INTERNAL MED EOR- CARDIO, PULM, GI, ORTHO, ENDO, NEURO, GU, CRITICAL CARE, HEME, ID
CARDIOVASCULAR 20% MI & Coronary Artery Disease
CARDIO About
HTN Causes:
1. Sympathetic NS & RAAS
2. Pressure/natriuretic
3. Renal/cardio development
4. Increase in Na & Ca levels
HTN Hypertensive Urgency
Urgency v. *>220/125 WITHOUT end-
Emergenc organ damage
y failure  brain, kidney, heart
Hypertensive Emergency
*>220/125 WITH end-organ
damage
Angina Substernal chest pain usually
Pectoris brought on my exertion
•Class I: strenuous activity
•Class II: more prolonged
rigorous activity
•Class III: daily activity
•Class IV: at rest
Hyper- Causes:
lipidemia -Hypercholesterolemia:
hypothyroidism, pregnancy,
kidney failure
-Hypertriglyceridemia: DM,
ETOH, obese, steroids, estrogen
Linkage between LIPIDS and
INFLAMMATION
Clinical Presentation
Risks:
OSA, smoking, alcohol, obesity,
metabolic syndrome, NSAIDs,
high sodium in diet (low K+)
•Urgency: poorly controlled
•Emergency: identify organ
History:
•Chest pain: poorly localized,
substernal
•Radiation: arm, teeth, jaw
•Duration: Short (<30 minutes)
•Alleviating: rest, NTG
•Aggravating: exertion
Other SX: diaphoresis, dyspnea,
fatigue, numbness, nausea
Exam: usually normal
•Xanthomas
•Xanthelasama (lipid plaques in
eyes)
Diagnostics
•UA, BMP, EKG, lipids
Evaluation goals: assess target-organ
damage, other risks, secondary causes;
•CBC, CMP, UA; EKG, CXR
•CT if neuro sx in emergency
Complications:
•Renal-nephrosclerosis
•Eye-retinopathy, cotton wool
•Vascular-atherosclerosis, aneurysm
•CVA (SPB); S4, heave
ALL: EKG and CXR
NSTEMI: high troponin, ST depressed
Unstable: normal troponin, ST depressed
Exercise Stress Test:
• (+) if ST-depressions, hypotension/HTN,
arrhythmias, symptomatic
Imaging Stress Test:
•thallium-201 or technetium-99
•patient with baseline EKG abnormalities
•Adenosine or Dipyridamole
•CI: asthmatics
Coronary Angiography (GOLD) “Cath”
Screening:
Ages 20-79 every 4-6 years
High risk: screening 20-25yo M, 30-35yo F
Low risk: 35yo M, 45yo F
Who to Treat:
1. DM between 40-75 years old
2. 40-75yo with risk 7.5% and higher
3. Age 21+ and LDL 190+
4. Clinical ASCVD
Management
•healthy >60yo-150/90;
•<60yo, CKD, DM-140/90
•1st line-ACE/ARB
•AA 1st line-CCB/thiazide, HF/MI-BB
Hypertensive Urgency: adjust medications
-hospital: Clonidine, Captopril, Nifedipine
-oral: labetolol, captopril, NTG, clonidine
Hypertensive Emergency: 1st line: BB, CCB
-ischemic CVA: keep BP 180-200
-hemorrhagic CVA: <130
-dissection: 100-110
Lifestyle modifications
Pharmacotherapy: M.O.N.A. (162-325mg)
*goal is to increase supply and decrease
demand on the heart
•NTG
•Beta-Blockers
•CCB (Diltiazem, Verapamil)
•Aspirin: does not work with supply/demand,
but prevents progression of stable angina to
acute coronary syndrome
Classic TX: ASA, BB, NTG, statin
Lifestyle: weight, exercise, dietary changes
Pharmacotherapy:
-LDL: Statin
-Triglycerides: Fibrates
-increase HDL: Niacin
High intensity: <75yo w/ ASCVD, LDL 190+,
10 year risk >7.5%
Atorvastatin 40-80 &Rosuvastatin 20-40
Goals: LDL <100, Cholesterol <200, HDL >60
CARDIO About
Congestiv •Acute: began last few days to weeks
e Heart •Chronic: sx present for months
Failure
•High: heart can’t meet demands
(supply<demand)
-thyrotoxicosis, anemia; decreased CO
•Low: insufficiency forward output (low EF)
•Systolic: reduced EF (HFrEF)
•Diastolic: preserved EF (HFpEF)
•Left: DOE, PND, orthopnea, fatigue
•Right *MCC of left sided HF
-JVD, hepatic congestion, ascities, edema
Cardio 20% About
Rheumatic •Due to GABHS (S. pyogenes)
Fever •autoimmune inflammatory muli-
systemic illness
•Children 4-9yo
•Diffuse inflammation of the heart
-exudative pericarditis
-myocardium infiltrated with
lymphocytes -> necrosis like MI
Endocarditis Cause: ORAL (dental, candy, brush)
-others: IVDU, EGD, TURP, cath,
•Localization of the infection is
determined by turbulent blood flow
•MC bug: S. aureus
•MC on Left side, TV MC in IVDU
•Acute: infection of normal valves
•Subacute: abnormal valve
•IVDU: MRSA, Pseudomonas
•Prosthetic: Staph epidermis
Clinical Presentation
•Chest pain, HTN, Flu-like sx
Physical Exam:
General: tachy, diaphoresis
•Narrow pulse pressure <25
Volume Assessment
•Rales or dull breath sounds
•Edema, JVD
Pulsus Alternans: LV HF
Precordial: lateral displaced PMI
Heart Sounds: S3 & S4
Clinical Presentation
Major: “JONES-FAR”
•J: joint pain (polyarthritis),
•O: oh my heart (carditis)
•N: nodules subcutaneous
•E: erythema multiform
•S: syndenham chorea
Minor:
•fever
•arthralgia
•hx RF
MC:
•fever (90%), chills, night sweats
•MSK pain (back)
•murmurs (80%)
•CHF (2/3 cases)
Peripheral Manifestations:
•petechia *strep or staph
•splinter hemorrhages *strep, staph
•osler nodes *strep *PAIN (finger)
•Janeway *PAINLESS (palms)
•Roth Spots (eyes on funduscopic)
Diagnostics
GOAL: confirm sx &
cause of HF
Initial Testing
EKG
CXR: kerley B, effusion,
congestion, cardiomegaly
Initial Labs:
•CBC, CMP, coagulation
studies, glucose, lipids
•BNP (>500 very likely)
•cardiac enzymes
Echo: GOLD
Diagnostics
Labs:
•high ESR, CRP, leukocytosis
•Increases ASO titers
Biopsy: ASCHOFF BODY
•monocytes and macrophages
Complications:
•rheumatic valvular disease
-MC: mitral, aortic
3 blood cultures, 1 hour apart
DUKE CRITERIA
Major criteria
• (+) blood culture (2 are +)
•endocardial involved on echo (TEE)
•new regurg murmur
Minor Criteria:
•heart condition or IVDU
•fever (>100.4F)
•vascular and embolic PNA
•immunologic phenomena
•microbiologic evidence
*1 normal, or 2+ abnormal
Interpretation:
•Definitive: 2 major or
1 major + 3 minor, or 5 minor
Treatment
Lifestyle modifications:
•Wt loss, sodium <2g, fluids <2L
•Daily weight monitoring
Pharmacotherapy: Loop Diuretics
Class I:
•ACEI (Check BMP for hyperkalemia)
•Entresto (Sabucitril + Valsartan)
•BB (Carvedilol, Metoprolol, Bisprolol)
-caution: 1st AVB, asthma, bradycardia
•Aldosterone Antagonists
-CI: K+ >5 or GFR <30
•Hydralazine/Nitrate (if black + ACEI/BB)
Acute: LMNOP: Lasix, Morphine, O2,
Nitrate, position
Treatment
•Penicillin or Erythromycin
•Aspirin (NSAIDS)
Prophylaxis: *1st 10 years
•Pen G 1.2m units IM monthly
•oral PCN or erythro is 2nd line
Acute Endocarditis: Nafcillin +
Gentamicin x4-6 weeks
Subacute Endocarditis: PCN or
Ampicillin + Gentamicin
Prosthetic valve: Vancomycin +
Gentamicin + Rifampin
Fungal: Amphotericin B
Prophylaxis: Amoxi 2g 30-60min
-prosthetic heart valves
-prior endocarditis
-cyanotic congenital heart disease
-cardiac transplantation
 Toxic: Alcohol, cocaine,
Doxorubicin
Other: pregnancy
Hypertrophic Inherited genetic disorder (autosomal
Cardio- dominant)
myopathy  mutation of sarcomeres
•MC effects interventricular septum
 LVH  diastolic dysfunction
•Impaired ventricular relaxation/filling
Restrictive •Ventricle is STIFF and has impaired
Cardio- filling  diastolic dysfunction
myopathy
Cause: Amyloidosis (MCC),
sarcoidosis, hemochromatosis,
scleroderma, fibrosis, cancer
Stress- •Can cause an ACS or STEMI
Induced *MC in postmenopausal women
(Takotsubo)
•Dyspnea (MC complaint)
•Angina, Syncope, Arrythmias
•Sudden cardiac death
•Right sided HF sx
•Pulmonary HTN
•Normal ejection fraction
Exam: Kussmaul sign
• psycho or physiological stress
 Systolic dysfunction of apex
and/or mid segments
Murmur:
Harsh, mid-systolic crescendo-
decrescendo murmur, at 3rd/4th ICS
louder with valsalva, quiet w/ squat
•EKG: LVH (V5, V6, aVL)
•Echo: DIAGNOSTIC-assymetrical
wall thickeness
•Echo: non-dilated ventricles with
normal wall thickness  dilation of
both atria
Echo/LV angiography:
•LV apical ballooning
•Avoid volume depletion
•Beta-blockers or Verapamil (CCB)
*1st line!
•Septal myetomy/alcohol septal
ablation *inject alcohol-kill off part
•Treat underlying cause if known
•Recover in a few weeks
•Beta Blockers for one year
Cardio 20% About Clinical Presentation Diagnostics Treatment
Pericarditis Inflammation in pericardial sac •PLEURITIC CHEST PAIN •Viral titers •FIRST LINE-NSAIDS
-worse with inspiration •Cardiac enzymes -Ibuprofen 600-800mg TID or
Causes: -worse when supine •Echo Indomethacin TID for 1-2 weeks
•Idiopathic *MC -relieved with sitting up and leaning *likely normal unless significant -ASA post MI
•Viral (enterovirus) (MC!) forward effusion present
•Systemic: thyroid, lupus, RA •CBC, BMP, ESR/CRP 2nd line: Colchicine
•Neoplasms: lung & breast CA •Fever -use for recurrence
•Drug Toxicity EKG: diffuse ST segment elevation
•Myocardial Injury Auscultation: pericardial friction -smiley face &diffuse
•Pericardial Injury rub *washing machine sound

Pericardial •Fluid in pericardial space Distant (muffled) heart sounds CXR: cardiomegaly Small/no tamponade: observe
Effusion EKG: low QRS voltage
•MCC: pericarditis Echo: increased pericardial fluid
•Others: infection, radiation, cancer
Cardiac Effusion causing significant pressure BECKS TRIAD: Echo: effusion + diastolic collapse of Pericardiocentesis
Tamponade on the heart  restricted filling  •JVD cardiac chambers
decreased CO •Muffled heart sounds
•hypotension EKG: electric alternans

Exam: Pulses paradoxus

Constrictive Thick, fibrotic and calcified heart
Pericarditis  diastolic dysfunction
MCC=TB *underdeveloped
MC is radiation, surgery, and viral
pericarditis *developed
•Dyspnea (MC sx)
•RHF: JVD, edema, N/V
Murmur: pericardial knock
-high pitched 3rd heart sound due to
sudden cessation of ventricular filling
from thickened pericardium
Echo: thickening of pericardium,
CXR: pericardial calcificiation
Cardiac CT/MRI: thickening
Cardiac Cath: *CONFIRMATORY
Diuretics for sx improvement
Definitive: pericardiectomy
-if unresponsive to diuretics

Cardio 20% About Clinical Presentation Diagnostics Treatment

Deep Vein Virchows Triad: Unilateral swelling of LE (>3cm), tender Venous duplex US: 1st line Anticoagulant therapy-First Line
Thrombosis 1. Venous stasis -noncompressible echogenicity -LMWH or heparin IV AND Oral x3mo
(DVT) 2. Endothelial damage Exam:
3. Hypercoaguability •WARM skin & Dusky cyanosis Venography: GOLD Heparin (antithrombin III): PTT
•Palpable cord, normal pulses
•Homans sign: calf pain with Warfarin (Vitamin K antagonist)
dorsiflexion (unreliable) -extrinsic pathway, monitor PT/INR

Varicose Veins •Varicose veins develop in LE
Dilated, tortuous superficial veins
Increased intraluminal pressure 
reverse venous flow
Hallmark: venous reflux & HTN
•Dull, aching heaviness or feeling of
fatigue in legs brought on by periods of
standing, relieved with elevation
•Itching , palpable
•No diagnostic evaluation
•Imaging needed for surgical
intervention-duplex US
•Nonsurgical: Elastic compression
stocking (20-30mmHg), leg elevation
•Surgical:
-sclerotherapy: inject sclerosing agent
-laser therapy: wavelength
-endovenous ablation
-vein stripping (last resport)
Cardio 20% About Clinical Presentation Diagnostics Treatment
Chronic Venous •Severe manifestation of venous Burning, aching, heavy leg pain Compression stockings, leg elevation
Insufficiency hypertension -worse with standing/sitting Regular exercise
-better with walking & elevation lipodermato
•Valve leaflets that do not coapt Ulcer: UNNA boot, wet to dry dressings
because thickened and scarred or Edema, hyperpigmentation,
in a dilated vein so impaired
function •Venous ulcers: medial malleolus atrophic blanche
 legs develop venous
HTN and high •Lipodermatosclerosis
hydrostatic force -pigmented, swelling, red, “bowling pin”
corona
MCC-prior deep venous •Atrophie Blanche
thrombophlebitis -star shaped ivory-white depressed Trendelenburg test: elevate one
atrophic plaque; red dots within scar leg at 90 degrees, occlude great
saphenous vein, have patient
•Corona Phlebectatica stand for 20 sec  slow ankle
-dilated veins around the ankle fillings suggests competency

Superficial •Inflammation of a vein due to
Venous clot in the superficial vein
Thrombophlebiti -thrombotic or septic
s complications
-great saphenous vein
Causes: IV catheter, trauma,
pregnancy, varicose veins
•MC pathogen-Staph Aureus
Trousseau’s sign: •CBC: WBC may be elevated 1st line: supportive therapy
migratory thrombophlebitis associated -elevate, warm compression,
with malignancy •Venous Doppler US: non- compression stocking, NSAIDs
compressible vein with clot
Local phlebitis: tender, pain, edema, Septic state:
erythema, induration •PCN + Aminoglycoside
•+/- palpable cord •Vanc + Rocephin
•Fever (if septic)

Cardio About Clinical Presentation Diagnostics Treatment

PAD Stenosis or occlusion in artery due to
atherosclerosis
•Coronary artery: angina
•Carotid artery: stroke, TIA
•Renovascular: HTN, renal
•PAD: claudication, limb ischemia
•Distal aorta & proximal iliac: smokers
•Femoral & popliteal: 60+, minorities
•Tibial artery: Diabetics
Atypical leg pain (MC)
•Intermittent Claudication
-aching, pain, tightness
-brought on by EXERCISE
-relieved with rest within 10 minutes
•Functional Impairement
-do not have claudication but have rest
pain or ulceration
•Limb ischemia: ulcer, gangrene
•Pulses (2+ normal)
•Blood pressure, carotid bruits
•Exam legs and feet
•Skin: COLD
Leg Lift Test: 60 degrees x1min
(+) if feet turn white when you lower
down
Dependent Rubor: seated to supine,
assess blood flow; longer red is more
severe
ABI: BEST TOOL
Abnormal is 0.90 or less
-use TBI if non-compressible (>1.40)
•Lifestyle: smoking cessation
•Exercise therapy
Pharm: Aspirin or Plavix
•Cilostazol (Pletal)
-supress cAMP degredation
-reversibly inhibits platelete
aggregation
-SE: edema, GI, HA, bleed
-CI: HF
Others:
•ACEI, statin, glycemic control
Cardio About Clinical Presentation Diagnostics Treatment
Acute Causes: 5 Ps: •MEDICAL EMERGENCY! Immediate revascularization
Arterial •thrombus: stable atheroma with fibrous cap -pallor
Occlusion  plaque rupture  acute occlusion -pain/ paresthesias (numbness/tingling) •Doppler: little to now flow 1. vascular surgery consult
of a Limb -pulseless •EKG: determine if Afib 2. begin IV Heparin bolus and
•embolus  AFIB MC cause -paralysis (muscles w/ no perfusion) •Labs: CBC, PT/INR, PTT continuous infusion
-polar (cold) •Echo: done LATER if embolic source
MEDICAL EMERGENCY! is suspected (TEE w/ bubble) •Once stable: Warfarin for at
least 3 months+, goal INR 2-3

Thrombo- NOT ATHEROSCLEROSIS •Starts at toes/feet  hand/fingers TOBACCO CESSATION!

angiitis •Segmental, inflammatory, thrombotic -severe ischemia  tissue loss
Obliterans processes that occur in small distal arteries -revascularization
(Buerger •Presents with distal ischemic rest -amputation frequently required
Disease) •Closely linked to tobacco use pain or ischemic ulceration on the -NSAIDS or opioids for pain
•Males <40, smokers toes, feet, or fingers
Aortic Valve General Features
Aortic Stenosis Congenital v. acquired
-Congenital: bi or quad
-Acquired: *MC in elderly
•rheumatic fever
•degenerative (Ca2+
deposit)
-Risk factors:
•HTN, HLD, smoke
thickening & calcification
 narrowing  LVH 
systolic dysfunction
Chronic Causes:
Aortic •Aortic leaflets:
Regurgitation rheumatic fever, congenital
abnormalities, endocarditis
•Aortic root:
dissection or dilation,
Marfan
*LVH due to dilation from
accommodating regurg
volume
Acute Aortic Causes:
Regurgitation •infective endocarditis
•trauma rupture of leaflet
EMERGENCY •aortic root dilation
•acute dysfunction of
prosthetic valve
Clinical Presentation
Most asymptomatic for years
Cardinal symptoms:
•angina, syncope, CHF
•Murmur:
-Harsh, Mid-systolic at R 2nd ICS
-Crescendo-decrescendo
-worse with leaning forward
-Radiates to CAROTIDS
-Thrill, S4 gallop, displaced PMI
EKG: may demonstrate LVH
*Asymptomatic for years
•CHF, angina
Murmur:
•Early diastolic, radiate to apex
•Decrescendo, blowing
•High pitch, 2nd and 4th L spaces
•Widened pulse pressure
•S3&S4 gallop
•Austin Flint Murmur maybe
•S/S of cardiogenic shock
•Pale, cool extremities
•Weak, rapid pulse
Murmur:
•low pitch, early diastolic
Diagnostic Studies
Echo *diagnostic study of choice!
-severe: <1 cm 2 -critical: <0.7 cm 2
•Cardiac Catherization
confirms severe AS and any CAD
•Echo*diagnostic of choice
-monitors progression of disease
Echo *diagnostic study of choice
-performed quickly and bedside
*LV in unable to accommodate the
increased diastolic volume -> increased
pressures and pulmonary congestion
Management
•1st line-AV Replacement with Sternotomy
-symptomatic patients
•2nd line-Transcutaneous Aortic Valve
Implantation/Replacement (TAVI/R)
*need a good myocardium
-poor candidates for open heart
-multiple comorbidities, high pre-op risk
-higher risk for stroke immediately after
•Balloon Valvuloplasty
-congenital AS; not used for degenerative
*no medical tx-manage symptoms of HF
•Valve Replacement (AVR): those with
symptomatic severe AR or with LV changes
•AR prior to LC dilation greater than 50mm
or reduction in EF to less than 50%
•Vasodilator therapy-unload the ventricle
 Arterodilation
 Reduce afterload -> less pressure to
push back into the ventricle
SURGICAL EMERGENCY
Vasodilator and diuretic if BP is stable
-Inotropic agents & vasopressors
**Treatment of choice: Urgent AVR
Mitral Valve General Features
Mitral Stenosis •2/3 are women
•Don’t develop sx until 20-40
years following disease ~30-40yo
Causes:
•Rheumatic fever is MCC!
•congenital abnormalities,
connective tissue disorders, left
atrial tumors, aggressive surgical
repair of MR
Clinical Presentation
•Dyspnea, orthopnea
•Atrial fibrillation *enlarged atria
•Hemoptysis (rupture of dialted bronchi)
•Blood tinged sputum *pulmonary edema
Additional findings:
•PE, edema, Ortner Syndrome (L recurrent
laryngeal nerve compression)
Murmur:
•Diastolic, Low-pitch, rumbling
•Heard at apex in LLD position w/ bel
•Opening snap following S2
Diagnostic Studies
EKG: LAE, RVH, A-fib
Echo: *diagnostic of choice
•Rhematic deformitity-doming
(hockey stick)
•Large LA compared to LV
-normal MV area: 4-6cm 2
-critical: <1cm 2
•smoke in left atrium
Cardiac cath: measure CO
Management
Mild to moderate: CONTROL HR
Moderate to Severe (NYHA III-IV):
•Percutaneous balloon valvuloplasty
*not common or definitive treatment
Surgery is definitive treatment with
bioprosthetic or valve replacement

Mitral Valve •1-3% population; MC in women Nonspecific sx (MVP syndrome): DX: Echo •NO TREATMENT if mild prolapse
Prolapse •superior displacement in systole •chest pain, palpitations, dizzy, anxiety *diagnostic study of choice and asymptomatic

Causes: Murmur: *treat when regurgitation occurs!

-connective tissue disorder •Mid-systolic click, usually followed by
-Marfans or SLE late-systolic murmur
-Autosomal dominant •Heard at the apex
•Squatting: delays click
•Standing: earlier click
*gallops won’t change with position!

