Orthostatic testing | Measure BP and HR from supine to standing; Sustained drop of SBP >20mg or DBP >10, HR ^ of 15 BPM: neurogenic Upright Tilt table testing
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