Chronic Abnormalities of mitral leaflets, •fatigue EKG: Reduce Afterload: *less mitral
Mitral annulus, chordae, papillary •dyspnea on exertion •LA enlargement, LVH, A-fib regurg
Regurgitation muscles •peripheral edema •vasoduilators (ACEI, hydralazine)
-MVP, LV dilation, posterior MI Echo: *Diagnostic of choice •diuretics
-rheumatic fever Murmur:
-endocarditis •blowing holosytolic murmur Cardiac Cath: Surgery: annuloplasty
•heard at apex & radiates to axilla/back •Assess function & filling pressures *DEFINITIVE
•Regurgitating blood flow from •mid-systolic click •should be performed before
LV to LA in systole irreversible myocyte damage and left
centricular remodeling occur

Monitoring: annual echo

Acute Mitral •Life threatening Signs of cardiogenic shock SURGICAL EMERGENCY

Regurgitation •LA does not dilate to
accommodate regurg volume - Murmur: Urgent valve replacement
increase in LA and pulmonary •Soft, low-pitched sound in early systole
EMERGENCY venous pressure  congestion *have high index of suspicion

Causes:
•acute MI, trauma, endocarditis
•tachyarrhythmia w/ chronic MR
 •MVP
Tricuspid Valve Causes/
Tricuspid *MC in women •Uncommon
Stenosis •Usually associated with AS or MS
Causes
•rheumatic heart disease MCC!
•carcinoid, congenital valve
abnormalities, tumors
•Reduced RA emptying 
Increased venous congestion and
reduced RV CO  fluid overload
Tricuspid •Regurgitating blood flow from RV
Regurgitation to RA
•Secondary to dilation of the RV
and tricuspid annulus due to RV
failure (pulm HTN or L failure)
•Increased RA pressure -> increased
venous congestion & reduced RV
output -> volume overload
Pulmonic Valve Causes
Pulmonic CONGENITAL (peds pt)
Stenosis •Rheumatic disease is RARE
•Noonan, Trisomy 13
•Isolated congenital lesion
fusion of pulmonary leaflets ->
pressure overload -> RVH
Pulmonic •Result of dilation of the PV annulus
Regurgitation secondary to pulm HTN
S&S/Physical Exam/Murmur
•Liver congestion
•Varices, Ascites, JVD, LE edema
•Palpable presystolic pulsation with
atrial contraction over liver
*always palpate liver with ascites
Murmur:
•soft, high-pitch, mid-diastolic, L 4th ICS
•Accentuated with inspiration
•Opening snap at left sternal border
•Well tolerated without pulmonary HTN
•As it progresses, may have RV failure:
-fatigue, abd bloat & peripheral edema
Physical Exam:
•JVD, hepatic congestion and palpable
systolic pulsation
Murmur:
•High pitch, pansystolic, tricuspid post
•accentuated with inspiration or leg raise
S/S
Critical at birth:
•Central cyanosis at birth
•otherwise asymptomatic until
adolescence or young adulthood
Moderate-Severe:
•fatigue, dyspnea
•-> RV dysfunction -> RV failure
•Sx due to primary disease and secondary
to RV failure
Diagnostics
•Echo-significant: <1cm 2
•EKG: RA enlargement
•CXR: cardiomegaly from
enlarged R atrium
CXR:
Murmur
Murmur:
•systolic at pulmonic post
•increases with inspiration
•RV lift on palpation of
precordium
•S1 followed by opening click
that’s louder with expiration
Murmur:
•High pitched, blowing
•Heard at 2nd L ICS
Treatment/Management
Diuretics
•Loop diuretics are best
•ascites  ADD aldosterone
antagonists (Spironolactone)
Surgery:
•TV replacement if symptomatic
•Treatment of underlying cause
•Repair TV with annuloplasty
*persistent symptoms
•TV replacement
*pts with underlying primary leaflet
pathologic condition
Management/Treatment
Mild: (pressure <30mmHg)
•asymptomatic and no intervention
Moderate-Severe: (>50mmHg)
•Balloon valvuloplasty or surgical
valve replacement
TREAT PULMONARY HTN!
•PV replacement is rare because its
being cause by pulmonary HTN, so it
will come back if that is still present
Sinus Dysrhythmias About Symptoms Management
Sinus Arrhythmia •Cyclic increase in normal heart rate with reflex changes in vagal influence on the normal No treatment required
inspiration and decrease with expiration pacemaker and disappears with breath holding or *not pathologic
increase in heart rate

Sinus Bradycardia Heart rate <60bpm
Rate increases with exercise, atropine
Causes:
•Increased ICP: hemorrhage
•Anterior MI: Inf. wall MI -> RCA supply SA
•OSA: decreased Hr <30bpm in apnea
•Other: hypothermia, hypothyroidism
•Increased vagal influence on the normal pacemaker •1st line-permanent pacemaker
or organic disease of sinus node
- Fear, bearing down, SSS Acute setting: transcutaneous pacing, temporary
transvenous pacing, Atropine (ACLS protocol)
•Severe <45bpm-sinus node pathology
SX:
•weakness, dizziness, confusion, syncope

Sick Sinus Syndrome •Commonly have recurrent supraventricular “When they go into AFIB its really fast then when Symptomatic  Pacemaker (PPM)
arrhythmias and bradycardia “tachy-brady” they go out of afib they go into a really slow sinus
brady”
•MC in elderly
•Cause: medications

Sinus Tachycardia •HR >100bpm Symptoms: palpitations, lightheadedness Physiologic: none needed, try massage
•Onset & termination usually GRADUAL *usually related to the cause *usually a compensatory mechanism

Causes: •2 types: inappropriate, POTS Symptomatic pts w/ or w/o correctable:

•MC-exercise, anger/stress *inappropriate sinus tach, POTS
- Beta-blockers (Metoprolol) or CCB

Dysrhythmia About Causes Signs and Symptoms Diagnose/Management

Premature ectopic focus in the atria that fires *frequently occurs in nml hearts Palpitations •Not required most of the time
Atrial before the next sinus node impulse •increased frequency with age
Contractions *diff P wave morphology •structural changes •Beta Blockers if significant symptoms
•precuroseor to afib, aflutter •Class IC antiarrhythmis is second-line

Premature Premature depolarization originates *frequently in normal heart •Many are completely asymptomatic •Symptomatic: BB (Metoprolol)
Ventricular from the ventricles •caffeine, stress, alcohol •Palpitations MC complaint •2nd line: Class Ic or III AAD
Contractions - wide QRS complex w/ pause •electrolyte abnormalities
•thyroid •Significant burden: cath ablation

Atrial About Causes Symptoms Management

Atrial Results from an ectopic atrial focus firing at a rate •severe COPD -palpitations •treat underlying conditions
Tachycardia faster than the sinus rate -> becomes pacemaker •structural heart disease -heart racing sensation
•may occur in normal hearts -SOB •CCB 1st line option
•Onset and termination occur abruptly *not commonly -dizziness *especially if have COPD
•Atrial rate about 100-160bpm •digoxin toxicity -near syncope
•Unifocal or multifocal •refractory: class IC or III
Dysrhythmia About
AV Block •First degree: PR >0.21 with all atrial
impulses conducted
•2nd-degree: intermittent blocked beats
Mobitz type I (Wenckebach) AV block:
AV conduction time (PR) progressively
lengthens with the RR interval
shortening before the blocked beat
*abnormal conduction AV node
Mobitx type II AV block: there are
intermittently non-conducted atrial beats
*block in HIS bundle
•Third degree: complete heart block, in
which no supraventricular impulses are
conducted to the ventricles
Causes
First Degree and Mobitz Type I:
•may occur in normal individuals
with heightened vagal tone
•drug effect
•electrolyte abnormalities
•organic disease: ischemia, infarction,
inflammatory, fibrosis, calcification,
infiltration
Mabotiz type II and 3rd degree:
•ORGANIC DISEASE involving the
infranodal conduction system
•transient or permanent
Signs and Symptoms
First Degree Block:
-diagnosed by EKG alone
Mobitz type I:
-most commonly asymptomatic
-may note palpitations, DOE,
dizziness
Mobitz type II:
irregular rhythm
-may be asympatomatic
-palpitations, DOW, weakness, dizzy
Third-Degree block:
-sx vary; worse w/ exertion
-palpitations, DOE, weakness, near
syncope, syncope, and/or HF
Diagnose/Management
Diagnostic Studies:
•Review medications & HX
*REVIEW FIRST!
•12 lead EKG
•telemetry monitoring (inpt)
•echo to r/o structural disease
•S/S ischemia -> cath
Labs: CBC, CMP, TSH
Management:
•First Degree:
-avoid medications that may prolong PR
interval and slow AV conduction
•Mobitz type I:
-avoid meds that slow AV conduction
•Mobitz type II/Third-Degree:
-unstable, usually require pacemaker

Dysrhythmia About Causes Signs & Symptoms//Diagnosis Management

Paroxysmal •Common cause of paroxysmal •MC mechanism for •Awareness of rapid heart beat Acute Management: STABLE PT
Ventricular tachycardia paroxysmal supraventricular •Chest pain, SOB 1. Mechanical measures *done by pt
Tachycardia tachycardia is reentry •Dizziness, syncope •valsalva*
Two common types of reentry: - typically initiated by •Abrupt onset and termination, last •stretching the arms and body, lowering the head
•AVNRT (AV node reentrant tachy) a PAC or PVC seconds to several hours or longer between knees*
*within the node •coughing, breath holding*
*Most Common EKG: •cold water
•Tachycardia (140-240) •carotid sinus massage-> PROVIDER
•AVRT (AV reciprocating tachy) •regular rhythm
 WPW: accessory path •QRS most commonly narrow 2. Drug Therapy (IV therapy): “ABCD”
*accessory path outside AV node •P wave is often buried in QRS •Adenossine, CCB, BB (Esmolol, Metoprolol)

3. Cardioversion (shock) *sedate if awake

•FIRST LINE if hemodynamically unstable
•synchronized electrical cardioversion at 100J

Prevention:
•Catheter Ablation: recurrent, sympt. PSVT
•Medication Therapy: BB & CCB are 1st LINE

** pts w/ AVRT (WPW) are prone to afib and

aflutter -> class IC or III or ablation
Arrhythmias Phases Risks/Causes/Complications
Atrial Paroxysmal: in and out on own Risks:
Fibrillation •CHF* & HTN*
Persistent: >7 days •Old age, CAD, valvular disease
Long Standing Persistent: 1 year Causes:
-alcohol
Permanent (Chronic): staying in -thyroid disease, lung, heart
-fhx
-pericarditis
Complications: HF, thromboemboli
Rhythm Control Anticoagulation
Hemodynamically unstable: CHA2DS2SASc Score
Cardioversion *calculate on EVERY Afib pt
•Score 0: no therapy
*any unstable patient in a fast heart •Score 1: consider oral anticoag or
rate needs to be carvioverted antiplat (ASA 81)
•Score 2: oral anticoagulant
•Valvular (mitral stenosis or
regurg) heart disease: Coumadin
Atrial Causes/Risks/Presentation Treatment
Atrial Flutter Presentation, risk factors, causes are Higher rate of cure with catheter-
the same as afib based radiofrequency ablatation
- FIRST LINE
Symptoms
Symptoms:
-may be asymptomatic
-palpitations, heart racing
-chest pain, SOB, fatigue, CHF
Physical Exam:
-irregularly irregular rhythm
-signs of CHF
-distal pulses may be difficult
Long-Term: “P-SEX”
*bridge with LMWH or Heparin
•Warfarin (INR goal 2-3)
•Pradaxa (reduce if CrCl 15-30)
•Xarelto (reduce if CrCl 15-50)
•Eliquis (reduce if 2+: 80+, wt
</=60kg, Cr 1.5+)
•Savaysa (reduce if CrCl 15-50)
-antiarrhythmics, cardioversion,
rate control same as AF
Management
Three-Fold:
1. Rate control
2. Rhythm control
3. Thromboembolic event prevention (ALL)
Rate Control:
•CCB (Verapamil, Diltiazem) *NOT in HF!
•Beta Blockers (Metoprolol)
•Digoxin
Rhythm Control: dependent on comorbidities
Maintenance/Education
Maintenance:
•CBC and BMP q6months
•outpatient ambulatory monitoring
*if on Amiodarone, then make sure they are
getting routine imaging and labs
Patient Education:
•avoid alcohol ANYTIME
•control underlying risk factors
•monitor for signs of bleeding if
anticoagulated
-anticoag same as AF
(4 weeks post ablation then no more)
Arrhythmias Definition/ Causes Symptoms Management
Ventricular •Three or more consecutive ventricular Patient may be asympatomatic, Acute sustained VT Long-Term therapy
Tachycardia premature beats especially with nonsustained •if hemodynamically unstable: immediate (prevention/recurrence):
-nonsustained: less than 30 seconds, synchronized direct current cardioversion •ICD
-sustained: greater than 30 seconds Majority have symptoms: •BB
•usual rate is 160-240bpm -palpitations, heart racing If stable and tolerating: •Amiodarone, Sotalol (class III)
-near syncope, syncope •IV Amiodarone likely will convert to sinus •catheter ablation
-confusion, fatigue •IV Lidocaine *MI or still in VT with Amio
-chest pain, SOB •Add IV Magnesium *everyone Non-sustained VT: Beta Blockers

Arrhythmias Definition
Ventricular •Not a sustainable rhythm IMMEDIATE UNSYNCHORNIZED
Fibrillation •Leading cause of sudden death DEFIBRILLATION

Arrhythmia About Mechanisms Causes/Management

Accelerated Regular wide complex rhythm with a rate Two possible mechanisms: 2. escape rhythm due to suppression of No treatment unless UNSTABLE
Idioventricular of 60-120bpm 1. Slow ventricular tachycardia higher pacemakers resulting from sinoatrial
Rhythm due to increased automaticity and AV block or depressed sinus node

IVC Delays About Causes Evaluation Management

Left Bundle •MC in pts with underlying heart
Branch Block disease; Can also be seen in
(LBBB) structurally normal heart
*Left anterior descending artery
provides the primary blood
Causes: Evaluation: Asymptomatic and isolated LBBB:
-structural heart disease •chest pain/ACS sx -no specific therapy
-functional LBBB (rate-related) -treat underlying cause (treat like MI)
Diagnostics:
•echo symptomatic pts with LBBB and low EF:
•stress test or LHC CRT

Right Bundle Receives blood supply from septal Conduction can be compromised by: Generally asymptomatic Do not require further dx or tx
Branch Block branches of the left anterior •Structural heart disease
(RBBB) descending •Functional factors
Bifasicular •Asymptomatic (BENIGN) Asymptomatic:
Block - no further dx tests •Screen carefully for symptoms and signs
suggesting occult cardiac disease
•Presyncope or syncope
- ECG monitor 24-48h Symptomatic:
- Echocardiography •Pacemaker if CHB is identified

PULM 15%
COPD Irreversible airflow obstruction •cough, dyspnea with exertion Screening: annual screen with Cat A (GOLD 1-2):
- Loss of elastic recoil of alveoli •excess sputum production CT in adults 55-80yo with 30yr •SABA, possible LABA
- Increased airway resistance pack history and currently smoke
or smoked within past 15 years Cat B (GOLD 1-2):
Risks •LABA or LAMA
•SMOKING (>15 pack years) CXR: hyperinflation
•secondhand smoke CT: better for emphysema Cat C (GOLD 3-4):
•alpha-1-antitrypsin deficiency •LAMA, + LABA, LABA +
Spirometry: inhaled steroids + SABA
FEV1/FVC <70%, FEV1 <80%
COPD •Productive cough x3mo for 2 consecutive years •Productive cough Cat D (GOLD 3-4):
(Chronic •cyanotic, edema, RHF A: mMRC 0-1, CAT <10, 0-1 •LABA/LAMA, triple
Bronchitis) •Chronic airway inflammation  hypersecretion of •rales and rhonchi exacerbation
B: mMRC 2+, CAT 10+, 0-1
mucus, airway narrowing, increased airway SABA: Albuterol
exacerbation
resistance  obstruction •respiratory acidosis C: mMR 0-1, CAT <10, 2+
LABA/ICS: “SAD”
•V/Q mismatch (normal in exacerbation, 1+ hospital LABA: Salmeterol,
emphysema) D: mMRC 2+, CAT 10+, 2+
exacerbation, 1+ hospital Combo LABA/LAMA: Bevespi

COPD •Irreversible enlargement of air spaces distal to •dyspnea with exertion GOLD 1: mild-FEV1 80%+ Triple (D): Trelegy
(Emphysema terminal bronchioles  destruction of air spaces; •pink complexion GOLD 2: moderate-FEV1 50-70%
) loss of elastic recoil in acinus  air trapping •thin, barrel chest, no edema GOLD 3: severe-FEV1 30-49% Others: Steroids, oxygen
GOLD 4: very severe-FEV1 >30%
•respiratory alkalosis *oxygen is only TX proven to
“lean forward w/ pursed lips” STOP SMOKING!!!!!!
decrease mortality in patient

Asthma Reversible; airway inflammation & •Dyspnea Pulmonary Function Test 1. SABA (all)
bronchoconstriction in response to trigger •Wheezing  Spirometry *GOLD 2. +ICS
•Cough (worse at night) low FEV1/FVC and FEV1 3. +ICS/LABA or med ICS
Pathophys: •Chest tightness 4. +med ICS/LABA
1. airway hyperactivity (IgE  T-cell) •Fatigue Bronchoprovocation: 5. +high ICS/LABA
2. bronchoconstriction: airway narrowing due to Bronchodilator  FEV1
6. +high ICS/LABA or oral
smooth muscle contraction, edema, mucus, Physical Exam: increases by 12% and 200ml
 hypertrophy  air trapping
3. inflammation
Mild Intermittent:
•SX ≤2d/wk, night awake ≤2x/mo, FEV1 >80%
Mild Persistent:
•SX >2d/wk, night 3-4x/mo, FEV1 >80%
Moderate Persistent:
•SX daily, night awake >1x/wk, FEV1 60-80%
Severe Persistent:
•SX throughout day, awake nightly, FEV1 <60%
PULM 15%
Idiopathic *MC interstitial lung disease
Pulmonary
Fibrosis Pathophysiology:
diffuse epithelial cell activation and
abnormal repair  fibrosis
Black Lung Pathophysiology:
*coal workers alveolar macrophages ingest coal 
pneumoconiosis form coal macules (2-5mm) that
deposit in the lungs (MC upper)
Silicosis •Rock or coal mining, stone cutting,
*pneumoconiosi tunneling, sandblasting, pottery
s •dust containing crystalline silica
Pathophysiology:
alveolar macrophages ingest particles
 inflammation  fibrosis
Asbestosis workers exposed to asbestos fibers
pneumoconiosis over many years (old homes, ships)
Pathophys:
macrophages ingest  inflammation
 fibroblasts  fibrosis
Sarcoidosis •Inflammatory Disease, immune
•Noncaseating (non-necrotizing),
granulomas involving 2+ organs
•Organs: lungs (MC!); skin, eye
Granuloma:
•Prolonged expiration
•Hyperresonance to percussion Peak Expiratory Flow (PEFR) Admit if:
•Decreased breath sounds *assesses asthma exacerbation •PEFR <50%
•Tachycardia, tachypnea severity and response •ER within past 3 days
•Accessory muscles •Normal is 400-600 •status asthmaticus
Samter’s Triad: asthma, nasal Culture: curschmann’s spirals,
polyps, ASA or NSAID allergy Charcot-Leyden crystals
Clinical Findings: PFT: restrictive (low TLC, RV) Early referral for lung
•gradual dyspnea with nonproductive cough DLco: reduced transplant
PE: HRCT: ground glass opacities,
•fine inspiratory crackles/rale traction bronchiectasis,
•maybe digital clubbing honeycomb
CXR: small upper lobe nodules Supportive
and hyperinflation
•Asymptomatic CXR Supportive
•Dyspnea on exertion •diffuse multiple small (<10mm) -bronchodilators
•Non-productive cough nodular opacities in upper lobes -oxygen
•”egg shell” calcifications of -vaccinations (flu, PNA)
PE: crackles on exam hilar and mediastinal nodes -pulmonary rehab
CT: masses of small nodules Increased risk of TB
Symptoms: CXR/HRCT: LOWER LOBES Supportive
•after a latent period of 20 years + DOE -linear (reticular) opacities
-pleural plaques INCREASED RISK OF
PE: -honeycomb bronchogenic carcinoma &
•bibasilar, fine end-inspiratory crackles malignant mesothelioma
•clubbing Lavage: asbestos bodies
Pulmonary: (MC) Labs: High Ca2+, ESR, ACE 1st line: watch and wait
•dyspnea & dry, non-productive cough x2-4wks *granulomas produce Vit D
•Fatigue, fever, night sweat, wt loss Standard: steroids
Pulmonary Function Tests: *reduce granulomas
Skin: (2nd MC organ) •DLco: <80% (most sensitive)
•erythema nodosum: bilat tender red nodules •restrictive disease (all low Second Line:
mass of immune •MC in black, N. European, females on anterior legs except ratio is normal or high) Immmunomodulators if no
cells made by •lupus pernio (pathognomonic): violaceous, improvement in 6 months
macrophages, Pathophysiology: raised discoloration of nose, ear, cheek, chin CXR:
epithelioid, giant T-cell response to variety of antigens •maculopapular rash (MC chronic) •Stage I: bilat hilar adenopathy Advanced: Lung transplant
cells  immune activation and immune •Stage II: combo
depression  granuloma formation Ocular: Anterior uveitis  blurred vision, •Stage III: infiltrates *upper Follow-Up:
 disrupt normal structure discomfort, photophobia, floaters •Stage IV: fibrosis -min yearly exam
-yearly PFTs, labs, CXR, EKG
Biopsy: noncaseating granuloma

HRCT: hilar adenopathy,

nodules, ground glass, infiltrates

Lavage: high CD4/CD8

PULM 15%
Cor Pulmonale Risks: pulm disease  COPD, ILD, pulm HTN JVD, ascites, edema DX: echo, R cath •diuretics & oxygen, anticoag

Pulmonary Increased pulmonary vascular resistance  RHF Symptoms:
HTN •dyspnea, chest pain
WHO Group1: pulmonary arterial hypertension •cough
•muscle hypertrophy & endothelial dysfunction •fatigue, lightheadedm syncope
•hemoptysis
WHO Group 2: *lungs  L heart disease
-pulmonary venous hypertension (heart) Classification: NYHA 1-4
1-no limitation
WHO Group 3: secondary to lung disease 2-mild sx with normal activities
3-marked limitation
WHO Group 4: pulm HTN secondary to 4-severe sx with rest
thromboembolism  occludes pulm arteries
Signs/Physical Exam:
WHO Group 5: heme, systemic & metabolic -JVD, LE edema  RHF
(sickle cell, sarcoidosis) - S2 & P2; tricuspid regurg
•Echo: *begin with echo
•EKG: RHF, RVH, RAD
•CXR: increased pulm arteries
•R Heart Cath (Swan-Ganz)
*GOLD STANDARD
-MAP >25, Wedge <15
•Vasoreactivity Testing
-vasodilator and measure
hemodynamic response
-Epoprostenol, Adenosine, NO
(+) if pressure decreases <10 and
to a value <40
Who Group 1:
1st line  CCB: Verapamil
Other options:
•PDE-5 (Sildenafil),
•Prostacyclins (Epoprostenol),
•Endothelin antagonists
(Bosentan)
Who Group 2: tx underlying
Who Group 3: Oxygen
Who Group 4: anticoagulant

Hypoventilation Risks: obesity, structural, fhx, alc, hypothyroid •snoring, interrupted sleep •Polysomnography (sleep study) weight loss, exercise, nonsupine,
Syndrome •daytime sleepiness, fatigue, avoid alcohol and sedatives
(sleep apnea) 1. pharyngeal wall collapse repetitively •wake up with breath holding, •Alternative: home sleep apnea
2. failure of upper airway dilator muscle gasping, choking testing (HSAT) Mild/moderate: CPAP
3. sleep-related obstruction and breath cessation •HTN, CAD, DM, mood Severe: CPAP, surgery

PULM 15%
Solitary Nodule: <3cm; Mass: >3cm Benign: SLOW GROWTH Malignant: RAPID GROWTH Low (<5%): watch
Pulmonary -round, smooth -irregular, speculated “<50yo and no smoking”
Nodule Risks: Thymomas (MC) -calcifications “popcorn” -cavitation with thick walls Intermediate (5-60%): biopsy
-cavitation High (>60%): resect

Carcinoid Neuroendocrine tumor •Asymptomatic (25-40%) •Secrete serotonin, ACTH, ADH, Definitive: surgical excision
Tumor •Wheezing, cough, recurrent PNA, hemoptysis melanocyte stimulating hormone
 MC sites: GI tract, lungs Carcinoid syndrome: diarrhea due to serotonin •Ocreotide may reduce SX
•Increased bradykinin and histamine  flushing, Bronchoscope: pink-purple tumor
tachycardia, bronchoconstriction, acidosis *well vascularized MC complication: bleeding

Bronchogenic MCC cancer deaths SCLC: fast growing, starts in bronchi (central) CXR & CT Scan NSCLC:
Carcinoma •SVC syndrome, SIADH/hyponatremia, cushing •Surgical resection treatment of
Risks: cigarettes, asbestosis •lambert-eaton (weakness improves WITH use) Central lesions: sputum, bronchoscope choice
*squamous cell, SCLC
Adenocarcinoma (MC!!): slow, periphery SCLC:
Squamous: central (bronchial) Peripheral lesions: FNA biopsy •Chemo treatment of choice
•CCCP: central, cavitation, hypercalcemia, *large NSCLC, adenocarcinoma
Pancoast (shoulder pain, horners, hand atrophy)

Large: rapid, periphery, AGGRESSIVE

PULM 15%
Bronchiectasi •Permanent, abnormal dilation and destruction of the •Chronic daily cough •Clinical diagnosis •ABX+ bronchodilator + chest PT
s bronchial walls of the large airway •copious, thick, foul- •CXR r/o PNA -Ampicillin, Amoxicillin, Bactrim
smelling sputum -FQ or Zosyn if Pseudomonas
MCC: H. flu, Pseudomonas (cystic fibrosis) •hemoptysis HRCT: STUDY OF CHOICE
•recurrent lung infection bronchial wall thickening (“tram-
 inflammation, edema, cratering, ulceration, track”) and dilated airways
neovascularization  abnormal dilation and PE: crackles
destruction of major bronchi & bronchial walls Sputum Culture: neutrophilia

Acute MC in the winter, self-limited ~5 days-3 weeks •non-productive cough CLINICAL *Reassurance and education
Bronchitis MCC: Adenovirus; Others: S. pneumo, M. cat, H. flu •Wheezing CXR: usually normal •rest and hydration, NSAIDs
•Rhonchi (clear with
Pathophys: infection  inflamed  exudate  spasm cough) •Procalcitonin *bacterial AVOID ABX unless indicated!
•Pharyngitis >0.25 (non-ICU) •Atypicals: Macrolide, FQs
Two phases: •Fatigue/Malaise >0.5mcg (ICU)
1. direct inoculation of tracheobronchial epithelium •Fever (low-grade)
2. Hypersensitivity of airway receptors (persistent sx
1-3wks)  increased sputum

Pneumonia rust: S. pneumo (MC)  RLL •productive cough CXR (PA and Lateral)  GOLD CAP Out: No comorbid/ABX:
(Bacterial) green: H, flu, pseudomonas •fever CT if unclear Azithro, Clarithro, Doxycycline;
red currant jelly: Klebsiella  upper lung •dyspnea Comborbid/ABX: Levofloxacin,
Foul smell/bad taste: anaerobic •pleuritic CP Azithro+Rocephin
•chills Labs: hospital: cx, NP, CBC, CMP;
•tachypnea HAP: new infiltrate CAP Inpatient:
Ventilator: Pseudomonas, Acinetobacter •accessory muscles Non-ICU: Levo; Moxifloxacin;
PSI: >90=hospital Rocephin+Azithro
CAP: within 48 hours of hospital or outpatient Dullness to percussion CURB-65 (2+=hospital): ICU: Rocephin + Azithro or Levo
Increased TF confusion, urea >19 (>7mmol), RR
-S. pneumo, Mycoplasma pneumo
(+) egophony 30+, BP <90/60, age >65 HAP (low risk drug-resistant):
HAP/VAP/HCAP: develops 48hours AFTER Levofloxacin, Zosyn, Cefepime
-Pseudomonas, Klebsillea, S. aureus
 HAP (high): Vanc +
1. Cefepime or Ceftazadime
2. Imipenem or Carbapenem
3. Zosyn+Cipro
4. Gent or Amikacin

Pneumonia •Influenza •Fever, chills •NP swab O2, rest, fluids, antipyretics,
(Viral) •adenovirus, parainfluenza, RSV, HMNV •nonproductive cough •CXR analgesics, IVF
•rhinorrhea, myalgia
•HA, sore throat

Pneumonia •Unicellular, Fungal pneumonia •Fever Labs: Elevated LDH & B-D-glucan •ART initiated if not already
(HIV/Fungal) •Associate with immunocompromised, esp HIV •dry cough, dyspnea
P. jivoreci •Person-person through airborne spread •respiratory failure CXR: diffuse, bilateral infiltrates •BACTRIM
CT scan: ground glass opacities •Prophlylaxis: CD4 <200

GI 12%
Hiatal Protrusion of the upper portion of •Type I: sliding hernia (MC) CXR •Type I: same at GERD
Hernia the stomach into the chest cavity
due to diaphragm tear •Type II: rolling hernia  fundus protrudes •Type II: surgery

Esophageal Dilated submucosal veins due to •Acute gastrointestinal hemorrhage Emergent Endoscopy STABILIZE: IV, fluids, blood
Varices portal HTN •Retching, Dyspepsia (+) red wale markings and FFP or plts if INR >2.0 or plt <50,000
•Bright red bleeding in esophagus cherry red spots
Risks: CIRRHOSIS •Hypovolemia w/ postural vitals or shock Pharm:
Vasoconstrict: Ocreotide (Somatostatin)
ABX: IV Rocephin or Fluoroquinolones

Emergent Endoscopy with banding

*Performed with pts hemodynamic status
stabilized within 2-12 hrs

Prevent Re-bleed: Beta Blockers

Infectious *MC in immunosuppressed patients Candida: linear white plaques Endoscopy with biopsy and Candidal: Fluconazole
Esophagitis -Candida albicans, HSV, CMV CMV: large superficial shallow ulcers brushings CMV: Gangciclovir
HSV: small, deep ulcers HSV: Acyclovir
MCC non-infectious: GERD

Mallory UGI bleeding due to longitudinal
Weiss Tear mucosal laceration at the cardia or
gastroesophageal junction
Due to increase in intragastric
pressure  vomiting after ETOH
•Hematemesis with or without melena Upper endoscopy: Superficial Supportive: fluids, transfusions
•H/o retching, vomiting, straining 50% cases longitudinal mucosal erosions
Severe: epinephrine, sclerosing agent,
•Upper endoscopy after resuscitation band ligation, clipping

GERD Transient relaxation of lower •Heartburn (pyrosis) ~30-60min after meals Upper endoscopy 1st: lifestyle modificiations
esophageal sphincter (LES) •Reflux of sour/bitter contents (regurg) -elevate head, avoid lying down x3hr,

*severity not correlated with degree
of tissue damage
•Dysphagia (1/3) Complications: avoid acidic food and alcohol
•Asthma, cough, laryngitis, CP, altered sleep Esophagitis
Stricture Pharm: H2-blockers (Ranitidine), PPI
ALARM: Esophageal adenocarcinoma (Omeprazole),
dysphagia, odynophagia, weight loss, bleeding Barrett’s Esopagus 
squamous to columnar

Esophageal Squamous cell: •Solid food dysphagia then fluids Endoscopy with biopsy Curable: surgery and chemo
Cancer -MC type worldwide •Odynophagia
-MC in upper 1/3 esophagus •Tracheo-esophageal fistula  cough, PNA Incurable: chemo, palliative
-risk: smoking, alcohol •Chest or back pain (mediastinal estension)

Adenocarcinoma:
-MC type in US; MC in lower 1/3
-risk: GERD

GI
Gastritis Inflammation/irritation of the stomach
mucosa with mucosal injury
Erosive: NSAIDs, alcohol, stress
Non-erosive: H. pylori, systemic
•MC asymptomatic H. pylori: urea breath test, stool H. pylori: CAP: Clarithromycin,
•Epigastric pain, N/V, anorexia Amoxicillin, PPI
EGD *MOST ACCURATE
•biopsy CONFIRMS NSAID: PPI (Omeprazole),
Misoprostol, Sucralfate

Peptic Ulcer Decreased mucosal protective factors and •Epigastric Pain (dyspepsia) worse at night Endoscope: GOLD 1. Triple Therapy x10-14d
Disease increased damaging factors •Dull, aching, “hunger” CAP: Clarithromycin,
•Food relief (duodenum) *returns in 2-4h H. Pylori tests: Amoxicillin, PPI
MCC OF UGI BLEED •endoscopy with biopsy (GOLD)
•Nausea, anorexia •urea breath test; stool 2. Quadruple Therapy
Causes: •GI bleed (melena, coffee ground emesis) •antibodies PPI + Bismuth (pepto) +
H. pylori infection *MC in duodenum *may be asymp until bleed Tetracycline + Flagyl
NSAIDS *MC in stomach Complications:
Zollinger-Ellison syndrome Physical Exam: tenderness over epigastric Bleeding, perforation,
ETOH, smoking, stress, obstruction, malignancy

Gastroenteriti Causes: •Vomiting, anorexia, fever, diarrhea Labs: Viral: symptomatic, fluids
s •Virus v parasitic v bacterial •HA, Cramp, Myalgia •CBC: WBC, bands Bacteria: Cipro, Doxy, Azithro,
•Viral: norovirus (#1), adenovirus, •BMP/CMP: CO2, BUN/Cr Bactrim
enterovirus, rotavirus Timing: winter •Stool: SSYC, O&P, virus (GE
*norovirus is vomiting and muscle Transmission: fecal oral panel) Concerns:
cramps Incubation: 12h-4d, last 4-7d •UA: dehydration •presence of blood or mucus
•Parasitic: cryptosporidium, giardia Age: <5yo •weight loss
•Bacterial: campylobacter, e. coli, •low BP, sunken fontanelle, dry
clostridium, salmonella (reptiles) Exposures: foreign travel, playing in creek, mucous membrane
daycare, poultry *want to know if crying, peeing
•decreased UOP

Gastric Adenocarcinoma MCC worldwide Asymptomatic until advanced Iron deficiency anemia •Surgical resection: gastrectomy
Adeno- Other: lymphoma •Dyspepsia, vague epigastric pain
carcinoma •Anorexia, wt loss, early satiety Diagnostic: EGD & biopsy •Chemotherapy and/or radiation
 Risks: H. pylori, high salt or nitrate foods
PE: •Palliative measures
•palpable mass (20%)
•left supraclavicular lymph (virchows)
•umbilical node (sister mary joseph)
•rigid rectal shift (Blumer shelf)

Zollinger- Gastrin-secreting neuroendocrine tumor •Multiple peptic ulcers •Fasting gastrin level HIGH Local: surgical resection
Ellison Associated with MEN1 •Refractory ulcers *best screening test
Syndrome •“Kissing” ulcers (each side of luminal Metastatic: PPIs
MC in duodenum, pancreas, lymph node wall touching each other) • (+) Secretin test: increase
•Abdominal pain, diarrhea gastrin release with secretin seen
in gastrinomas

GI
Celiac •Response to GLUTEN •Diarrhea, steatorrhea, flatulence Diagnostic work-up: *bloods! REMOVE GLUTEN!
Disease •Presents in childhood, early adulthood •Wt loss, weak, muscle wasting Serologic antibody tests •Sx improve in 1-2 weeks once
•IgA TTG (best!) most sensitive gluten is taken out of diet
Triggers autoimmune response that •Iron, B12 or folate deficiency •IgG DGB (gluten sensitivity)
damages proximal S.I. mucosa  loss of •Osteoporosis, bone pain •IgA Endomysal SEVERE reactions:
villi  malabsorption •Detmatitis herpetiforms (10%) •Prednisone 40-60mg/day
*severity depends on amount of SI affected *very confirmative of celiac after (+) blood test: •Fluids
•Confirm with EGD with duodenal
mucosal biopsy

Irritable •Idiopathic Rome IV Criteria: ALARM sx: •Food diary and dietary changes
Bowel •Chronic GI sx NOT explained by the •Crampy, abdominal pain 1x/wk x3mo •Severe progressive pain *avoid triggers, avoids gas
Syndrome presence of structural/biochemical abnorm. AND 2/3: pain with anorexia or wt loss producing, low FODMAP diet,
(IBS) -relieved with defecation! •severe constipation or diarrhea fiber supplementation
Causes: abnormal motility, visceral -Change in stool frequency •hematochezia
hypersensitivity, enteric infection, -change in stool form •weight loss Diarrhea: Dicyclomine or
psychosocial (functional dyspepsia) •fever Loperamide

Constipation: laxatives

GI
Crohns Transmural inflammation and skip •Crampy RLQ abdominal pain Labs: (+) ASCA Goal: *NOT curative!
Disease lesion •Diarrhea (intermittent, non-bloody)
 malabsorptive, steatorrhea GOLD=Colonoscopy w/ biopsy •Diet
Can occur anywhere in GI •weight loss, fatigue  skip lesions with cobblestone appearance •Stop smoking
*MC-ileum and cecum •Symptomatic medications
perianal disease: fistula, abscess Barium study: “string sign”
*see infectious s/s with fistulas  barium flows through narrow 1st line: oral mesalamine
 inflammaed/scarred area due to transmural
malabsorption: iron and B12 deficiency strictures Maintenance:
5-ASA (Asacol, Pentasa)
extra-intestinal manifestation:
•arthralgia, arthritis, iritis, uveitis
•skin: Pyoderma gangrenosum
erythema nodosum

Ulcerative Relapsing and remitting episodes of •Crampy lower LLQ abdominal pain Labs: H/H, ESR, albumin, (+) P-ANCA CURATIVE
Colitis inflammation, spreads proximally •BLOODY diarrhea, pus/mucus
*mucosal layer of colon ONLY, •Fecal urgency and tenesmus Imaging: Pharmacology
*can mimic rectum is always involved Gold Standard-COLONOSCOPY 1. Aminosalicyclates
diverticuliti Complications:  uniform inflammation, ulceration, polyps (Sulfasalazine, Mesalamine)
s *smoking decreases risk for UC •Severe bleed -CI IN ACUTE COLITIS 2. Steroids *acute flares only
•fulminant colitis (>10BMs/day) 3. Immunomodulators
•toxic megacolon, perf Barium: “stovepipe sign”  loss of haustra 4. Anti-TNF

GI
Anal Fissure •Linear tears/ulcerations around anus •Tearing pain with defecation Inspection •Proper toileting, Sitz bath, Fiber
*MC posterior midline •Bleeding
*small amount with bright red Chronic fissures:
•Due to trauma to anal canal during blood (streaking on TP) •Topical NTG, Botulinum injection
defecation  constipation/hard, straining •Surgery- sphincterotomy

Perianal ½ perianal abscesses are caused by fistulas Abscess: swelling, pain Clinical rectal exam •Perianal Abscess: I & D, Antibiotics;
Abscess and MC in posterior rectal wall •worse with sitting, cough, poo sitz baths, high fiber
Fistula Fistula DX: US/CT
Fistula: open tract b/w two epithelium areas Fistula: anal discharge and pain •Fistula treatment: Fistulectomy

Hemorrhoids •Internal and/or external •Asymptomatic PE: Conservation (stage I and II)
•Engorgement of rectal and hemorrhoidal •peri-anal inspection •proper toileting & high fiber diet
veins Internal (superior vein) •Anoscopic evaluation
•Bleeding Medical (stage I & II with bleeding,
Causes: constipation, low fiber, straining, •Prolapse Staging: stage II-IV)
pregnancy, obesity •mucoid discharge •I: confined in anal canal, no •Preparation H, Anusol, Proctofoam
prolapse
Complications: External (inferior vein) •II: prolapse with straining Surgical (III-IV, recurrent bleed)
•Thrombosed external hemorrhoids *painful •perianal pain and bleeding •III: require manual reduction •band ligation (MC)
•sitz bath, topical ointments, clot evacuation •IV: always out, irreducible •sclerotherapy

Diverticulitis Infection/inflammation of diverticuli •Acute LLQ abdominal pain Labs: leukocytosis Diet:Clear liquid initially
•Fever, N/V, Bowel changes *eliminate seed, nuts, popcorn
Diverticuli: outpouching due to herniation of Imaging: CT abdomen/pelvis
the mucosa into the colon wall Physical exam: ***BEST TEST ABX:
*MC in sigmoid colon •LLQ tenderness, •Augmentin 875mg BID x7-10d,
•palpable mass Complications: peroration, bleed, •Flagyl + Cipro
abscess, stricture •Bactrim
Colon Cancer Causes: Proximal Screening Staging and Management: TNM
•Adenomatous polyp  malignancy •Anemia •FOBT (yearly) colonography *tumor, node, metastasis
•Familial adenomatous polyposis •Weakness, fatigue •flexible sigmoidoscopy q5 years
•Melena, (+) FOBT •colonoscpy age 50-75 Treatment:
Risk factors: •Wt loss •Surgical resection: stage 1-II
•>50yo Diagnostic: •Chemotherapy/radiation: III +
•family hx Distal colon Colonoscopy with biopsy 
•diet (red meat, fat) •Change in bowel habits diagnostic study of choice!
•smoking •Obstruction
•obesity •Hematochezia Barium enema: apple core lesions
•Urgency/tenesmus (rectal) Labs: HIGH CEA

Familial •Inherited mutation (APC gene) Soft tissue tumors in skin and Diagnosis confirmed with genetic Prophylactic colectomy
Adenomatous •Development of hundreds and adenomatous osteomas testing recommended!
Polyposis polyps
*stomach and duodenum

GI
Cholelithiasis Gallstone form from: Asymptomatic •Ultrasound Symptomatic (Biliary Colic):
•Ratio of cholesterol too high *procedure of choice •Laparoscopic cholecystectomy
•Ratio of bilirubin too high Symptomatic (biliary colic)
•Gallbladder not emptying bile •RUQ pain (hallmark) •CT No surgery:
-follow fatty meals Ursodeoxycholic acid
Types: Cholesterol gallstones (MC!) -may radiate to back and
right shoulder blade! Complications:
Risks: 5 Fs: fat, female, fertile, fair, choledocholithiasis, acute
forty *don’t typically see N/V, fever, chills cholangitis, acute cholecystitis
with biliary colic

Choledocolithiasi Choledocolithiasis: gallstones in Choledocolithiasis Choledocolithiasis •IV fluids, pain control, NPO
s and Cholangitis common bile duct (CBD); symptomatic •Intermittent RUQ pain Labs: normal •ERCP w/ stone extraction &
-passes are “uncomplicated” •Jaundice sphincterotomy
-typically symptomatic •Intermittent N/V Cholangitis
PE: normal Labs: •ABX with acute cholangitis
Cholangitis: gallstone lodged and •Leukocytosis -mild-moderate: Cipro + Flagyl
obstruction in CBD  infection Cholangitis •high alk phos, GGT, bilirubin -severe: IV Zosyn + Flagyl
-Bacterial infection or hepatic injury •Charcot Triad
*when become a problem -RUQ pain, Fever, jaundice Diagnostics: Complications:
•Reynolds Pentad: •US/CT (FIRST!) •liver damage
-Charcot + low BP •ERCP-diagnostic test of choice •septic shock with acute
+mental status changes cholangitis
PE: RUQ pain & hepatomegaly

Cholecystitis Acute: •RUQ Pain Labs: Leukocytosis Management: NPO, IVF, ABX
•MC due to stone lodged in cystic duct -steady, sharp pain, continuous •Ceftriaxone +/- Flagyl
•Sudden onset, severe -precipitated by meal Imaging: •IV Morphine or Demerol for pain
•N/V & Fever •Ultrasound-1st line •Laparoscopic chole in 24-72hr
Bugs: E. coli, Klebsiella, Enterococci -thick gallbladder, sludge, stones
 PE: Complications:
(+) Murphy Sign •HIDA scan: GOLD •Gangrene
(+) Boas: referred pain to R shoulder (+): no visualization of gallbladder •Chronic Cholecystitis
 irritation of the phrenic nerve

GI
Hepatitis A •Fecal-oral route •Incubation ~30 days •Hep A Antibody (Anti-HAV) Symptomatic  rest & fluids
•Crowding and poor sanitation -IgM peak in first week of sx *active Vaccine
•Contaminated food •Malaise, myalgia, N/V, anorexia infection
•Aversion to smoking (no craving) -IgG rises for months *previous, immunity
•RUQ abdominal pain, jaundice
•Mild hepatomegaly, liver tenderness Blood smear: Atypical large lymphocytes

GI
Acute Causes: •Epigastric pain that radiates into the back •Serum amylase & lipase Assessment of Severity:
Pancreatiti •gallstone *because retroperitoneal -elevated 3x normal •Ransons Criteria “LAAWG”
s •heavy alcohol -sudden, steady -lipase better for dx 3+ indicates severe course
-worse w/ activity & supine •CBC -age >55
Pathophysiology: -improve w/ leaning forward -leukocytosis -bld random glucose >200
•Edema/obstruction at ampulla of Vater •N/V •CMP -serum LDH >350
•acinar cell injury  premature or over •Weakness, sweating, anxiety -elevated glucose -AST >250
activation of enzymes  self-digestion -electrolyte abnormal b/c N/V -WBC >16,000
PE: *can dehydrate quickly •elevated alk-phos, LFTs
•Epigastric tenderness •High TGs Treatment:
•Distended abdomen •UA: proteinuria, glycosuria **Supportive: IVF, NPO, pain
•Absent BS if with ileus ABX: broad spectrum if severe
•Fever, Tachycardia, hypotension *baseline 3 tests are serum amylase
•Cullens & Grey Turners (side) sign and lipase, CBC, CMP

X-ray: Sentinel loop, colon cut off

CT: diagnostic study of choice

Chronic Chronic inflammation causing •Chronic, steady or intermittent epigastric X-ray: calcifications in pancreas Oral pancreatic enzyme
Pancreatiti parenchymal destruction  loss of pain *often radiates to back replacements
s exocrine function, sometimes endocrine •Anorexia, weight loss CT (best): pancreatic enlargement,
•N/V, constipation pseduocysts, calcifications
Causes:
•Alcoholism –MC! Pancreatic insufficiency Endoscope US: honeycomb
•Recurrent biliary pancreatitis exocrine: malabsorption & steatorrhea
•Severe high TGs endocrine: glucose high or low
•Autoimmune
•Genetic mutations TRIAD: calcifications, steatorrhea, diabetes
•Idiopathic
GI
Acute •Double stranded DNA •Incubation 12-14wks (up to 6mo) •HBsAG (surface antigen)-infective state! •Rest, increase fluids,
Hepatitis B •Inner core protein and outer *first to elevate, first sign nutrition
surface coat •Flu-like: Malaise, myalgia, fatigue •Avoid activity, alcohol,
•Low grade fever, anorexia •Anti-HBs  (+) and rest (-)= vaccine hepatotoxic
Causes: Bloodborne, sex, mother •Recurrent infections (URI)
Risks: IVDU, inmates, healthcare •Distaste for smoking •Anti-HBC (antibody to core antigen) •Hepatitis B Immune
•Mild RUQ pain and hepatomegaly - indicates diagnosis of Hep B Globulin (HBIG)
•Jaundice, enlarged lymph nodes *must give within 7d
•BEeAG (envelope antigen) *definitely infected
- indicates rapid viral replication & infectivity Prevent:
•Universal precautions
•HBV DNA: parallels presence of HBeAG •Safe sex
•Needle sharing education
•Elevated ALT/AST (LT > ST), bilirubin, ALP •Vaccination: 0, 1 and 6mo

GI
Chronic 90% of infants and Periods of remission with acute flares Elevated HBsAG and ALT/AST x6 months! •Antivirals: *1st LINE
Hepatitis B immunocompromised adults Increased risk of hepatocellular carcinoma -Tenofovir, Adefovir

Hepatitis C •Bloodborne, Sex, parenternal Incubation period 6 weeks Acute: (+) HCV RNA and +/- anti-HCV Interferon alpha 2-B AND
•Initially asymptomatic Resolved: (-) HCV RNA and +/- anti-HCV Ribavirin
Risk: IVDU, inmates, healthcare •Fatigue, myalgia Chronic: (+) HCV RNA and anti-HCV
•Jaundice wax and wane

Hepatitis D Hep B co-infection Increased risk of fulminant hepatitis •serum antibodies •Worse prognosis

Hepatitis E •RNA virus; Waterborne •Arthritis •IgM anti-HEV in serum •Self-limited

•Asia, Middle East, North Africa •Pancreatitis •Oral Ribavirin x3 months
•Thrombocytopenia
Spread: swine, pet, organ meats •Neurologic-Guillain Barre, neuropathy •Recombinant vaccines

GI
Cirrhosis •Fibrosis and nodular regeneration S/S: Insidious onset Minimal changes early •No cure w/o liver transplant
throughout the liver  •Weakness, fatigue, sleep changes •Treat complications!
replaces functional hepatocytes •N/V, abdominal pain, ascites •AST/ALT & ALP elevated
with nonfunctioning nodules •Bilirubin elevated Avoid alcohol
•Portal HTN: esophageal varices, •Hypoalbuminemia •Strict dietary management: protein, low
Causes: splenomegaly •Anemia carb and sodium; reduce protein if
•Alcoholic hepatitis (MCC US) •WBC fluctuations encephalopathy
•Hepatitis C •Skin: spider angioma, palmar erythema, •Thrombocytopenia •Nutritional supplements
•NASH ecchymosis •Prolonged PT/PTT •Vaccinations
•Drug toxicity *May have normal AST/ALT but
•Autoimmune hepatitis •Menstrual abn, ED, gynecomastia craziness everywhere else Encephalopathy: Lactulose, Rifamixin
•Hemochromatosis Ascities: Diuretics
•Genetic, metabolic •Vitamin & nutrient deficiencies: Diagnostics: Pruritis: Cholestyramine
 -anemia, glossitis, cheilosis •US/CT
•Biopsy: definitive DX Staging: Child-Pugh classification
•Jaundice, ascites, edema, effusion (late) •EGD: look for varices

Hepatic encephalopathy  confusion,

lethargy, asterixis (flapping hands),
increased ammonia levels

Hepatocellula Types: Patient that has already had cirrhosis •Alk phos spike (higher then before) Screening:
r Carcinoma •Hepatocellular *parenchymal and now they are declining •Alpha fetoprotein HIGH Cirrhosis & chronic HBV/HCV patients
•Cholangiocarcinoma *ductal •Liver US & a-feroprotein q6mo
•Cechexia Imaging:
Risks: •Severe wt loss, anorexia •CT: 1st line imaging! Treatment:
•hepatitis B, C, D; Cirrhosis •Weakness, muscle wasiting •Liver biopsy: CONFIRMS! •resection if not invading vasculature and
•male gender, fhx •Bloody ascities *necrotic tumor preserved liver function
•Alcohol •Tender hepatomegaly Staging: TNM •other: transplant

ORTHO
Polymyalgia •Idiopathic inflammatory •Pain and stiffness of proximal joints •HIGH ESR! *characteristic 1. Prednisone 10-20mg/day po
Rheumatica condition  neck, shoulder, pelvis •Elevated CRP *dramatic improvement in 72hr
(PMR) •MC in women >50 years old “difficulty putting on shirt/coat, comb hair” •Normocytic anemia
•symmetric & bilateral •ANA, RF, anti-CCP all (-) 2. DMARDs
•Associated with giant cell •worse in morning, resolve w/ movement
arteritis •fever, tired, weight loss Criteria for Chuang & 3. Calcium 1200mg and vitamin
Colleagues/Healy D 800 units daily
•Genes: HLA-DR4 *Healy-rapid response to Prednisone

Polyarteritis •Necrotizing inflammation of Constitutional: fever, myalgia, arthritis •Increased ESR and CRP Mild:
Nodosa medium/small arteries •ANCA (-) Prednisone 1mg/kg x4 weeks
•Systemic vasculitis Renal: HTN (increased renin), renal failure
P-pulmonary Definitive: biopsy  necrotizing Moderate & severe:
A-arteries •NO glomerulonephritis CNS: neuropathy, mononeuritis multiplex inflammatory lesions AND…
N-not •Associated with hepatitis B Oral Cyclophosamide 1.5-2mg
involved  “hePANitis B” Derm: livedo reticularis, purpura, ulcers, Renal angiography: microaneurysms with
gangrene, Raynauds phenomenon abrupt cut-off of small arteries

ORTHO
Systemic •Chronic, systemic multi-organ
Lupus autoimmune disorder of connective tissues
•MC in females 20-40, minorities
Risks: sun exposure, estrogen, fhx (HLA)
Drugs: Procainimide, Hydralazine,
Isoniazid, Quinidine
•Joint pain, fever, pericarditis, conjunctivitis • (+) ANA *initial test Sun protection
•malar “butterfly” rash *spares nasolabial
• (+) Anti-Smith and Anti-DNA Skin: topical steroids
Discoid: annular, erythematous patches on *most specific test
face, scalp that heals with scarring Rash/joints: Hydroxychloroquine
Lupus profundus: firm, deep nodules Pain: NSAIDs or Tylenol
causing dented scars as fat cells destroyed
Systemic: glomerulonephritis, retinitis, ulcer
Scleroderm Systemic connective tissue disorder •Tight, shiny thickened skin • (+) anti-centromere Raynauds: CCB, Prostacyclin
a (Systemic *associated with CREST
CREST Syndrome *spares trunk
Sclerosis) 2 types: Reflux: PPI, H2-blocker
•C-calcinosis cutis
1. limited (CREST)  distal extremities • (+) anti-SCL-70
•R-raynauds
2. diffuse  proximal extremities *associated with diffuse Nausea: Reglan
•E-esophagus motility disorder
•S-sclerodactyly (claw hand)
Pulm HTN: Sildenafil
•T-telangiectasias

Polymyositis •Idiopathic inflammatory muscle disease of •Progressive PROXIMAL muscle weakness •Increased aldolase and CK Prednisone 40-60mg
proximal limbs, neck, pharynx • (+) Anti-Jo 1 and Anti-Mi
Dermatomyositis: deep purple (heliotrope) • (+) Anti-SRP; Anti-155/140
•MUSCLE WEAKNESS rash of face, neck, shoulder, chest, back, eye
DX: 1st-MRI, definitive: biopsy
Sjogren •Autoimmune disorder of exocrine glands •Dry mouth (xerostoma) and dry eyes • (+) AntiSS-A and B (Ro/La) Eyes: artificial tears
Syndrome (keratoconjunctivitis sicca) • (+) RF and ANA Xerostoma: Pilocarpine
Types: primary (alone) v. secondary •Parotid enlargement & Thyroid dysfunction • (+) Schirmer test (low tears) -MOA: cholinergic

ORTHO
Reactive •Autoimmune response to infection •asymmetric arthritis (knees, ankles) • (+) HLA-B27 1. NSAIDs
Arthritis in another part of the body conjunctivitis/uveitis, urethritis
(Reiters Synovial Fluid: high WBC 2. DMARDs
Syndrome) •MCC: Chlamydia, gonorrhea, GI •mucocutaneous lesions: -bacterial culture (-)
infections (SSYC) balanitis, stomatitis 3. Anti-TNF

•Keratoderma blennorrhagicum:
hyperkeratotic lesions on palms & soles

Rheumatoid •Chronic inflammatory disease with
Arthritis persistent symmetric polyarthritis 
T-cell mediated
•Formation of pannus  erodes
cartilage, bone, ligaments, tendons
•Symmetrical swelling
•MC in PIP of fingers and MCP of
wrists, knees, ankles•
Worse in the morning, improves with
movement
Complications: ulnar deviation, swan
neck deformity, boutonniere deformity
•High ESR and CRP
• (+) RF *best initial test
• (+) anti-CCP *most specific
X-ray: joint space narrowing
Joint fluid: inflammatory
1. NSAIDs *symptom control
2. DMARDs (Methotrexate)
3. TNF-inhibitors
*give NSAIDs with DMARDS; NSAIDS
don’t prevent disease course

Gout Uric acid deposition in soft tissue, •Joint pain, erythema, swelling X-Ray: “mouse bite” “punched-out” 1st line: NSAIDs
joints, bone •MC 1st MTP great toe (podagra) erosion -Indomethacin, Naprosyn

Cause: under-excretion of uric acid Tophi deposition: collection of uric acid Arthrocentesis: (-) befringement 2nd line: Colchicine
-purine rich foods: alcohol, liver, crystals *CHARACTERISTIC LESION
seafood, yeast Preventative: Allopurinol
-MOA: Inhibits xanthine oxidase
-meds: diuretics (thiazide, loop),
ACEI, pyrazinamide, ethambutol,
aspirin, ARBs
 Pseudogout Calcium pyrophosphate deposition •Red, swollen, tender joint• X-ray: chondrocalcinosis 1st line: NSAIDS; joint injections
MC in the knee
•MC in elderly females >60yo Arthrocentesis: (+) befringement Propohylaxis: Colchicine
rhomboid shaped CPPD crystals

Fibromyalgi •Widespread muscular pain •Diffuse pain •Pain in 11/18 “trigger points” •Exercise
a •MC in middle aged women •Fatigue, sleep disturbances 3 MONTHS +
•depression Pharm:
•TCAs (Amitriptyline)
•SNRI (Duloxetine-Cymbalta)
•SSRI (Fluoxetine)
•Gabapentin
•Pregabalin

ENDOCRINOLOGY 8%
Adrenal Gland: Cortex = GFR-ACE outer  inner: Glomerulosa (Aldosterone-Na+), Fasciculata (Cortisol), Reticularis (Estrogen/Androgens)
ENDO 8%
Addison’s Autoimmune disease *gluco & mineralcorticoid deficiency •CBC: Eosinophilia, lymphocytosis Chronic: Oral glucocorticoids
Disease •CMP: low Na, glucose; high K+, -Hydrocortisone 15-30mg daily
*Adrenal ↓ cortisol •skin and mucosal hyperpigmentation BUN/Cr 2/3 in morning, 1/3 later
Gland ↓ aldosterone •Anorexia, weight loss, fatigue, decreased •Culture: Blood, sputum, urine
stamina •Plasma Cortisol and ACTH •Glucocorticoid Stress therapy
Adrenal Crisis: •Hypotension, dehydration, dizzy, hypoglycemia, •Serum DHEA (<1000) -Increase dose by 50% with stressors
MCC: abrupt weakness, fever, lymphoid hyperplasia, N/V/D •Plasma Renin
withdrawal of •Rapid ACTH Stimulation •Mineralocorticoid: Fludrocortisone 0.05
steroids Chronic: *add Cosyntropin IM, test cortisol in 45
•vitiligo (10%)  ACTH binds to melanocyte min, abnormal= increase <20 Acute Adrenal Crisis
•Changes in hair *loss CYP11+17, gain CYP21 •Hydrocortisone: Loading IV  IV q6h
•Generalized pain Adrenal Crisis: for 24h  oral when tolerate oral food
•Psychiatric: anxiety, irritable Low Na and glucose, high K+ •Fludricortisone, IVF (normal saline)
•Neurologic: gait, coma •Broad ABX, tx electrolytes/glucose

Acute: Sudden “Adrenal Crisis” Education: medical alert bracelet

-MC symptom: Shock  low BP and volume

Cushing’s ↑ cortisol Cushing Syndrome/Disease CBC: leukocytosis, low eosinophils Cushing SYNDROME Management
Disease •Fatigue, reduced physical endurance CMP: elevated glucose •hydrocortisone=DOC
*Adrenal Cushing Syndrome: •Central obesity with protuberant abdomen,
Gland Cortisol excess plethoric “moon face”, supraclavicular fat Dexamethasone suppression test Cushing DISEASE Management
pads, “buffalo hump” 1mg @ 11pm then check cortisol at •surgical removal of pituitary tumor
Cushing Disease: •Large purple striae, thin skin 8am: (+) if cortisol >5 •Hyperandrogenism: Flutamide
Increased ACTH •Hirsutism, male hair loss •Hypercortisolism: Metrypone
secretion from •Muscle weakness 24 hour urine free cortisol •HTN: K+ sparing diuretics, CCB
anterior pituitary •Elevated BP, immune suppression (+) if increased 3x normal
 Monitor/treat cortisol related conditions:
Causes: Late night salivary cortisol osteoporosis, psych, DM, hypokalemia,
•Iatrogenic (steroid muscle weakness, infections
therapy) Serum ACTH
•Pituitary adenoma <20  adrenal CT, >20  MRI
•Ectopic ACTH pituitary
•adrenal tumor

Pheo- Rule of 10s: Triad: episodic palpitations, HA, diaphoresis Plasma Free Metanephrines Management: resection of tumor
chromocytom •10% bilateral •Anxiety, pallor, syncope, tachycardia •sit 15min; elevated  assess urine
a •10% extra-adrenal •Paroxysms <1hr Awaiting Surgery:
*Adrenal •10% malignant •emotions/physical stressors, change in position, 24h Urine Metanephrine and Creatinine •Maintain BP < 160/90
Gland urination, various medications • (+) if >2.2mcg/mg of creatinine •Alpha-Adrenergic Blockers:
Catecholamine Cardura, Minipress, Hytrin
secreting adrenal *triad + HTN is HIGHLY suggestive Imaging: CT/MRI with contrast
tumor  NE and E Diet-high salt and water intake

ENDO 8%
Diabetes Primary central DI: •Polydipsia (thirst)-craving for ice •24hr urine for volume and creatinine Mild: no tx, consume fluids (WATER)
Inspidious •Genetic or autoimmune water Urine volume <2L/24hr without ↑Na
•Polyuria rules out DI Central AND Vasopressinase-induced DI:
Resistance or Secondary central DI: •large urine volumes •desmopressin  nose sprays
↓Vasopression •Damage to hypothalamus/stalk, •Serum glucose, urea nitrogen, calcium,
hemorrhage, surgery If no access to water: Potassium, Na, and uric acid
*AD •Partial DI Hypotension should be normal Nephrology:refer to nephrology
* posterior Vasopressinase-induced DI: •dry skin *wont respond to Desmopressin
pituitary •3rd trimester •+/- ↑Na and dehydration •Central DI: Vasopressin challenge test
*circulating enzyme destroys *measure urine 12h before & 12h after
vasopressin *aggravated by STEROIDS people w/ DI have ↓ polyuria/thirst Psychogenic-resolves with water
If positive, then get an MRI! restriction
Nephrogenic DI:
Defect in tubules •Nonfamilial: MRI pituitary/hypothal
•Nephrogenic: measure vasopressin
Congenital DI:
•Defective vasopressin *usually vasopressin is high
•present from birth (X-link)

Acromegaly/ Gigantism: child (before fuse) •frontal bossing (frontal bone •increased IGF-I Goal: control GH and IGF-I
Gigantism Acromegaly: adult (after fuse) enlargement)
•soft tissue swelling CONFIRM DIAGNOSIS: •SURGERY  transphenoidal
↑GH ↑IGF-1 *most commonly caused by •hyperhidrosis (deep voice) •glucose load does not cause a •Somatostatin analogues
somatotrope adenoma •kyphosis, macroglossia. suppression of GH <0.4 w/n 1-2h •Dopamine Agonists
*anterior sleep apnea, DM, polyps •Radiation
pituitary •Cardiomegaly, thyroid enlarge

Pituitary MC: Microadenoma Prolactinomas (MC) Diagnostics: Transphenodial surgery

Adenoma *lactation and suppressing MRI *study of choice •active and compressive tumors
Types: pregnancy, low FSH  sellar lesions, pituitary tumors
•Functional: secretes hormones •oligomenorrhea, amenorrhea, Prolactinomas: MEDICATION
•Nonfunctional galactorrhea Labs: •Dopamine Agonists: Cabergoline,
•Compressive: local symptoms •decreased libido, hypogonadism •Prolactin, FSH, LH Bromocriptine
•GH, IGF-1
Somatotropinoma •ACTH Acromegaly: surgery and Bromocriptine
•secretes GH  acromegaly •TSH •

Adrenocorticotopinomas
•Cushings disease

TSH secreting: thyrocotixosis

ENDO
Type I DM no insulin due to destruction of beta-cells (islet 3 Ps: Monitor: •insulin (multiple-dose basal bolus)
cells of the pancreas) *antibodies •polyuria (pee) •check glucose 3x daily -short acting: Humalog, Novalog
•polydipsia (thirst at home, increase fiber in -basal: Glargine, Lantus, Levemir
•Islets of Langerhans infiltrated by lymph •polyphagia (hunger) diet •Pramlitide (Symlin) *adjunct only
islet cell autoantibodies, T-lymph proliferate, •GFR and urine
release of cytokines within infiltrated islets albumin/year Dawn Phenomenon:
•Weight loss (low
•nml glucose until 2-8am
water)
preproinsulin (A, B, and C)  proinsulin (A & Labs: •decreased insulin sensitivity & nightly hormones
B)  insulin (C chain cleaves off) •postural hypotension •treat with bedtime injection of NPH
•weakness, blurred • glucose >200, fast>126
Insulin functions: glucose transport; stops vision, neuropathy, •A1C >6.5%, GGT Somogyi effect:
protein & TG breakdown, and gluconeogenesis fatigue •C-pep/Insulin ratio (low) •night hypoglycemia  rebound hyperglycemia due
*longer t ½ then insulin to surge of GH
•treat with decreased night NPH dose
Incretin: hormone that stimulates the release of
insulin and decrease blood glucose (+)GAD-65 with type IA

Type II DM Risks: •polyuria, polydipsia •self-check glucose 1- 1st line-Metformin + diet + exercise
•(+) fhx; N. American, AA, Hispanics, Asians •blurred vision 2x/d 2nd line-GLP1 ag., SGLT-2, DPP-4
•overweight (obese), birth wt >9lbs •poor wound heal •weight loss (5-10%) GLP1: “-tide”, DDP4: “-gliptin” SGLT2: “-glifozin”
•hyperglycemia •neuropathy •caloric restriction *insulin 0.1-0.2U if A1C>9 or sig. sx
•dry and itchy skin •eye exam, neuropathy
DM Treatment: •A1C 2x/year
Hypoglycemia: Sulfon, Meglit, Pramlintide, Insulin
Affordable: Metformin, Sulfonylureas Yearly eye exams
Weight Loss: GLP-1 Agonists, SGLT2 inhibitors; Recheck meds q3mo
Weight Gain: Sulfonylureas, TZDs, insulin

Diabetic metabolic acidosis 1+ days of ↑ thirst with •Glucose: 350-900 1-Fluid: 1L/hr 0.9% NS or LR 1-2h
Ketoacidosis
•Relative/absolute insulin def.
•Excessive counter hormones
•↓ Bicarbonate b/c depleted by ketoacids
•↓ Insulin, ↑Glucagon
-↑ hepatic gluconeogenesis and glycogenolysis
-↑ free FA release -> ↑ ketones
*triggered during increased physiologic need
Hyperglycemi Insulin deficiency and inadequate fluid intake
a weakness, decreased oral
Hyperosmolar •Triggered by stress:
State -infection, infarction, ↓ water
ENDO
Hyper- Causes:
thyroidism •Graves Disease (MC)
•Toxic multinodular goiter
•TSH secreting pituitary adenoma
•Excess intake
•Iatrogenic thyrotoxicosis
Hypo- Causes:
thyroidism •Iodine deficiency (MC worldwide)
•Hashimotos thyroiditis (autoimmune)
•Potpartum thyroiditis
•Pituitary hypothyroidism
•Hypothalamic hypothyroidism
Primary: failure of thyroid T3, T4
Secondary: failure of pituitary TSH
polyuria and polydipsia
•GI: N/V, fruity breath
•Cardio: ↓ BP, ↑ HR
*due to volume
depletion
•Neuro:
Mild-alert or drowsy
Severe-confusion, coma
•Respiratory: kussmaul
polyuria, polydipsia,
intake, wt loss
•Neuro: altered mental
•Cardio: ↓ BP, ↑ HR
HIGH BMR
•Heat intolerance
•Weight loss, hyperglycemia
•Diarrhea
•Warm, moist skin & hair
•Hyperactive: anxiety, tremor, nervous,
fatigue, weakness
•Tachycardia, high output HF
•Scanty period
Graves Eyes: lid lag with downward
gaze, “staring” appearance
Graves dermopathy (pretibial
myxedema): red, rough plaques
LOW BMR
•Cold intolerance
•Weight gain, hypoglycemia
•Constipation
•Dry, thick skin; brittle nails
•Loss of outer 1/3 eyebrows
•Hypoactivity: fatigue, sluggish,
memory loss, depression
•Bradycardia, decreased CO
•pH: acidic (6.8-7.3) *if Na rises, change to 0.45%
2-monitor cap glucose/hr & BMP/4hr for 1st 24hrs
•Potassium nml or ↑
•Sodium ↓Bicarbonate ↓ 3-IV regular insulin 0.1U/kg/hr
*change to dextrose when glucose 200mg/dL
•Renal: ↑BUN/Cr, ↓GFR Goal glucose: 150-200mg/dL
•Ketones: acetone, 4-Potassium 10meq if <5.2
acetoacetate, B-hydroxy 5-Bicarb if pH <7.0 (50meq/L/2hrs)
*serum checks B-hydroxy,
•Glucose: 600-1200 1-Fluid management
Infusion 1-3L/hr 0.9% NS 1-3h
•pH: nml or minimal acid
*if Na rises >150, change to 0.45%
•K+ and bicarb nml
2-monitor *same as DKA
•Renal: ↑BUN/Cr, ↓GFR
3-IV regular insulin 0.1U/kg/hr *NO if K <3.3
•Osmolality: 330-380 *change to dextrose when glucose 250mg/dL
*often >350 Goal glucose: 250-300mg/dL
4-Potassium-10meq/hr, ↑ if K+ <3.5
Thyroid labs: Treatment: PTU
•Primary: ↓TSH, ↑ FT4
Hypercalcemia, ↑ alk phos, Anemia Thyroid Storm:
Decreased granulocytes •marked delirium, tachy, V/D,
dehydration, high fever
•Graves-(+) TSI,(+) anti-TPO, anti-Tg
increased RAI and vascularity •Thiourea Methimazole or PTU
•Iodinated contrast
•Thyroiditis: ↑ ESR •Beta Blocker
•Hydrocortisone
Thyroid Storm Definitive tx:
radioactive iodine surgery
•serum TSH +/- FT: ↑ TSH, ↓ FT4 Treatment: Levothyroxine
Hashimoto: Myxedema Crisis-
• (+) (anti-TPO) *MC and (=) anti-Tg *triggered by infection, illness,
cold, drugs
Imaging:*not indicated in simple cases
•thyroid US •Treament Myxedema:
•CT MRI views gland IV levothyroxine (LT4)
 Tertiary: Failure of hypothalamus TRH •Menorrhagia •Supportive Myxedema: blankets,
intubation, tx underlying

Thyroid papillary thyroid carcinoma *MC
Cancer •single thyroid nodule
•least aggressive, slow, confined for
Follicular Thyroid Carcinoma
•metastasize, ↑ iodine uptake
Medullary Thyroid Carcinoma
•Secrete calcitonin, prostaglandins, 5HT,
ACTH, CRH, other chemicals
•Local mets, NO good iodine uptake
Anaplastic Thyroid Carcinoma
•Most aggressive, worst survival
•Rapidly enlarging mass in MNG
•Does not have good iodine uptake
*local resection and radiation
•Palpable, firm, nontender nodule/mass
Symptoms:
•Asymptomatic
•Metastasis ~3% cases
*MC sites-lymph, lungs, bone
•Anaplastic-s/s of metastasis
•Medullary-flushing, diarrhea
*rare Cushing-like syndrome
Serum Tg Surgery-First Line
•↑-metastatic papillary and follicular >1cm cancer: total
<1cm cancer: lobectomy
Serum Calcitonin <4cm inderterminate: lobectomy
•↑-medullary thyroid carcinoma >4cm indeterminate: total
Serum CEA RAI therapy
•↑-medullary thyroid carcinoma CI-prego, nursing
*low iodine diet for 2wkbefore
Thyroid US *size, location of mass
Chemo: aggressive CA
RAI Scan *use after thyroidectomy
•reveal metastatic tissue
High uptake: follicular
CT or MRI: Distant metastases
Malignant: COLD & LOW UPTAKE

ENDO
Hyper- Primary: increased PTH (MC) •Signs of hypercalcemia •Increased PTH and Ca2+, vit D Primary:
parathyroidism •parathyroid adenoma •Decreased DTR •Low phosphate •Parathyroidectomy

Secondary: 24 urine calcium: HIGH Secondary:

•hypocalcemia or vitamin D deficiency •Vitamin D, calcium supplementation
•CKD

Hypo- Causes: •Signs of hypocalcemia •Low PTH and Ca2+, Calcium supplementation and Vit. D
parathyroidism •post-surgical thyroid/parathyroidectomy •Increased DTR •High phosphate (Ergocalciferol, Calcitrol)
•autoimmune

ENDO
Pagets of Bone •Abnormal bone remodeling and disorganized •MC asymptomatic-incidental finding Labs: Asymptomatic: none
(Osteitis osteoid formation HIGH ALP
Deformans) •Bone pain (MC symptoms) Normal Ca & Ph Symptomatic:
•Increased osteoclast bone resorption  •Soft bones  bowed tibia, kyphosis Calcitonin & Bisphosphonates
abnormal trabecular formation  large, weak, less •Deafness X-ray: (Aldendronate, Risedronate)
compact bones with more vasculature and prone “blade of grass/ -MOA: inhibit osteoclasts
to fracture flame” lucency -take with water 1-2h before meals
-CI: nephrotoxic, thrombocytopenia,
•MC in western Europeans Skull: cotton wool atypical femure fx, jaw osteonecoris

Hypercalcemia Causes: “stones, bones, abdominal moans, psychic EKG: shortened Mild: no treatment
•hyperparathyroidism (high PTH & Ca, low Ph) groans” QT interval
•malignancy (low PTH) Severe/symptomatic:
 IV saline  Furosemide (Lasix)
NO HCTZ (increases Ca2+)

Hypocalcemia Causes: •Chovstek (touching cheek) EKG: prolonged Mild: oral calcium and vitamin D
•hypoparathyroidism (low PTH) QT internal (Ergocalciferol, Calcitriol)
•Renal disease (high PTH) •Trousseu (BP cuff), cramps, spasms,
•Hypomagnesemia tetany  lower action potential Severe/sympatomatic: Calcium
threshold gluconate IV or calcium carbonate IV

Hypernatremi Causes: Body loss of water  diarrhea, sweating, CNS dysfunction: confusion, lethargy, Na >145 Fluid replacement  hypotonic fluids
a diuretics, hyperglycemia coma, muscle weakness (water, 0.45% NS, D5W)

Hyponatremia Hypertonic: increased solutes dilute out sodium- •CNS dysfunction: Na <135 hypovolemic: Isotonic 0.9% NS,
increased glucose-pull water into interstitial space *cerebral edema
Isotonic (normal free water): usually due to HA, AMS, seizure, decreased DTR, hypervolemic: hypertonic 3% saline
hypertriglycerides or hyperproteinemia
•GI: N/V
Hypotonic: kidney unable to excrete free water
-Hypovolemic: diuretic; •Other: muscle cramps, lethargy
-Hypervolemia: fluid overload (CHF, nephrotic),
-Euvolemia: SIADH, thyroid

NEURO 8%
Tension HA Trigger: STRESS; depression, anxiety •Band-like/vise-like or tight in quality Clinical diagnosis •NO TRIPTANS
•Pericranial tenderness, poor concentration •Analgesics (NSAIDs, Tylenol)
•Bilateral, generalized, non-pulsatile
•NO FOCAL/NEURO COMPLAINTS Relaxation:
massage, bath, behavior

Cluster HA •activation of cells in ipsilateral
hypothalamus, triggering trigeminal
autonomic vascular system
*MC middle aged men (30-40yo)
•Trigger: alcohol
•Minutes -> hours, severe, unilateral, temporal •Typically occur at night & •100% O2 via non-rebreather
HA in grouped attacks over a period of time awaken patient •Sumatriptan and DHE
IPSITALERAL SYMPTOMS: •Clinical Diagnosis Preventative:
•ptosis, miosis, lacrimation, conjunctival •lithium, verapamil, Topamax,
injection, rhinorrhea, congestion, horner Valprate, prednisone. Ergotamine

Migraine Neuronal dysfunction in the
HA trigeminal system vasoactive
neuropeptides such as calcitonin gene-
related peptide leading to neurogenic
inflammation, sensitization, and HA
•3x more common in women
•90% have a family history
•MC type is WITHOUT an aura
Triggers:
stress, menstruation, visual stimuli,
Classic migraine attack typically has 4 phases: Criteria without aura: •NSAIDS (FIRST!)
1. Prodrome (24-48h prior to HA) A. 5 attacks + B-D -ASA, Ibuprofen; Naproxen
•euphoria, depression, irritability, cravings, B. HA last 4-72h -Ketorolac (Toradol)-ER
constipation, stiffness, and yawning C. has 2/4 following: -IM/IV, give w/ Zofran
-unilateral •Triptans (FIRST LINE)
2. Aura (75% don’t have) -pulsating •Ergotamines
•attributed to cortical spreading depression -moderate or severe •Antiemetics (Zofran!)
•transient neurologic sx -aggravated by activity
*MC visual; sensory, verbal, motor D. 1+ of following: *sx treatment: rest in quiet, dark
-nausea, vomiting, or both room until sx subside, cold cloth
3. Headache -photophobia or phonophobia
•unilateral, throbbing, or pulsatile Prophylaxis indication:
•anorexia, N/V, photophobia, phophobia, •Topiramate, valproic acid
 weather, nitrates, fasting, wine, sleep cognitive treatment, cutaneous allodynia (touch •Propranolol (BB), CCB, TCA
disturbances, aspartame hurts), blurry vision, hyperalgesia, blurry vision

4. Postdrome-drained, exhausted, euphoria

Giant Cell •Chronic vasculitis of large and •HA, jaw claudication, scalp tenderness, visual increased ESR, anemia, elevated •High dose corticosteroids
Arteritis medium sized vessels abnormalities CRP and alk phos
(Temporal)
•Varicella-zoster antigen is found in •Temporal artery may be normal to nodular, •Temporal artery biopsy
nearly 75% of temporal arteries tender, or pulseless *GOLD*

Intracranial HA that are typically worse w/ •Fever, Night sweats

Tumor awakening or lying down •Immunocompromised/ malignancy hx DX: MRI
•May awaken person at night
•New onset HA age >40

Concussion Mild traumatic brain injury •HA, vision changes, vomiting, LOC, confusion, CT: study of choice •Allowing brain to heal  rest
dizziness, amnesia  normal •No contact sports until cleared

NEURO 8%
Bacterial Acute infections of the arachnoid
Meningitis mater and subarachnoid space
Adults:
•Community Acquired
-S. pneumo (adults >20), N.
Meningitidis, GBS, Listeria
Monoctogenes, H. flu
•Healthcare Acquired: Staph aureus
Pediatrics:
•Neonatal: GBS, E. coli, Gram (-)
•Children >1 month: S. pneumo, N.
meningitides, GBS, H. flu
Adults:
•Fever, HA, Nuchal, Meningeal
•N/V, photophobia, seizure
increased ICP:
-papilledema, N/V, LOC change
-meningococcal rash
Pediatrics:
•Fever, lethargy, seizure
•Respiratory distress
•Jaundice, N/V/D
•Poor feeding/decreased appetite
•Restlessness/irritability
•Bulging fontanel (infants)
•Blood cultures x2 + stain, C/S GOAL: TX WIHTIN 60min
•PROMPT LP first, UNLESS:
Standard for all (3mo-55yo)
-immunocompromised
1.Dexamethasone 0-20minutes
-history of CNS
2.Ceftriaxone (Cefotaxime <1mo)
-new onset seizure
3.Vancomycin
-papilledema
-abnormal LOC PLUS ONE additional below:
-focal neurologic deficit •Acyclovir (HSV encephalitis)
•Meet any above=CT first! •Doxycycline (tick season)
*DO NOT DELAY ABX! •Ampicillin (<3mo or >55yo)
•Metronidazole (OM, sinus, mastoid)
Lumbar Puncture:
Rifampin prophylaxis if:
•low glucose
•Exposure H. flu, S. pneumo, N.mening
•high protein & WBC
•GBS (+) 35-37 weeks gestation
•cloudy, pressure 200-300
•Neurosurgery

Viral Evidence of meningeal inflammation Present similar to bacterial meningitis Work-Up: same as bacterial •Most cases self-limited (7-10d) &
Meningitis with a negative bacterial cx; MCC- but less severe treatment is supportive: fluids, rest, sx
Enterovirus Lumbar Puncture control
•HA, nuchal rigidity •CSF analysis, Gram stain and
Risk factors:
•Photophobia •PCR amplification Specific treatments:
•Infants <1 month
•Constitutional symptoms •clear, pressure <200, rest •HIV  refer; HSV  Acyclovir
•Immunodeficient patient
•mildly diminished LOC nml/low
•Exposure to someone with viral
Empiric ABX: old & immunocomp
meningitis
*NO seizures or focal neuro CT scan
 Historical features:
•travel and exposure history
•TB exposure
•ill contacts with similar sx/viruses
•vaccination history
•sexual history (HSV, HIV, syphilis)
Encephalitis •Inflammation of brain parenchyma
•Meningoencephalitis: meninges
•Encephalomyelitis: spinal cord/nerve
Causes:
•MC=herpes (HSV, VZV, EBV)
•Enterovirus, MMR, rabies, HHV6,
History:
•Travel/Exposure history
-camping/hiking, animal bite
•Sexual history (HSV 1 or 2)
•Ill contacts
•Vaccine history
NEURO
Carpal •A set of neurologic symptoms resulting
Tunnel from compression of the median nerve
Syndrom -Increased pressure in intracarpal canal
e -direct compression damages nerve
•MC in women
•MC mononeuropathy
Causes: synovitis of flexor tendons,
anatomically small canal, mass lesion,
edema, inflammation
Tarsal •Compression of the tibial nerve as it
Tunnel passes under flexor retinaculum at ankle
Syndrom
e Causes: posterior tibial nerve passes
through tarsal tunnel
-MC=fracture or dislocation
-not needed in uncomplicated Indeterminate diagnosis on CSF:
indications: focal neuro, 1. administer ABX after cultures
immunocompromised OR
2. observe w/ repeat LP in 6-24h
Prevention: IPV, MMR, VAR/Zoster
•Altered LOC, Seizures Work-Up: Treatment: Supportive, control sx
•Fever, HA, NV •LP with CSF analysis •Seizure: IV Lorazepam
•Focal neurologic signs (focal) -CSF PCR amplification
-speech/hearing, CN deficits, Therapy:
involuntary movements, MRI •HSV/VZV/EBV: Acyclovir IV 21 days
muscle weakness, partial •MRI for sensitive than CT *first dose within 30 minutes
paraylysis, memory loss •HSV etiology-90%, EEG-75% *all cultures before antiviral!
•Psychotic symptoms
Labs: Clinical Course:
Involvement of HPA: •CBC, CMP, PT/PTT •CSF analysis for PCR repeated at
•temp dysregulation, DI, SIADH •Blood cultures (no sepsis) completion of antiviral
•Culture any herpetic lesion for a •continue therapy until (-)
•Tzanck smear
-dull, aching discomfort, paresthesia, weak •Electrodiagnostics 1st line! •Relief of pressure
-NCS/EMG -neutral position (cock-up)
•Aggravating: sleep, sustained hand/arm -confirm dx & assess severity wrist splints, esp at night x3mo
positions, repetitive movements of hand/wrist -severity needed to know if -steroid injection
•Alleviating: posture change, shaking/ringing surgical candidate -OT, PT, chiropractic
-surgical decompression
•inspection: atrophy of thenar eminence (late) US/MRI: identify structural
abnormalities Plan of care:
•Tinel Sign: wrist percussion over capral tunnel •mild CTS: conservative (splint,
injection) 4-12weeks
•Phalen/”Prayer” Sign: flex/extend hands
•moderate/severe: conservative
•Carpal compression: pressure for 30 seconds while awaiting NCS/EMG test
-surgery referral
•Hand Elevation Test: hands above head x1min
*HIGHEST sensitivity & specificity; longest
•Paresthesias involving sole of foot, distal foot, •X-ray and/or MRI of the foot 1. Conservative: NSAIDS, shoe
toes, and occasionally heel -evaluate for bony deformity modification, orthotics
-worse at night, walking, standing, dorsiflex
- +/- tinels sign •NCS/EMG 2. Steroid injection if
-sensory loss over plantar surface -may be helpful in confirming conservative fails
Severe: atrophy of intrinsic muscle 3. Surgical decompression
Ulnar •Compression of ulnar nerve at one of
Nerve two locations: cubital tunnel, guyon canal
Palsy
Causes:
•Cubital tunnel: trauma of distal
humerus or elbow, compression/friction
(osteophytes, arthritis, synovitis)
•Guyons canal: trauma (laceration, carpal
fracture, blunt), space occupying lesion
Risks: occupation (lean on elbow) cycling,
baseball, karate
•Sensory: paresthesias in 4th and 5th digits, Diagnostics: Conservative: (mild-moderate)
aching elbow/wrist pain, worse at night •NCS: localize compression to -avoid leaning on elbows,
-triggers: sustained elbow flexion, elbow or wrist prolonged flexion
repetitive grip, leaning on, repeated -brace or wrap elbow at night to
pronation/supination •EMG: muscle weakness limit flexion
•Motor: “claw hand” in 4th/5th digits •MRI/US: demonstrate •Surgical Options:
compression at elbow or wrist -decompress (elbow/wrist)
Physical Exam: -MRI: nerve impingement -decompress w/ nerve
•Tenderness, decreased sensation & increased signal intensity transportation (elbow)
•tinels sign at elbow or wrist -US: thickening of nerve and
•atrophy of hypothenar (pinky) eminence altered echogenicity
•froment sign: thumb adductor weakness

Radial Compression of nerve at various sites:
Nerve •axilla (crutches), humerus, proximal
Palsy forearm, wrist
Risks: crutches, position, frequent tight-
fitting straps or gloves, fractures
•Motor: weakness of wrist extensor (“wrist •Often made with H/P ALONE Acute-conservative
drop”), finger extensors, thumb abduction •cock-up wrist & finger splints,
•Confirm with NCS or EMG if avoid compression
•Sensory: hand (radial distribution) atypical presentation
Severe secondary to trauma
-surgical decompression

NEURO 8%
Guillain- •Acute inflammatory •Onset 1-4wks after respiratory of GI illness Labs: CMP, CK, ESR, thyroid, stool IMMUNOTHERAPY WITHIN
Barre polyradiculoneuropathy with culture for C. jejuni, rheumatologic, 4WK OF ONSET
resultant weakness with possible Symptoms: vit B12, folic acid, A1C,
paralysis and diminished •dyesthesias (finger/toes and move proximal) electrophoresis, metal •Plasmapheresis
reflexes •proximal muscle weakness of LE ascending -removes autoantibodies, immune
symmetrically Electrodiagnostic (EMG/NCS) complexes, cytotoxic constituents
•Age: bimodal •diminished or loss of DTRs early on •confirms polyneuropathy
(15-35yo, 50-75yo) •pain-throbbing, aching •IVIG: donated plasma
*shoulder, back, buttocks, thighs Lumbar Puncture -requires less time, once daily
Variants: •progression of weakness over hrs -> days •reveals albuminocytologic
•acute inflammatory -CN involvement dissociation  high protein, normal •Pain: NSAIDS, Gabapentin
demyelinating polyneuropathy -respiratory: dyspnea, SOB, diminished WBC
(AIDP)=MC •ANS dysfunction (dysautonomia) •Motor Dysfunction: PT, OT
-tachycardia(MC), bradycardia, arrhythmias MRI with Gadolinium
•other neurological findings •spine: thick intrathecal spinal nerve •DVT Prophylaxis: LMWH
-neuro: unsteady to complete gait loss roots and cauda equine
-sensory: impaired proprioception •brain: enhanced CN III, VI, VII

Myasthenia •Autoimmune disorder with
Gravis progressively reduced muscle
strength with repeated use
•Females 20-30; Males 50-70
eye/face -> neck -> UE
•Fluctuating skeletal muscle weakness and fatigue Ice Pack Test x 2 minutes 4 treatment option available:
•worse later in the day/evening or after exercise •(+) if improvement 1. symptomatic therapy
•Ocular (CN II, IV, VI): EOM weak  diplopi  anticholinesterase
-diplopia disappears when close one eye Serology: (Pyridostigmine)
-unilateral or bilateral ptosis •AChR antibodies (85%)
•MuSK Antibodies (if AChR (-)) 2. Chronic immunomodulating
•Bulbar muscle weakness (CN IX-XII) -not likely to have thymic therapy  glucocorticoids
 -> hands -> LE
•Antibodies are produced (by
thymus) against the ACH
nicotinic postsynaptic receptors
(AChR) at the neuromuscular
junction
 AChR destruction and a
loss of postsynaptic
folds
 Over release of Ach
Etiology:
•Idiopathic derangement of
immune system regulation
-anti-AChR antibody (MC!)
-anti-MuSK antibodies
•Thymic disease found in 75%
•Various drugs
-weakness with prolonged chewing •Seronegative MG (both (-))
-dysphagia, dysarthria(speech), dysphonia(voice) -purely ocular disease
•Anti-striated Muscle(anti-SM)
•Facial Muscles (CN VII) -(+) in about 80% w/ thymoma
-flat affect, cant smile or close eye
Imaging: CT chest  thymoma
•Neck Muscle Weakness *anterior mediastinal mass
-“dropped syndrome” later in day  weak
extensor muscles Electrodiagnostic Studies
•Repetitive Nerve Stimulation
•Limb: proximal muscle weakness, UE>LE (RNS) *MC study for MG
-repetitively stimulated the NMJ of a
•Myasthenia Crisis (resp. muscles) specific muscle
-diaphragm and IC muscle weakness (+) test: smaller EPSPs due to
repetitive stimulation
•Single-Fiber Electromyopgraphy
*Most sensitive test for MG
-2 muscle fibers w/ same axon
-(+) if increased time frame between
1st and 2nd AP
3. immediate immunomodulating
therapy Prednisone
-Other immunomodulators:
Azathioprine, Mycophenolate
mofetil, Cyclosporine
4. Surgery (thymectomy)
Rapid Immunomodulating
Therapy
Indications: myasthenic crisis,
pre-op, bridging meds, maintain
remission
•Plasmapheresis
•IVIG

NEURO 8%
Essential MC adult onset movement disorder •Rapid action/kinetic tremor of arms Clinical Diagnosis •1st line-Propranolol (off label)
Tremor -trouble writing, eating, fine motor skills •Primidone + Propranolol if no response
Defined by: •Head and arm tremor MC *speech *refer if 1st line options don’t work
-enhanced by emotional stress changes
-decreased with ETOH •NO tremor at rest •2nd-Alprazolam, Topiramate, Gabapentin
-fhx common (dominant)
-no other abnormal findings •3rd line-Deep brain stimulation, botox

Parkinson’s •Uncommon under age 40, increase after
Disease age 60
•MC in men
•Reduced Risk: caffeine, coffee, ibuprofen,
statins, cigarette smoking, moderate alcohol
•Increased Risk: age, fhx,
herbicide/pesticide exposure
Pathophysiology:
Degeneration of the dopamine-producing
neurons in the pars compacta of the
substantia nigra and locus coeruleus in
brainstem Dopamine/Ach imbalance
•resting tremor, rigidity, bradykinesia Clinical features from hx •Aim: blocking the effect of Ach or
& PE administration of Levodopa
Tremor
•resting tremor of distal muscles; “pill Must have bradykinesia •1st line: Levodopa & Carbidopa
roll” with either rigidity
•less with voluntary movement and/or tremor •Dopamine Agonist: <65 and mild sx
•spreads unilaterally up the body -Bromocriptine (Cycloset)
-Pramipexole (Mirapex)
Rigidity -Ropinirole (Requip)
•unilat  spread up then contralateral -Amantadine
• “cogwheel” rigiditiy & lead pipe
•Anticholinergic-Benztropine
Bradykinesia 80% of patients -young patient w/ tremor as primary sx
•generalized slow movement
•starts distally: fingers  loss of arm •COMT Inhibitors
swing  feet and legs (shuffling) -Talcapine, Entacapone
-extend life of Levodopa; adjunct tx
 •Lewy bodies within neurons
Huntingtons •Incurable, inherited, autosomal
dominant neurodegenerative disorder
•Chromosome 4
•Expanded & unstable CAG trinucleotide
repeat in HTT gene at 4P16
NEURO 8%
Multiple •MC autoimmune inflammatory
Sclerosis demyelinating disease of CNS
•Cause: autoimmune
•Women > Men
Pathophysiology:
•lesions effect white matter in the optic
nerve, brainstem, basal ganglia and
spinal cord
-demyelinating lesions (plaques)
-myelin loss, destruction of
oligodendrocytes, reactive
astrogliosis (increase in astrocytes)
•lesions affecting signal in grey matter
Risks: far from equator, viral infections,
HLA on chromosome 6
•Characterized by motor, cognitive, and
psychiatric deficits with cell loss in
neurons of basal ganglia and cortex
•Chorea, Dystonia
•Eye movement abnormalities
•Wt loss and cachexia
•Psych: irritable, moody, antisocial
•Cognitive: judgement, memory
•Behavior changes: dementia *gradual
•Initial: abnormal movements or
intellectual changes
•Early: abnormal behavior & restless
•Later: dementia & choreiform, dystonia
Spinal cord
•sensory loss, weakness, numbness,
sphincter (urgency, hesitancy, sexual)
brainstem: optic neuritis, diplopia,
lateral gaze, dysphagia
psychological: cognitive disability,
depression, euphoria
motor: unsteady, spastic, cramp, gait
transient features
•lhermitte sign: electric shock like
sensation that runs down back or limbs
upon neck flexion (looking down)
•uhthoff phenomenon: worsening sx
when overheated
•History and PE
•CT/MRI: cerebral &
caudate nucleus atrophy
•PET scan: reduced
striatal metabolic rate
•Genetic Testing
CLINICAL
•2+ attacks followed by
objective evidence on exam &
2 lesions
McDonald Criteria
•clinical findings + MRI
•2+ regions of central white
matter (space)
•different times (time)
Imaging:
T1/T2 MRI of brain/cervical
cord
-T1: hypointense “black holes”
showing axonal damage
-T2: high signal intesntity
lesions associated with total #
of lesions, highlight active
inflammation
LP: oligoclonal IgG
*Symptomatic; No cure
•Tetrabenazine for dyskinesia
-MOA: blocks Dopamine release
-SE: extrapyramidal
•Reserpine for chorea
•Haloperidol for behavior & chorea
•Amantadine for chorea
•Supportive care
Acute Attacks
•Methylprednisolone
•Plasma exchange if steroids CI
Symptomatic
•fatigue: Amantadine, Methypheidate
•Depression: SSRI
•Spasticity: Baclofen, Diazepam
•Pain: TCAs
•Optic Neuritis: Methylprednisolone
Disease-Modifying
RRMS, SPMS with exacerbations
relapse prevention 1st line
•IFN B-1a (Avonex, Rebif)
•IFN B1b (Betaseron or •Extavia)
•Glatiramer acetate (Copaxone)
•Fingolimod (Gilenya)
•progressive MS
-SPMS: high dose IFN-B
-PPMS: Ocrelizumab (Ocrevus)
•Aggressive MS: Cyclophosphamide
Complex •Typically follows an injury, surgery, or •Pain •History and PE •Multidisciplinary approach
Region Pain vascular event (stroke) -burning, stabbing *send to a pain clinic!
Syndrome -grinding, throb •Labs: CBC, ESR, CRP, ANA,
(CRPS) •Onset about 30-60yo, MC females -exacerbated by limb movement, RH, complement fixation panel, •Meds: antidepressants, corticosteroids,
•cigarette smoking contact, temperature, stress serum immunoelectrophoresis anticonvulsants (pain), COX-2 inhibitors
(Reflex (Celebrex), GABA, opioids, calcitonin,
Sympathetic Pathogenesis: •motor impairment •Imaging: radiograph, bone sympathetic blockers
Dystrophy) •diagnosis requires presence of regional scan, MRI/CT
pain and sensory changes following event •other sensory: hyperalgesia, •PT & OT
 Surgery, trauma, stroke allodynia, hyperesthesia *should not •EMG and NCS •Local anesthetic block/inject
•3 things: cause pain •Vascular studies •Tactile discrimination training
-persistent painful lesion •Sweat testing •Botox injection
-predisposition •autonomic: temp, color, sweat, edema •Spinal cord stimluators
-abnormal sympathetic reflex arc: •Thermography: visual displays •Amputation
increased sensitivity of injured axons •trophic: increase hair and nail growth, the amount of infrared energy •Sympathectomy (remove ganglion)
skin atrophy emitted, transmitted, and
reflected •Prevent: early mobilization, vit C sup,
aggressive tx, stop smoking

NEURO 8%
CVA A sudden onset of neurologic
deficit resulting from a loss of
blood flow to a part of the brain
*cell death and irreparable damage
to brain tissue w/n 5min
Types:
Ischemia: thrombotic, emboli
*MCC is atrial fibrillation
Hemorrhagic: intracerebral
(HTN), subarachnoid (aneurysm,
AV malformation)
•hemi/mono/quadriparesis
•hemisensory deficit
•visual loss; one or both eyes, diplopia
•dysarthria, facial droop, ataxia, vertigo
•aphasia (Brocas or Wernickes)
•decrease in LOC
Exam:
ABCs and vitals
Skin: petechial, janeway, osler, livedo
reticularis, purpura
HEENT: trauma, funcoscope, mouth
Cardio: rhythm, M/R/G, bruit
Respiratory: breath sounds
Neuro: CNs, NIHSS sale
•Oxygen Saturation
•Finger stick blood glucose
•CT brain w/o contrast
-GOAL: w/n 25min of arrival
Other Immediate Studies:
•CBC, BMP, PT/PTT, troponin
•EKG/cardiac monitoring
•Keep NPO  IVF
•Hypoglycemia: dextrose
•Blood pressure: Labetolol,
Nicardipine, Clevedipine
•Cerebral edema: Mannitol
•Seizure: Lorazepam
Ischemic Stroke
•goal of SBP < 185 + DBP < 110
•TPA (Altepase): maintain BP
<180/105 for 24 hours after
Intracerebral Hemorrhage
-lower BP within one hour to 140

Transient •transient episode of neurologic Assessing severity of symptoms ABCD2 scoring: 1. Order US of carotids (CAD)
Ischemic dysfunction caused by cerebral 3+ should be admitted 2. EKG, Echo (emboli)
Attack acute infarction 3. MRA/CTA (vessel disease)
(TIA) -most resolve within 1-2 hours
Pharm: Plavix, Control BP, Statin

Coma 1. lesions that damage the RAS in •Sleep-like state with no purposeful GCS: 3 When to intubate:
the upper midbrain or its projections response to the environment and which the •apnea upper airway obstruction,
 pt cannot be aroused for >1hr hypoventilation, emesis
2. Destruction of large portions of -closed eyes, do not open •liable to aspirate because of coma
both cerebral hemispheres -lack verbal communication
-no purposeful movement Prognosis:
3. Suppression of reticulocerebral -verbal stimulation  no response •rarely lasts more than several wks
function by drugs, toxins, or -painful stimulation may produce no •either recover or revolve into brain
metabolic derangements response or nonpurposeful reflex death or a persistent vegetative state
(hypoglycemia, anoxia, uremia,
hepatic failure) *MC

Disease Presentation Clinical Presentation Diagnostics Management

Dementia Impairment in 2+ domains Triad: memory impairment, visuospatial problems, History 1st line: Cholinesterate inhibitors-
language impairment Donepezil, Rivastigmine,
MCC: Alzheimers *little to no insight to condition Galantamine

Delirium ACUTE onset & fluctuating Cognitive: rambling speech CBC, CMP, glucose, O2 stat Reorient, encourage family
over 24 hours Inattention: difficulty maintaining conversation, trouble involvement, avoid restrains,
with instructions Brain MRI or CT: if trauma, maintain mobility, glasses and
Risk factors: medications Disorganized thinking: memory FUO, new neurologic hearing aids
Altered LOC: Sleeping disturbances, symptoms, no obvious cause
hallucinations/illusions, delusions, emotional lability

NEURO 8% About Cardiac/Other Neuro Diagnostics and Treatment

 Syncope Cardiac: carotid sinus,
aortic stenosis, HOCM
Neurologic: basilary artery,
subclavian steal syndrome
Other: orthostatic,
vasovagal
Epidural •middle meningeal artery
Hematoma •MCC: temporal FX
Subdural •cortical bridging veins
Hematoma •MC in elderly
•MCC: blunt trauma
Subarachnoi •berry arterial aneurysm
d •MCC: rupture, AVM
Hemorrhage
Intracerebral •intraparenchymal
Hemorrhage •MCC: HTN, AVM, trauma
UROLOGY/RENAL 8%
GU 8%
Epididymitis •Inflammation of epididymis
•STD: men <40
•Non-STD: men 40+
Hydrocele •peritoneal fluid between
layers of tunica vaginalis
•common in infants
•resolves by 1yo
Testicular •Twisting of spermatic cord
Torsion
Neonate: cord above insertion
of tunica vaginalis
Adolescent: bell clapper
Varicocele Dilated, engorged, tortuous
veins w/n the pampiniform
Carotid sinus: slow SA and AV node due
to pressure on carotids (turtleneck)
Aortic Stenosis: low CO due to stenosis
HOCM: murmur increases with valsalva
Vasovagal: decrease in arterial pressure
and HR mediated by parsympathetic tone
•LOC, HA, N/V, focal sx, CN III palsy
•LUCID INTERVAL  coma
•varies, may have focal neuro sx
•”thunderclap” sudden HA
•meningeal symptoms, no focal neuro
•HA, N/V
•+/- urethritis, prostatitis, cystitis sx
•fever
•pain and swelling in scrotum
-late-hard to distinguish from testis
•+/- retractive hydrocele
•+- inguinal lymphadenopathy
• (+) phrens sign
Communicating: patent processus vaginlais-
fluid into tunica vaginalis; fluctuates
Noncommunicating: processus vaginalis
closed, fluid trapped, not reducible
•pain worse with activity, N/V
•Red, tender, swollen scrotum with a tender
swollen, elevated testis
•Absent creamsteric reflec, (-) phrens sign
•Exquisite pain on palpation from testis
•Can compromise spermatogenesis in 4-6hr
•Scrotal enlargement or heaviness
•Infertility as initial complain
Basilary Artery: vertigo, visual
dysfunction, perioral numbness, ataxia
Subclavian Steal: Stenosis of subclavian
artery proximal to the vertebral artery 
sx with left arm exertion  angina, finger
ulceration
Orthostatic: rapid change from lying to
sitting or sitting to standing
•CT of brain: convex (lens) bleed
-does NOT cross suture lines
•CT of brain: concave (cresecent)
-DOES cross suture lines
•CT of brain
•LP: CT (-)  xanthrochromia, high CSF
•CT: intraparenchymal bleed
•DO NOT PERFORM LP (herniation)
•UA-pyuria, bacteriuria, hematuria,
culture
•Urethral swab
-gonorrhea: G- diplococci
-chlamydia: WBC w/o organism
•PCR for gonorrhea/chlamydia
•CBC: WBC with left shift
DX: transillumination
-scrotal US to check contents
DX: US
Labs: Rule out other disorders
Diagnostics:
•Head CT: focal neuro, hx SAH
•Position of patient at time of syncope
-lying: seizure, cardiac arrhythmias
-standing: orthostatic, vasovagal
Orthostatic vital signs: SBP drop >20
or SBP <90 or pulse increase >30bpm
Treatment: varies on cause
•high ICP: Mannitol
•evacuate with massive 5mm+ midline
shift
•supportive tx: bed rest, stool soft
•lower BP: Nicardipine, Nimodipine,
Labetalol
•supportive treatment: +/- Mannitol
•gradual BP reduction
•Bed rest, scrotal elevation, ice packs
•NSAIDS
•ABX (improve ~3d, resolution ~2-4wk)
-STD: Ceftriaxone + Doxycycline
-unlikely STD: Levofloxacin 500mg
TX: supportive until about 1-2yo
Surgery indications: not resolved by 1-
2yo; sx; compromised skin
•Urgent urological consult and surgery
•Orchipexy; Detorsion with in 4-6hr
Manual Detorsion:
-twisted clockwise/counterclockwise
-successful= rapid return of blood
Asymptomatic: observe
Conservative: scrotal support, NSAIDS
 plexus of scrotal veins
*most surgically correctable
cause of male infertility
*MC on left side
US: confirms DX
Physical Exam: Surgical:
•Dilated veins in sac “bag of worms” •Occlusion (balloon) or embolization
•Increased with standing, valsalva •Injected ablation of vein
•Improve while supine •Surgical ligation of pampiniform plexus

Erectile 1. Failure to initiate erection
Dysfunction *psych, endo, neuro
2. failure to fill penile tissue
*arteriogenic
3. failure to store adequate
blood in lacunar network
*venoocclusive dysfunction
>80% cases: DM,
atherosclerosis, medication
Meds: BB, thiazides, estrogen,
GnRH, H2, TCA, SSRI
Vasculogenic causes: MCC! PE: cardio, genital, neuro Psychogenic component:
•atherosclerosis, arterial disease, structural •behaviorally oriented sex therapy
Labs: lipids, glucose, T, prolactin •counseling, stress reduction
Neurogenic *target towards underline cause
•surgery, radiation, spine, MS, neuropathy Organic component:
*esp w/ DM & alcohol Education: •medications:
•diet and exercise -PDE-5 inhibitors
Endocrinologic: Low T, increased prolactin •avoid smoking, ETOH, drugs -injection therapy (prostaglandin)
-testosterone replacement therapy
Diabetic: Vascular, neuropathy Associated Factors:
*Decreased NO •DM, obesity, BPH •surgery:
•HTN, CV disease, low HDL -vacuum devices
Psychogenic: •smoking, radiation, surgery -penile implants (prosthesis)
•inhibit reflexogenic responses, increase •depression, anxiety, stress, anger -vascular surgery
smooth muscle tone

GU 8%
Acute •Gram – rods most common •Fever, chills, malaise Labs: •IV: fluroquinalone +/- aminoglycoside,
Bacterial •E. coli, Pseudomonas, Proteus •Pain-perianal, sacral, suprapubic •CBC: leukocytosis, left shift or amp/gent
Prostatitis •Irritative & obstructive voiding •UA: pyuria, bacteriuria, hematuria
MC route: ascent up urethra •Urine culture: + for bacteria •Oral (MC): Bactrim 800-160mg BID
•Digital rectal exam (DRE): *KEY! or Fluoroquinalone (Cipro)
Risks: hot, exquisitely tender prostate Imaging: rarely indicated
•catheter, prostate biopsy, stricture *prostatic massage CI due to sepsis

Chronic •Gram – rods most common •Dull, poorly located, in suprapubic, Labs: Fluoroquinolones or Bactrim x6wk
Bacterial •E. coli perineal or low back pain •Prostatic secretions: increased WBCs
Prostatitis •Pseudomonas, Proteus, Klebsiella, •Irritative & obstructive voiding (>10) with a (+) culture SE of prolonged use:
•Enterococcus •HX UTI or (+) cultures C. diff, CNS, tendinopathy
•UA: normal unless cystitis also present
MC route: ascent up urethra DRE: nml (MC), may see boggy Supportive: anti-inflam, sitz baths
*may be complication of ABP, but (spongy), tender, enlarged, and/or •Urine culture: negative; + for
most have no hx indurated prostate organism AFTER massage! Difficult to cure! Common relapses

Benign •MC benign tumor in men •Obstructive voiding-hesitancy, Labs: Mild (0-7 score): watchful waiting
Prostatic •More common with increasing age decreased force and caliber of •UA: normal, possible hematuria
Hyperplasi *become more sensitive to stream, sensation of incomplete Surgical Procedures:
a (BPH) androgens and GF bladder emptying, double voiding •PSA: screening for prostate CA •Transurethral Resection of the
•Increase in both glandular and (urinating within 2 hr), straining, *can be elevated in BPH Prostate (TURP) *MC!
stromal component post-void dribble *can cause retrograde ejaculation

Risks:
•Genetics (blacks more likely,
Asians less likely)
•Increase Risk: Higher PSA levels,
prostatitis, heart disease, BB use,
lack of exercise, obesity
•Decreased risk: NSAIDS, ETOH,
smoking, regular exercise
•Irritative voiding
-urgency, frequency, nocturia
*secondary response of bladder to
increased outlet resistance
*detrusor muscle hypertrophy and
hyperplasic, collagen deposit
DRE: smooth, firm, symmetric,
elastic enlargement of prostate
*induration & asymmetric -> cancer
Imaging: *often not needed
•US: if high serum Cr or UTI
•Upper GU tract image: only if
complications arise or comorbid GI
disease present
2 mechanisms of obstruction:
•Mechanical: narrowed urethral lumen
•Dynamic: A-receptor stimulation
causing increased tone (constriction)
•Transurethral Incision of Prostate
(TUIP)
•Open Simple Prostatectomy
Minimally Invasive:
•Laser Therapy (TULIP)
•Transurethral Needle Ablation of
Prostate (TUNA)
•Transurethral Electrovaporization of
Prostate
•Hyperthermia
•Implant to Open Prostatic Urethra

Prostate MC non-skin cancer in men DRE: focal nodules or induration •PSA Observation small, well-differentiated
Cancer most are adenocarcinomas
Large or locally extensive CA: •BUN/Cr: high if urinary Radiation: beam or pellets
Risks: •obstructive voiding retention/obstruction Chemotherapy: metastatic disease
•Black ethnicity
• (+) fhx of prostate cancer Axial skeleton metastasis: •Alk Phos/Calcium: high if bony mets Cryosurgery: liquid nitrogen in prostate
•high dietary fat intake •low back pain, fracture
•old age *MC 1st site of metastasis Imaging: Transrectal US: stage/biopsy Androgen Deprivation Therapy
•LNRH agonists (Leuoprolide)
Staging: Gleason system •LNRH antagonist (Degarelix)
•Ketoconazole or steroids
•Orchiectomy (remove testicles)
GU 8%
Acute E. coli •Irritative voiding (dysuria) Labs: Short term antimicrobial Therapy
Cystitis Proteus •Frequency urgency •Pyuria •Nitrofurantoin (Macrobid) 100mg po BID x5-7d
“Bladder Klebsiella •Suprapubic pain •Hematuria •Bactrim 800/160mg po BID x3d
Infection” Pseudomonas •+/- gross hematuria •Bacteriuria •Fosfomycin (Monurol) 3g po x1
“UTI” Staph •Leukocyte esterase •Fluoroquinalones, Augmentin, Cephalosporins
Exam: •Urinary nitrate
MC route: •Suprapubic tenderness •Urine culture + bacteria Urinary Analgesics: Phenazopyridine (Azo)
ascent up urethra •NO CVA!
•NO TOXICITY! COLONY COUNT >100,000 Non-Pharm: *in addition to antibiotics
*MC in women •Sitz baths, fluids +/- crandberry juice, probiotics

Acute G-bacteria MC •Irritative void (dysuria) Labs: Outpatient:

Pyelo- E. coli •Suprapubic pain •Pyuria, hematuria, bacteriuria •1st line: FQ (Cipro or Levo); Bactrim, Augmentin
nephritis Proteus •+/- gross hematuria •+/- WBC Casts
“kidney Klebsiella •Fever, chills, N/V/D •Leukocyte esterase & Urinary nitrate •Adjunct Tx: if high risk for fluoroquinalone resistance
infection” Pseudomonas •Flank pain •CX: + heavy growth of bacteria or if using 2nd line tx  1g Ceftriaxone (Rocephin)
•CBC: leukocytes w/ left shift
MC route: Exam: Inpatient:
ascent up urethra •Fever Imaging: •IV ampicillin/gentamicin, FQ, fluoroquinalone
hematologic route •Tachycardia •CT (preferred): renal inflam, abscess •IV carbapenem (Imipenem)
•CVA tenderness •US: hydronephrosis, abscess •IV extended-spectrum cephalosporin (Cefepime)
Renal *MC in males
Calculi •Calcium oxalate- MC!
(Nephro-
lithiasis) Risks:
•high protein and salt
•inadequate hydration
•humidity & elevated temp.
•sedentary lifestyle
•GI malabsorption syndromes
•HTN, obesity, gout
*stone size does NOT
correlate with severity
S/S:
•Acute, severe pain (flank)
•radiate to abdomen or groin
•Urgency and frequency
•Nausea/Vomiting
<5mm pass spontaneously
10mm+ do NOT pass
Labs:
•hematuria (micro or gross)
•<5.5: uric acid or cysteine
• 5.5-6.8: calcium oxalate
• >7.2: calcium phosphate/struvite
Frequent or + family history:
•Low Na & protein, high fluid
Diagnostics:
•KUB abdominal xray (cheapest)
•Renal US (good if noradiation)
•Spiral CT-most accurate
•Pain control-NSAIDS, opioids
•Hydration-NO FORCED IV because may worsen pain
•Alpha-1 blocker-Tamsulosin
•Steroids-Prednisone 10mg daily for 3-5d
Prevention:
•Increase fluids-best thing to do! 1.5-2L of urine/d
•Diet (Eat bran to decrease calciuria)
*do not need to decrease calcium!

Autosoma 90% from autosomal dominant •Abdominal or flank pain Hematuria & Mild proteinuria •Vasopresssin receptor antagonists
l •+hx of UTI & HTN •Tx HTN, protein restriction
Dominant Two genes: •+fhx of PKD •US confirms DX; CT if unclear •Rest, analgesics, hydration, avoid caffeine
PKD •ADPKD-1 (MC!): more severe <30: 2+ renal cysts
(ADPKD) •ADPKD-2: slow progression Exam: 30-59yo: 2+ cysts in each kidney Infected: Floroquinalone, Bactrim 2wk IV
•large kidneys, +/- palpable 60yo+: 4+ cysts in each kidney

Autosoma Enlarged kidneys with small •Enlarged kidneys & HTN •Large, echogenic kidneys •No specific therapy
l Recessive cysts on collecting tubules only •Impaired urine •Cysts visible after birth •Manage HTN
PKD *most neonates die from concentration absence of cysts in parents •Dialysis & transplant
pulmonary hypoplasia •Metabolic acidosis

GU 8%
Prerenal Bad perfusion (hypoperfusion) •Uremia •￬GFR and ￪BUN/Cr *BUN: CR ratio >20:1 treat underlying!
Azotemia •Arrhythmia •Low excretion of Na+ (<20 •Maintain euvolemia
*most •Hypovolemia •Nonspecific diffuse abd •Normal urine osmolality (>500) •Correct electrolytes
common •Decreased CO pain & ileus •Avoid nephrotoxic drugs
•Changes in vascular resistance urinary sediment: Hyaline casts

Postrenal obstruction of urinary outflow •Anuria or polyuria ￬GFR and ￪BUN/Cr *BUN: CR ratio >20:1 Studies/Imaging:
Obstruction *get blood in, but no urine out urine backed up  leak •Bladder Catherization,
•Na+ in urine varies •Abdominopelvic US
least common ￪ pressure  damaged parenchyma •Lower abdominal pain •Urine osmolality <400 can be helpful to look for hyroureter and
obstruction
causes: BPH (MC), obstructed catheter, •Large prostate, distended Urine sediment: nml
anticholinergic meds bladder •maybe RBC, WBC, crystals due to underlying

Acute AKI from tubular damage •Underlying cause ￬GFR and ￪BUN/Cr *BUN: CR ratio <20:1 •Remove cause & avoid complications
Tubular 85% of intrinsic AKIs •Arrhythmia •￪K+ and Phosphate, •AVOID volume overload & ￪K+
Necrosis •abdominal pain •￪Na+ in urine (>20)
(ATN) 3 causes: •uremia •Urine osmolality <400 (250-300) volume overload-loops or dialysis
*intrinsic •Ischemia: inadequate GFR and blood •Oliguric or nonoliguric
renal injury •Nephrotoxins: endogenous, Urine sediment: diet: restrict protein, adjust Ph, Ca, Mg
exogenous(MC) •pigmented granular or “muddy brown” casts, renal
•Sepsis: hypoperfusion and direct injury tubular cells, epithelial cast cells

Glomerulo- Types: Classic presentation: •Serum Cr increases over days -> months •High dose corticosteroids
nephritis •Immune complex deposition •HTN *slows immune process
*intrinsic *complexes in glomerular BM •Edema •Hematuria, moderate proteinuria
renal injury causes: infections (strep), lubus, Bergers (scrotal, periorbital) •RBC casts •Cytotoxic agents if cell mediated
disease (IgA nephropathy) •Proteinuria
•RBC, WBC, RBC casts •Complement low in immune complex •Plasma exchange: Goodpasture disease
•Anti-GBM .*Goodpasture (renal & pulm) •ASO titers (post-infectious) and pauci-immune
•Anti-GBM antibodies
•Pauci-Immune *churg-strauss •ANCA levels (Pauci-Immune)

Acute Interstitial inflammatory response with Classic triad: Sediment-WBCs, RBCs, eosinophiluria, WBC casts •Remove cause, supportive care
Interstitial cell-mediated immune rxns •Fever •IV or oral corticosteroids if persists
Nephritis •Rash ￬GFR and ￪BUN/Cr *BUN: CR ratio <20:1
*intrinsic Causes: •arthralgia •Urgent dialysis ~1/3 pts
renal injury •Medication (70%) Renal biopsy: inflam cells w/n renal interstitium
•Infections (staph, strep, CMV…), •Peripheral blood
Immunologic (SLE, Sjogrens…) •eosinophilia Abdominal Pelvic US: enlarged kidneys

Nephrotic Usually due to DM ! Subnephrotic: •Hypoalbuminemia (<3g) & Hypoproteinemia (<6g) Protein loss
Syndrome •little to no s/s •Hyperlipidemia •IF >10g, then intake INCREASE
*low protein low osmotic pressure  high lipids •ACE/ARB
Nephrotic: *low clearance of VLDL -> high TG
•peripheral edema •Elevated ESR Edema: salt restriction, diuretics
•dyspnea •Vit D, zinc, copper deficiency
•pleural effusions Hyperlipidemia: diet, exercise, statins
•ascities UA: Proteinuria 300mg/d or more
spot urine protein: urine Cr ratio Hypercoag *If albumin <2g
•loss of antithrombin, protein C & S
Sediment: oval fat bodies, grape cluster, maltese cross •anticoag for 2-6mo in pt with thrombosis

GU 8%
Chronic Epidemiology: Early: asymptomatic •↓ RBC, H/H SLOW PROGRESSION
Kidney •70%+ cases due to DM or Late CKD: waste build-up, uremia •↓ Ca, Na+, pH (acidosis)
Disease HTN/vascular •↓ GFR •HTN & proteinuria: ACE/ARB
(CKD) •Independent risk of cardio disease Stage I-II: no sx from low GFR •↓ vitamin D •Reduce further kidney damage
•possible edema, HTN •↓ HDL *obstruction, nephrotoxins, flare of
↑↓ Risk Factors: underlying disease
Patient demographics: old, AA Stage III and IV: all organs affected •↑ K+, Phosphate •Control bld glucose AIC <7%
•Anemia, fatigue, anorexia •↑ uric acid
Historical Factors: •Abnormal Ca, Ph, vit D, PTH •↑ BUN/Cr Dialysis Indications:
•previous AKI •Abnormal Na, K, water, acid/base •↑ PTH •GFR 10 or less
•fhx renal disease •↑ triglycerides •Uremic symptoms
•smoking Stage V/ESRD: uremia syndrome •metabolic disturbances
•lead exposure •Marked disturbance in ADL, well-being, Urinalysis: •Fluid overload unresponsive to
nutrition, water, electrolytes •broad, waxy cast (dilated nephron) diuretics
Comorbid Conditions: •proteinuria
•GU-structural, proteinuria, sediment Physical Exam:
•Metabolic-DM, HDL, obese, •MC=hypertension!
•Other-HTN, autoimmune •Uremic frost

Bladder 2nd most common urologic cancer Hematuria, painless Labs: Hematuria +/- pyuria, anemia Superficial (Ta and T1):
Cancer MC in men and older patients (~73yo) Weight loss •transurethral resection of tumor
+/- irritative voiding Cytology: epithleial cells
 MC-epithelial cell malignancy Invasive (T2+): radical cystectomy
(urothlial cell carcinoma) Large: possible abdominal mass Imaging: CT, MRI, or US •+/- chemotherapy, radiation

Risks:Smoker; Industrial solvents Metastatic: Hepatomegaly, LAN Cytoscopy with biopsy-GOLD!

 Local anesthesia, local resection

Renal Cell •Peak incidences in 60s
Carcinoma •2x more common in males
*primary •MC cause=sporadic tumors
*most •most are clear cell carcinoma
common  arise from proximal tubules
renal
cancer Risks: obesity, HTN, chronic
analgesics, environmental toxin
exposure, chronic HCV,
nephrolithiasis, smoking
•Gross or microscopic hematuria Labs: •Surgical excision
•Flank pain •Hematuria -standard: radical nephrectomy
•Abdominal mass •Anemia (MC!) or erythrocytosis - kidney & adrenal, lymph nodes
•Hypercalcemia
Classic triad: •Stauffer syndrome: hepatic •very limited effective chemotherapy
•flank pain dysfunction with elevated LFTs for RCC
•hematuria
•abdominal mass Imaging: Prognosis: 5 years survival rates
•Solid renal mass •renal capsule only 90-100%
Metastatic: cough, bone pain •Standard-CT abd/pelvis •beyond renal capsule 50-60%
•MRI-evaluates spread into IVC •lymph node involvement 0-15%

Renal Atherosclerotic occlusive disease
Artery 5% of pts with HTN have RAS
Stenosis
*MC >45yo w/ atherosclerotic disease
*suspect if unexplained HTN in
woman <45 year old
•HTN (refractory new onset)
•Pulmonary edema with poor HTN
PE:
•HTN
•audible abdominal bruit
Elevated BUN/Cr if ischemia
Imaging:
•US: asymmetric kidney (unilat) or
small hyperchoic kidney (bilat)
•Doppler US *BEST
•Renal angiography *GOLD
don’t use ACE if BILATERAL
•Medical management
•Angioplasty +/- stent
•Surgical bypass
*more risks, no greater efficacy

GU 8% Causes Labs Treatment

Metabolic Anion Gap-MUDPILERS Non-Anion Gap-HARDUPS •Low bicarb Correct underlying
Acidosis •Methanol •Hyperalimentation •low ph
•Uremia •Acetazolamide
•DKA •Renal tubular acidosis
•Propylene glycol •Diarrhea
•Isoniazid, infection •Ureto-pelvic shunt
•Lactic acidosis •Post-hypopcapnis
•Ethylene glycol •Spironolactone
•Rhabdo.renal failure
•Salicylates (ASA)

Metabolic CLEVER-PD •Increased Bicarb

Alkalosis •Contraction •increased pH
•Licorice
•Endo (Cushings)
•Vomiting (loss of H+ from GI tract)
•Excess Alkali
•Refeeding Alkalosis
•Post-hypercapnia
•Diuretics
 Respiratory Hypoventilation-CHAMPP •High CO2
Acidosis •CNS depression (acute/chronic resp failure) •low ph
•Hemo/pneumothorax
•Airway obstruction
•Myopathy
•Pneumonia
•Pulmonary Edema

Respiratory Hyperventilation-CHAMPS •Low CO2

Alkalosis •CNS disease •high pH
•Hypoxia
•Anxiety
•Mechanical Ventilators
•Progesterone
•Salicylates

GU 8% About Clinical Presentation Diagnostics Treatment

Hydronephrosis Water inside kidney  distention/dilation of •May be palpable abdominal or •Increased BUN/Cr •Remove obstruction/drain urine
pelvis and calyces by obstruction of free flow of flank mass •Electrolyte imbalance
urine from kidney •IV urogram, US, CT, MRI •Nephrostomy tube: upper tract
•Catheter: lower tract

CRITICAL CARE 7% Angina Pectoris, Cardiac Arrest, Cardiac arrhythmias/blocks, cardiac failure, Tamponade, Coma, MI, HTN crisis, pericardial effusion, seizures
CRITICAL
Appendicitis Rectocecal: •dull periumbilical or epigastric pain  RLQ •CBC, UA, pregnancy •Consult surgeon
abd and flank pain •N/V, anorexia; SX increase over 24h •Preoperative preparation
•CT scan: STUDY OF CHOICE IVF, ABX  Zosyn
Pelvic: PE: McBurneys point & Appendicitis signs *don’t need contrast
tender abd and rectal pain Rovsing: RLQ, Psoas: SLR, Obturator: twist

Volvulus •Torsion bowel  bowel Infants: bilious vomiting Complications: •Endoscopic decompression
obstruction • intestinal ischemia, gangrene •IV Fluids
•MC in elderly Adults: distention, abdominal pain, N/V
•Sigmoid (MC!) 80% Fever, tachycardia Imaging:
•X-ray: SBO, “double bubble”
•GI series & CT: “birds beak”

Acute Decrease of blood supply •Crampy, abdominal pain DX: CT angiogram •NPO, rest, fluids; SURGERY
Mesenteric to bowel •Bloody diarrhea •Pain control, anti-emetics
Ischemia MCC: emboli, thrombus •HALLMARK: pain out of proportion Labs: CBC, lactate

Ischemia Colitis MCC: hypotension or •LLQ pain •Colonoscopy •Restore perfusion and observe for
atherosclerosis •Bloody diarrhea perforation

Toxic Total/segmental non- •colitis present for at least 1wk prior to onset XRAY (best!): •Complete bowel rest & NG tube
Megacolon obstructive colonic
dilatation (>6cm) +
toxicity
Complication of IBD,
radiation, ischemia
Acute GI bleed •Ligament of Treitz is
defining location
seperating UGI from LGI
bleed
Medications:
•NSAIDS, anticoags,
antiplatelets,
•Iron (melena)
•Beets (hematochezia)
Social:
•Alcohol  gastris, liver
hx similar sx: 60% UGI
from same lesions
CRITICAL
Pneumo- spontaneous:
thorax •primary: no lung disease
-rupture of subpleural apical bleb
-tall, thin males 10-40yo
•secondary: underlying lung dx
traumatic: penetrating or blunt,
iatrogranic ((+) pressure)
tension (EMERGENT)
-air entering pleural sac
-MCC: cardiopulm, (+) pressure
Pulmonary Thrombus of the pulmonary artery
Embolism or its branches
Types: thrombus MC!
Risks (Virchows Triad):
•venous stasis
•Severe bloody diarrhea, abd pain, distention
•Malaise
PE: FAT BAT
•Fever, AMS, Toxic
•BP low, (postural), abdominal pain, tachycardia
Hematesmesis: bleed proximal to ligament
-coffee-ground: mild, frank blood: severe
Hemathochezia: maroon/bright red  LGI
Melena: black, tarry stool (altered hgb from
digestive enzymes )  UGI
•Pain, dixzzy, syncope, confusion, diaphoresis
signs of significant bleeding: hypotension,
tachycardia, low pulse pressure, tachypnea
•sign of shock: cool, pale, low cap refill
•hyperactive BS: UGI bleed
•tenderness: inflame/infectious
•non-tender: vascular
•ascites/hepatosplenomegaly: liver
Rectal exam: if LGI suspected  guaiac test
Sudden chest pain-pleuritic,
unilateral, non-exertional
Dyspnea
Physical Exam:
•diminished breath sounds & TF
•increased resonance to percussion
•mild tachypnea
•pneumothorax under tension
-resp. compromise & CV collapse
-tracheal deviation, displaced PMI
Symptoms:
•Dyspnea (sudden onset)
•Pleuritic chest pain
•Hemoptysis (pulm infarction)
•Cough, wheeze
•DVT symptoms (Homans sign)
-dorsiflexion causing pain
Transverse or R colon is dilated,
6-15cm supine
•type and crossmatch
•CBC
-normocytic: acute
-microcytic: chronic
•CMP: high BUN: CR >30-UGI
•PT/INR: endoscopy can not be
performed until INR <2.5
•EKG & cardiac enzymes
NG Tube (suspected UGI)
•visual inspection of gastric content
 MOST SENSITIVE
CLINICALLY
•PA CXR with expiratory view:
diagnostic *stable pt
•Chest CT, bedside US *large
EKG: sinus tachycardia, S1Q3T3
CXR: Hamptoms Hump or westmark
VQ Scan: poor perfusion, good vent
Spiral CT: BEST
•DC all antimotility agents (opiates,
anticholinergics)
•prophylaxis PPI & DVT
•IV steroids & surgical consult
•Flagyl + Amp/Gent or Ceftriaxone
Upper GI Bleed
ALL GET ENDOSCOPY
Stable: consult GI/surgery
Unstable: IVF, PRBC: FFP (4:1)
Lower GI
•consult GI/general surgery
•consider endoscopy to r/o UGI
•discuss colonoscopy v angiography
Others:
PPI: acid suppression
•Pantoprazole 80mg IV bolus
•indicated for bleeding from PUD
Somatostatin analong
•Ocreotide 50mcg bolus
•use for variceal bleeding
Tension Pneumothorax:
Needle decompression
•large-bore needle (14-16 guage) at 2nd ICS at
midclavicular line-leave in until thoracostomy
tube places
•Oxygen 2-4L nasal cannula
Small Primary (<15-20%): observe x6hr
Large: chest tube (thoacostomy) & admit
1. Oxygen, IV Fluids if needed
2. Anticoagulation
•Anti-thrombin III: Heparin (renal), LMWH
•Factor Xa inhibitor: Xarelto, Eliquis
*good for outpatient, no heparin
•Direct thrombin inhibitor: Pradaxa
 •injury (to vessel wall)
•hypercoagulability: medications
Acute MC form non-cardiogenic
Respirator pulmonary edema
y Distress
•acute hypoxemic respiratory
failure following systemic or pulm
insult WITHOUT evidence of HF
•inflammatory alveolar damage 
increased permeability of
alveolar-capillary barrier 
pulmonary edema  low O2
Causes: MCC-sepsis
-critically ill, trauma, aspiration
CRITICAL
Acute “Addisonian Crisis”
Adrenal •Sudden worsening of adrenal
Insufficiency insufficiency due to “stressful” event
Triggers: surgery, trauma, volume loss,
hypothermia, MI, fever, sepsis,
hypoglycemia, steroid withdrawal
Thyroid •Potentially fatal complication of
Storm untreated thyrotoxicosis
Triggers: surgery, trauma, infection,
illness, pregnancy
Status •Episode of abnormal neurologic
Epilepticus function caused by inappropriate
electrical discharge
•Seizure activity 5+ minutes or two +
PE:
-tachypnea, tachycardia
-hypoxemia; rales
-hypotension and syncope
-JVD & S3 and S4 sounds
(+) homans: calf pain w/ dorsiflex
•rapid onset of profound DYSPNEA
within 12-48h after event
•SOB, tachypnea, intercostal
retractions, crackles
•hypoxemia (no response to O2)
•multiple organ failure: kidney,
liver, CV, CNS
HALLMARK: diffuse alveolar
damage
•Hypovolemic Shock (MC!)
•Hypotension
•Hypovolemia
•Abdominal pain, N/V
•Fever
•Weakness, lethargy, confusion
HYPERMETABOLIC
•N/V/D
•Tremors, psychosis (AMS)
•Lid lag
•High fever
•Palpitations, tachycardia
•Liver failure
•Abrupt onset
•Memory loss of activity
•Purposeless movement during
attack
•Postictal confusion/lethargy
Pulmonary angiography: GOLD
Wells Score >6: high, 2-6: mod
+3: DVT, alt dx not likely
+1.5: HR >100, VTE hx,
immobilization for 4 weeks
+1: malignancy, hemoptysis
•CXR: bilateral pulmonary infiltrates
-AIR BRONCHOGRAMS
-spares costophrenic angles
•ABG: PaO2/FIO2 <200 and is NOT
responsive to 100% O2 (refractory
hypoxemia)
•Swanz-Ganz cath: pressure <18
*differentiates from pulm edema
•BMP
-hyponatermia
-hyperkalemia
-hypoglycemia
•Insulin resistance
•Increased free T3 & T4
•Decreased TSH
ALL: Glucose, hcg
HX seizure disorder: + serum drug
levels
*requires Heparin for 5-10d
•Vitamin K inhibitor: Warfarin
TPA: *hemodynamic compromise
•begin UFH or LMWH after infusion
Thromboembolectomy:
•pts with life-threatening PE and CI to TPA
Non-invasive or mechanical ventilation
PEEP ((+) end-expiratory pressure)
-prevents alveolar collapse
-give at lowest effective levels
-does not improve mortality
-risks: barotrauma, pneumothorax, auto-peep
Treat underlying disease
•IVF: normal saline (D5NS if
hypoglycemia)
•IV HIGH dose Hydrocortisone
•Reversal of electrolytes
•Fludricortisone
1. Propranolol
2. PTU
3. Iodine
4. Glucocorticoids
Definitive: radioactive iodine surgery
•insert nasopharyngeal airway
•DOC is Lorazepam x2
- alternates: Diazepam, Midazolam
•monitor airway and oxygenation
 seizures without regaining NO HX: +CMP, magnesium •second line: Fospheytoin or Phenytoin
consciousness -phenytoin incompatible with benzos,
fluids glucose/dextrose
CT scan of the head w/o contrast
Refractory: peristant seizures despite IV -SE: cardiac arrhythmias, resp dep,
•indications: first-ever seizure, change
of two anti-epileptics hypotension w/phenytoin
in pattern of normal seizure activity,
concern for acute intracranial process
Refractory Status Epilepticus
•persistent seizure after first and second
Lumbar Puncture
line treatments  coma and intubation
•Indications: febrile,
•Midazolam or Propofol or Pentobarbital
immunocompromised, suspicion for
subarachnoid hemorrhage
Eclampsia: IV Magnesium sulfate 4-6g
•CI: avoid during active seizing Alcohol use: benzos, educate on alcohol

Acute Angle •Obstruction of aqueous humor outflow
Closure due to the lens or peripheral iris
Glaucoma blocking the trabecular network
History: dark room (movie), reading,
dilating, anticholinergics, coke
•Sudden eye pain & HA
•colored halos around light
•peripheral “tunnel” vision loss
•N/V
•Fixed mid-position pupil,
hazy cornea, injection
•Increased IOP 60-80 (normal 10-20):
•firm to palpation
fundoscope: cupping of optic nerve
•Supine position
1. Acetazolamide (lower pressure &
aqueous humor production)
2. Timilol (reduce pressure without
affectiving visual acuity)

3. Pilocarpine or Carbachol (cholinergic

 pupil constriction)

CRITICAL
Hypovolemic •Loss of blood or fluid volume •pale, cool extremities •CBC: increased hgb and hct ABCDEs
Shock •slow cap refill *decreased in late shock
*circulatory Causes: hemorrhagic, GI, •low skin turgor •Volume resuscitation: NS or LR
shock pancreatitis, DKI, burn •Increased HR •Vasoconstriction •Blood: PRBCs
•Decreased BP and CO •Low wedge pressure

Cardiogenic •Insufficient CO to meet •cool, mottled skin •Decreased BP and CO •ABCDEs

Shock metabolic needs •oliguria •Increased wedge pressure •Isotonic fluids (AVOID a LARGE amount!)
*circulatory •AMS •Revascularization if ischemic: PCI is the
shock Causes: Acute MI (MC!), •LVH, pulmonary edema
cardiotoxic drug effects, •frothy sputum •Ionotropic support: decreased contractility & CO
infection, mechanical, valve Norepinephrine, dobutamine, dopamine if persistent

Obstructive •Physical obstruction of blood •S/S of underlying disease •CXR ABCDEs

Shock flow of heart or great vessels •EKG •PE: heparin, TPA
*circulatory •Increased wedge pressure
shock Causes: •Tamponade: pericardiocentesis
•PE •CBC, CMP, lactate, coagulation
•Pericardial tamponade studies, cultures, ABG •Pneumothorax: needle decompression
•Tension pneumothorax
•Aortic dissection •Aortic dissection: surgery
Septic Shock •Bacteria  systemic
*distributive inflammatory response 
shock peripheral vasodilation 
increased capillary perm.
•Hypotension
•WIDE pulse pressure
•INCREASED CO***
•WARM extremities
SIRS Criteria: 2/4 •ABX (Vanc or Ceftriaxone + Zosyn)
•Temp >100.4 (38) •IVF
•Pulse: >90bpm •Vasopressors if no response to fluids
•RR: >20 or PaCO2 <32
•WBC: >12,000 or <4,000

Neurogenic •Acute spinal cord injury  •Bradycardia •Clinical •fluid and vasopressors
Shock blocks sympathetic system  •Hypotension (alpha-activity to increase sympathetic tone)
*distributive increased vagal tone •Warm, dry skin
•WIDE pulse presure

Anaphylacti •IgE mediated severe systemic •Pruritis, hives •ABCDEs

c Shock hypersensitivity reaction •Angioedema •Epinephrine 0.3mg IM repeat q5-10min prn
*distributive •Respiratory distress •Epinephrine 1mg IV if cardiovascular collapse

HEMATOLOGY 5%

HEME/ONC
Iron •MCC blood loss •Fatigue, hair thinning •High TIBC, RDW Ferrous Sulfate
Deficiency •pallor, pica, cheilitis •Low iron, ferritin, transferrin *take with Vitamin C
Microcytic •koilycia, plummer vinson syndrome •Low MCV, low MCH, nml MCHC

Alpha •Decreased alpha-globin •¼-silent •Smear: target cells •Moderate: folate, avoid oxidative
Thalassemia •MC in Asians •2/4- minor (trait) stress, avoid iron supplementation
•¾- HbH •Electrophoresis:
Microcytic •4/4- hydrops fetalis all equal b/c all contain A •Severe: transfusions, splenectomy
iron chelation (IV Deferoxamine),

Beta •Decreased beta-globin •½: Minor (trait)-asymptomatic electrophoresis: Major: blood transfusions
Thalassemia •MC in Mediterranean •2/2: major (cooleys) •increased HbA2 and HbF,
-symptomatic around 6 months definitive=bone marrow transplant
Microcytic HbF=2a2y -Frontal bossing & maxillary growth smear: target cells, nucleated cells
HbA=2a2b, HbA2=2a2d X-ray: crew-cut skull appearance

Folate •MCC=diet  leafy greens •Glossitis, cheilosis •high MCV and homocysteine Folate supplement
Deficiency •NO NEUROPATHY •normal MMA
Macrocytic
 Smear: hypersegmented
neutrophils, macro-ovalocytes

B12 •MCC=pernicious anemia  damaged glossitis, NEUROPATHY high MCV, homocysteine & MMA B12 Injections
Deficiency parietal cells  lack of intrinsic factor *B12 needed to convert MMA to
Macrocytic SCoA Smear: hypersegmented, macro-
ovalocytes, basophilic stippling

Anemia of increased hepcidin and decreased EPO Increased ferritin EPO

Chronic  not able to produce heme Rest of labs are low
Disease
Normocytic •MCC: Chronic Kidney Disease (CKD)

Sick Cell •Autosomal resessive Jaundice, HSM, cardiomegaly •Electrophresis: HbS •PCN at 2 months, folic acid at 1 yr
Anemia •Abnormal substitution of B chain Ill appearing, poor healing, •Smear: Howell-Jolly •Hydroxyurea
Normocytic retinopathy •Labs: increased reticulocytes
•Unstable HbS  abnormal shape  vaso- Acute: HOP: hydration, oxygen, pain
occlusive episodes  destroyed by spleen Triggers: SHITAE Definitive: stem cell

G6PD •X-linked recessive; MC in AA males •Jaundice, dark urine Smear: Prevent: avoid oxidative drugs,
Normocytic •Malaise, weakness, pain •Bite & Blister cells; Heinz Bodies triggers
•Deficit in G6PD enzyme
Labs: •Folic acid supplementation
•RBC is vulnerable to oxidative state  Triggers: •Low hgb & hct
hgb denatures  forms Heinz bodies  infection, food (fava beans), ABX •High reticulocytes & High MCH
damages membrane  destroyed by spleen •G6PD assay

HEME
ITP • antibodies against platelets •Bleeding, petechiae, bruising ISOLATED thrombocytopenia •Steroids
•MC after URTI •IVIG, splenectomy

TTP •deficiency in ADAMTS13 • “FATRN”  fever/FFP, anemia, •increased vWF, low ADAMTS13 FFP
“Adults, fever, neuro, vWF” thrombocytopenia, renal(hematuria), •smear: shistocytes
neurp

DIC Pathologic activation of coagulation system •Widespread hemorrhage & •Increased PTT/PT/INR •Treat underlying cause
 widespread microthrombi  consumes thrombosis •Decreased fibrinogen •FFP if severe bleeding
clotting factors  thrombocytopenia and •MC at venipuncture sites •Increased D-dimer
diffuse bleeding

vWF •Autosomal Dominant •recurrent nose bleeds, heavy •Decreased vWF, decreased VIII DDAVP
Disease periods •prolonged PTT and bleeding time
•family history
Hemophilia X-linked recessive •hemarthrosis (joints, MC ankle) •prolong PTT & bleeding time •Hemophilia A: Factor VIII or
MC in children •hemorrhage due to trauma •normal platelets DDAVP
A: factor VII B: Factor IX C: factor XI •possible purpura/petechiae •Hemophilia B: Factor IX
•Hemophilia C: Factor XI
HEME
Factor V Leiden Factor V: activated by thrombin and helps •DVT Activated protein C Anticoagulant
convert prothrombin to thrombin •PE resistance assay
•Clotting  confirm with DNA test
MCC inherited thrombophilia

Mutation of Factor V  does not respond to

protein C  does not turn off and keeps clotting

Protein C/S Autosomal dominant •DVT Heparin  oral

Deficiency Vitamin K dependent •PE anticoagulation

Protein C: risk warfarin induced necrosis

Anti-thrombin Autosomal dominant •Venous thrombosis, DVT, PE Asymptomatic: anticoag

III deficiency •MC in deep veins and mesenteric veins before surgery
Normal: inactivated thrombin, IX-XII
Thrombosis: high-dose IV
heparin  oral
Antiphospholipi •Acquired hypercoaguable condition •Thrombotic events Antibodies
d Syndrome •Cardiac: Libman-Sacks, endocarditis
•Autoantibody antiphospholipid antibody (aPL) •pulmonary HTN
in plasms •necrosis of hip
•Livdeo reticularis
HX: pregnancy complications •adrenal insufficiency

ONC
Multiple •Proceeded by a premalignant
Myeloma plasma cells proliferative disorder-
MGUS
*monoclonal=ONE CELL
•proliferation of plasma cells in the
BM  decreased hematopoiesis
•increased neoplastic cells  bone
tumor and hypercalcemia
•secrete M-proteins  harm
kidneys, nerve, organs
MC in the axial skeleton
•bone pain-back, hips, ribs
•spinal cord compression-median*
•pathologic fracture
•hypercalcemia
confusion, somnolence, bone pain,
constipation, nausea, and thirst
•anemia, neutropenia, thrombocytopenia
•impaired renal, oliguria, proteinuria
•radiculopathy
•plasmocytomas
CBC: anemia, thrombocytopenia *INCURABLE
Smear: RBC rouleaux formation *refer to heme/onc
BM Biopsy/Aspiration: infiltration by Chemo, stem cell, radiation
abnormal monoclonal plasma
Complications:
Electrophoresis: (+) paraprotein (M) •fractures
24hr urine: Bence Jones protein •vertebral body collapse
Quantitative Immunoglobulin: suppression •spinal cord: steroids
of IgG, IgA, IgM •hypercalcemia: Reclast
•Renal impairement 
Beta-2 microglubin: elevated plasmapheresis to remove
M-proteins
X-ray: COMPLETE skeletal survey

Hodgkins •Germinal B cells undergo •PAINLESS cervical/supraclavicular LAD •Staging: Ann Arbor Chemo
transformation •Mediastinal mass, fatigue, wt loss •CBC normal, elevated ESR
•MC in males •B SX: wt loss >10%, T >38C, sweats •Biopsy: Reed Sternberg cells

Non- Accumulate in lymph tissue (spleen, •Cough, dyspnea, edema Burkitt: BBBB Chemo
Hodgkins nodes, thymus) •Mediastinal mass, RLQ mass • boy, B-cells, belly, chromosome B

ALL MC malignancy in children
Leukemic BLASTS replace marrow
AML Risks:
•radiation, chemo
•downs, NF1, twins
CLL MC LEUKEMIA IN US!
MC elderly
Complications:
•obstructive lymphadenopathy
•transformation into aggressive large
cell lymphoma (Richter syndrome)
CML Single specific genetic mutation
(translocation) of gene 9:22
 PHILADELPHIA on PCR
First (Chronic): MC  mature cells
Second (Accelerated): cytogenic
Third (Terminal Blast): immature
ID 5% About
Botuslism Clostridium botulinum
(Gram +) •Endotoxin ingested or inhaled 
inhibition of Ach  weak
Transmission: canned goods (adult),
wound, honey (infants)
Tetanus Clostridium tetani
(Gram +)
Transmission: spores from soil
Neurotoxin (tetanospasmin) block
neuron inhibition (ach)  severe
muscle spasm
Diptheria Corynobacterium diphtheria
(Gram +)
Transmission: inhale drops
Lymphoblastic: TT “teen, T-cells” Large Cells: B and T cell
•Fever, weakness, fatigue •CBC with diff: ANC <1000 Chemo
•Bone pain, pallor, anemia •Smear: lymphoblasts (~25%)
•Petechia, purpura, infection •Marrow FNA & biopsy confirms
•Fatigue, infection, nodules, HSM •CBC: all WBC low Chemo
•Smear: auer rod
•CONFIRM with marrow biopsy
Slow onset! Usually found incidentally CBC: WBC > 20,000 Immediately begin multi-
•lymphadenopathy (MC!) Isolated lymphocytes (>5,000) drug chemo if high-risk
•recurrent infections (PNA, HSV, HZV) +/- decreased RBC, platelets
•hepatosplenomegaly FLOW CYTOMETRY: *confirms
 upper abdominal discomfort/fullness Confirms abnormal B-lymphocytes
•anemia/thrombocytopenia
BM Aspiration/Biopsy: small lymphocytes
•Fatigue! *often first symptom CBC: WBC 100-150,00 w/ L shift Chronic:
•Low-grade fever, night sweats, wt loss Alk Phos: low Tyrosine kinase inhibitor
•abdominal fullness, bone tenderness
•pruritis, flushing, GI ulcers with elevated PS: Accelerated: blast cells, promyelocytes Accelerate or Blast:
basophils due to histamine TKI + multidrug chemo
BM Aspiration/Biopsy: hypercellular with *possible stem cell
PE: HSM, LAD increased granulocytes and progenitors
Clinical Presentation Diagnostics Treatment
8 Ds: •toxin assay Antitoxin (EVERYONE)
•Diplopia •drooping eyelids •dilated/fixed pupil
•dry mouth •dysphagia, dysarthria (speech), + PCN or Metronidazole if wound
dysphonia transmission
•”floppy” baby syndrome
•Early: local muscle spasms, neck/jaw stiffness, Clinical DX Antitoxin + Metronidazole or
trismus *DO NOT CULTURE Penicillin
•Later: drooling, risus sardonicus (facial contraction)
•increased DTR
•Tonsillopharyngitis with white/grey patch that •cllinical diagnosis •Antitoxin + Erythromycin or PCN
bleed when scrapped •PCR
•Bull neck due to enlarged cervical LAD •Culture Prevention: DtaP, Erythro
•myocarditis  arrhythmias, HF
Chlamydi Chlamydia trachomatis Women: urethritis, cervicitis, PID; inflamed, friable, Nucleic acid test Azithromycin
a (Gram -) red cervix, conjunctivitis, cervical motion tenderness
MC STD in US Complication:
Men: urethritis, epididymitis, prostatitis PROM
-water, mucoid discharge, conjunctivitis Fitz-Hugh Curtis

Gonorrhe Neisseria gonorrhoreae Yellow-green purulent discharge, urethritis, Nucleic acid:Intracellular Rocephin + Doxycyline
a (Gram -) prostatitis, conjunctivitis (infants), septic arthritis gram (-) diplococci Azithromycin

Pertussis Bordatella Pertussis
(Gram -)
Pathogenesis: A & B toxin
A enters cells & inactivates cAMP
 increase mucous
B cell surface (adenylate cyclase)
coughing spells, hemorrhage and petechiae; clinical, high suspicion Azithromycin, Bactrim
Stages: children >2wk Vaccine: DTaP
1. Catarrhal-MOST contagious, resp symptoms,
2. Paroxysmal (rapid cough  whoop) GOLD-Culture
3. Convalescent: chronic cough x2-3 weeks definitive: cough >3wk

Transmission: droplets

Cholera Vibrio cholera •Severe and voluminous disarrhea Culture •Doxycycline

(Gram -) Transmission: food/water •Liquid grey “rice water” stool w/o odor •Azithromycin, Bactrim, Cipro

Salmonell Typhoid fever: S. typhi  food Typhoid fever: Culture Typhoid:

a (Gram -) •flu like  rose spots  blood pear soup Cipro, Azithro, Bactrim, Doxycyline
Enterocolitis: Salmonella
thypimurium/enteritidis  reptiles Enterocolitis: inflammatory diarrhea (blood, mucous) Enterocolitis: supportive

Shigellosis Shigella •Inflammatory diarrhea Culture Rehydration

(Gram -)
ID 5% About Clinical Presentation Diagnostics Treatment
Herpes •HSV-1: Mouth •Burning, tingling, low fever •Dendritic lesions on slit lamp Acyclovir
Simplex Virus •HSV-2: Genitals •Herpetic whitlow: lesions on fingers with HSV-1 •PCR: most sensitive, BEST
(HSV) (Viral) •Tzanck: multinucleated giant cells

Varicella Transmission: resp droplets, •“dew drop on a rose petal”  clear vesicles on an Clinical diagnosis Acyclovir
Zoster (VZV) direct contact erythematous base, different phases
(Viral) •along dermatome Complication: PHN
-Gabapentin, TCAs

Epstein-Barr Transmission: “kissing •posterior cervical lymphadenopathy heterophile monospot test supportive  NO CONTACT
Virus (EBV) disease”, saliva, blood •fever, fatigue, malaise, splenomegaly SPORTS
(Viral) •maculopapular rash (worse with Ampicillin!) Smear: atypical lymphocytes

Cytomegalo- •MC in immunocompromised •ok immune: mono-like, •Serology Gangcyclovir

virus (CMV) •CD4 <100 •congenital: retinitis, sensorineural hearing
(Viral) •Reactivation: retinitis, ulcers on upper endoscopy •Fundoscope: eggs/ ketchup
appearance (hemorrhage w/ exudate)

•Biopsy: Owl’s eye apperance


Influenza Transmission: respiratory
(Viral) droplets, touching
contaminated surfaces
3 types: A (most pathogenic),
B&C
Rabies (Viral) Transmission: bats,
woodchucks, skunk, raccoon,
fox, coyote
•animal saliva  nervous
system  encephalitis
HIV (Viral) Retrovirus: changes RNA into
DNA via reverse transcriptase
Transmission: sex, IVDU,
mother, blood contact
ID 5% About
Cryptococcosi Cryptococcis neoformis
s (Fungal)
Source: inhalation of spores
from PIGEON POOP
Histoplasmosis Histoplasmosis capsulatum
(Fungal)
Source: Bird/bat poop, river
areas (Ohio/Mississippi)
•Ingested by macrophages
•CD4 <150
Pneumocystiti Pneumocystic jirovecii
s (Fungal)
(epithelial cells with enlarged nuclei)
Sudden fever, chills, malaise, sore throat, HA, non- •rapid flu Tamiflu (neuramidase
productive cough •RT-PCR (1-3d) inhibitors A & B) w/n 48hr
•NP viral culture (3-7d)
Hemaglutinin: bind to epithelium (cellular infection) Prevention: influenza vaccine,
<9yo need two in one seasons
Neuraminidase: cleaves bond holdings new virions
(spread of infection)
S/S: initial=fever, chills, tingling & itching at site •negri bodies in the animal, ONE dose of immunogolublin
clinically FOUR vaccines (day 1,3,7,14)
 neurologic=behavior change, agitation, anxiety,
hallucination, hypersalivation, fear of water
(hydrophobia)
Acute seroconversion: flu-like illness •ELISA  western blot 2 NRTIs: nucleotide reverse
transcriptase inhibitor
AIDS: CD4 <200, diarrhea, wt loss, dementia •HIV RNA viral load -Zidovudine (Retrovir)
-Tenofivir
Prophylaxis
<200: Bactrim
<150: Itraconazole
<100: Fluconazole
<50: Azithromycin;
Valgangcilovir
Clinical Presentation Diagnostics Treatment
S/S: •fungus in CSF  low glucose, high Amphotericin B + Flucytosine 
•Pulmonary: cough, pleuritic CP, dyspnea WBC + protein Fluconazole
•meningitis (MCC of fungal): HA, meningeal
India ink stain: encapsulate yeast CD4 prophylaxis: Fluconazole
CD4 < 100
acute pulmonary: •high LDH, ALP, ferritin mild/moderate=Itraconazole
fever, non-productive cough, myalgia
CXR: severe=Amp B
disseminated: •acute/disseminated=mediastinal
flu-like, wt loss, HSM, bloody diarrhea LAN & infiltrates
“Wear hats at the river so you don’t get pooped •chronic=apical cavities & infiltrate
on before the mediastinal Ice cave”
•fever CXR: bilateral infiltrates “batwing” Bactrim
•dyspnea on exertion
 •CD4 <200 •non –productive cough •Sputum & blood cx
•O2 desaturation with ambulation • (+) Wright-Giemsa
•definitive=bronchoscope lavage

Oral Candida albicans Beefy, red edematous mucosa with white •KOH  budding yeast and Nystatin, Fluconazole
Candidiasis papules that CAN be scraped off pseudohyphae

Esophageal Candida albicans Odonyphagia +/- oral thrush •Endoscope  white plaques Fluconazole
Candidiasis

Vulvovaginal Candida albicans White “cottage cheese” discharge, burning, •KOH  fish smell Monistat
Candidiasis itching

Intertrigo Candida albicans Itch, erythema, “satellite” papules and pustules •KOH Nystatin, Fluconazole

Tuberculosis Mycobacterium tuberculosis
(Atypical)
Transmission: person to person
by airborne droplets
Primary TB: active initial
infection  contagious)
Chronic (latent): caseating
granuloma formation  not
contagious
Secondary (reactivate): apex of
upper lobes  contagious
ID 5%
Lyme Disease Deer tick  Ixodes tick
(Spirochete) summer & spring
Borrelia burgdorferi
Pulmonary: productive cough, CP, hemoptysis
Constitutional: night sweats, fever, chills,
fatigue, anorexia, weight loss
Extra-pulmonary: vertebral (Potts), lymph
nodes (scrofula)
(+) 5mm+  HIV/immunosuppressed, (+)
CXR, close contact
(+) 10mm+  high risk populations: IVDU,
homeless, age <5yo, immigrant, travel
(+) 15mm+  no risk factors
early localized: erythema migrans
early disseminated: arthritis, CN VII palsy, cardio
late: neurologic worsening, synovitis, arthritis
•sputum cultures & acid-fast stain
•Mantoux TB skin test
CXR: apical cavities
-reactivation: apical, upper lobes
-primary: middle/lower lobe
•ELISA test  if (+) then
confirm with Western Blot
RIPE x6-12 months
Rifampin: orange fluids, low plt
Izoniazid: hepatitis, neuropathy
Pyrazinamide: hepatitis, hyperuric
Ethambutol: optic neuritis (E=eye)
Latent: Isosinizid + Pyridoxine
*not contagious in latent period
*no sx, (+) PPD, (-) CXR
Doxycycline; Amoxi (<8, prego)
Prophylaxis: <72hr of rick
removal if the tick present >36h

Rocky Wood/dog tick  Blanching, erythematous macular rash on wrists/ankles •Clinical diagnosis Doxycycline
Mountain Dermancentor tick  palms/soles  centrally Chloremphalone (pregnant)
Spotted Fever •serology  indirect
(Spirochete) Ricketssia ricketsii immunofluorescent antibody
Gram (-) obligate intracellular

Syphillis Trepenoma pallidum Primary painless chancre on genital, painless lymph •RPR/VDRL Pen G Benzathine
(Spirochete) •dark field microscopy
Secondary: mucous patch, condyloma, scaly papule

Latent: first year=contagious, > one year=not contagious

Tertiary: anytime after untreated secondary  gummas

 Neurosyphillis: asymptomatic invasion  meningeal 
tabes dorsalis (wide gait)  paresthesia (cerebral cortex)

Tapeworms Taenia sainata (beef) Instetinal: vague abdominal sx Proglottids in stool BIltricide once
(Parasite- Taenia solium (pork) Brain: epilepsy Albendazole
Helmith)
Roundworms Ascariasis •Eosinophilic PNA Eggs in stool Albendazole
(Helmith) *MC helmith infection •Vague abdominal sx Mebendazole

Hookworms Ancylostoma duodenale; •Pruritis maculopapular rash •Eggs in stool Albendazole

(Parasite- Necator americans •Pulmonary and GI sx •Low hgb, hct, albumin Mebendazole
Helmith) “vampire worm”  sucks blood  low hgb, hct, protein”

Trichinosis Trichinella spiralis  larvae •GI: abdominal pain, N/V/D •ELISA Albendazole
(Parasite- to intestine  striated muscle •Muscle: myositis, muscle pain, periorbital edema •High CK/LDH Mebendazole
Helmith) •HALLMARK: eosinophilia
Transmission: Uncooked pork

Malaria Plasmodium falciparum •paroxysm=HIGH fever, chills, sweats  okay  •Giemsa stain on blood •Chloroquine
(Parasite) cyclical smear •Atovaquone + Doxy or Clinda
Vector: Anopheles mosquito •Effects RBCs •Low WBC, plts, anemia

Toxoplasmosis Toxoplasmosis gondii •primary (good immune): asymptomatic or mono-like PCR, IgG/IgM pregnancy=Spiramycin
(Parasite) •primary (bad): necrotizing lesion, encephalopathy
•Fecal oral, cat feces •congenital: retardation, hearing loss, chorioretinitis immunocompromised:
Pyrimethamine & Sulfa
“The toxic cat spiraled out of control with the sulfa pyramid
due to necrotizing brain lesion. This caused her retina to swell
& the marines/guards were called in.”