PCM III Final Exam Material Flashcards
What do these terms mean:
- Anuria
- Oliguria
- Polyuria
- Azotemia
- Uremia
- urine output < 50-100 mL/day
- urine output < 400-500 mL/day
- urine output > 3000 mL/day
- elevated blood urea nitrogen (BUN) W/O symptoms
- elevated BUN WITH symptoms, though they are NON-SPECIFIC (N/V, confusion, pruritis, fatigue)
What is AKI and what does it staging depend on?
AKI = inc. serum creatinine or dec. urine output
- staged based on whichever of the two above issues is worse
What are the two most common causes of Acute Kidney Injury?
What does Pre-renal Azotemia lead to and why?
- Acute Tubular Necrosis
- Pre-renal Azotemia
- Prerenal Azotemia leads to activation of RAAS and ADH release, causing dec. urine output as a mechanism to help try and restore extracellular volume
What are the two most common forms of Acute Tubular Injury?
- Ischemia (50% of cases) –> MOST COMMON
- Toxins (35% of cases)
- Abx (vancomycin/aminoglycosides), IV iodine contrast, heme pigments, light chains
What is the difference in FeNa levels in Prerenal Azotemia vs Acute Tubular Necrosis?
Prerenal = FeNa < 1% (inc. tubular Na/water reabsorption)
ATN = FeNa > 2%
What are the two major blood supplies of Renal Tubules and why are they important?
Efferent arterioles –> Peritubular Capillaries and Vasa Recta
- kidneys receive 20% of cardiac output with most blood being directed to the renal CORTEX
- renal MEDULLA is primarily a watershed area that receives blood from the VASA RECTA –> relatively starved of oxygen and is MORE susceptible to ischemia
What are the two most common sites of Acute Tubular Necrosis and why?
What are the two reasons that GFR decreases in Acute Tubular Necrosis?
- Proximal Tubule segment
- medullary Thick Ascending Limb of the loop of Henle
- these two areas have HIGH METABOLIC ACTIVITY because of sodium reabsorption by basolateral membrane Na/K-ATPase
- GFR dec. due to tubular obstruction from cast formation and back-leak of urine filtrate due to loss of tight junctions
What is Interstitial Nephritis and what is its major cause (3 examples)?
What is the difference between Acute and Chronic Interstitial Nephritis?
IN = inflammatory cells within the renal interstitium and +/- granulomas
- most common due to DRUGS
- ex: NSAIDs, Abx, PPIs
AIN: fever, rash, arthralgia, pyuria/WBC casts
CIN: bland urinary sediment, slow decline in renal function, more fibrosis on renal biopsy
What are clinical presentations of Acute Kidney Injury?
- edema, hypertension, dec. urine output, foamy urine (PROTEINURIA), uremia
- pericardial friction rub, asterixis, uremic frost
What three labs should be obtained for ALL Acute Kidney Injury pts?
What are two ultrasound findings that are more indicative of Chronic Kidney Disease?
- urinalysis with urine microscopy
- urine albumin/Cr or protein/Cr ratios on RANDOM sample
- Renal ultrasound
CKD U/S: small kidneys and cortical thinning
What patients are FeNa and FeUrea only valid in?
OLIGURIC PATIENTS (<400-500 mL/day) - if pt is NON-oliguric, they cannot be prerenal
- RAAS and ADH would both be increased if a patient was volume depleted
in most cases FeNa and FeUrea are not needed to differentiate etiology of AKI because history and physical exam are sufficient
What etiology do these urinary patterns allude to:
- renal tubular and transitional epi cells, granular casts
- WBC, WBC casts, urine eosinophils
- dysmorphic RBCs, RBC casts
- proteinuria (<3.5g/day), hematuria, dysmorphic RBCs
- heavy proteinuria (>3.5g/day), lipiduria, minimal hematuria
- hyaline casts
- WBCs, RBCs, bacteria
- acute tubular necrosis (ATN)
- acute interstitial nephritis (AIN) or pyelonephritis
- vasculitis or glomerulonephritis
- nephrITIC syndrome
- nephrOTIC syndrome
- non-specific, prerenal azotemia
- urinary tract infections (UTI)
What are the AEIOU indications for dialysis?
A - severe ACIDOSIS
E - ELECTROLYTE disturbances (hyperkalemia)
I - INGESTION (ethylene glycol, methanol)
O - volume OVERLOAD
U - UREMIA
What causes these heart sounds:
- S1
- S2
- S3
- S4
S1 = closure of AB valves (mitral and tricuspid)
- specifically MITRAL valve closure
S2 = aortic valve closure due to left ventricle emptying and drop of LV pressure
S3 = conditions where there is LV overload or failure
- pt w/abnormal myocardial stiffness and high filling pressure (occurs just after S2)
S4 = audible forceful left atrial contraction into a non-compliant left ventricle
- auscultate in left lateral decubitus position at apex
- inc. LV end-diastolic pressure
Who is Mitral Valve Prolapse most commonly seen in and what can be heard?
- diagnosed w/maneuvers that rapidly dec. venous return and is MOST COMMON in thin, tall young women
- hear MID-SYSTOLIC “click”; late-systolic murmur
- associated with Marfan/Ehler-Danlos
Where is Aortic Stenosis best heard and what is the triad of critical aortic stenosis? (S/A/D)
What is AS associated with in the 6th decade of life vs the 7th decade of life?
- heard at base of heart with crescendo-decrescendo murmur best heard at RUSB and radiates into bilateral carotid areas
Triad: chest pain (angina), syncope, dyspnea
6th decade: due to congenital bicuspid valves
7th decade: due to atherosclerotic calcific AS
Where is Tricuspid Regurgitation best heard and what is it most commonly associated with?
- holosystolic murmur best heard at the LLSB that inc. with deep inspiration due to right heart association
- seen with PULMONARY HYPERTENSION
- treat left heart failure (MCC of right heart failure) by relieving CHF and using diuresis
What two complications is Acute Aortic Regurgitation associated with and what kind of murmur is it?
- associated with endocarditis and aortic dissection (typically presents as medical emergency –> cardiogenic shock)
- AR is a DIASTOLIC murmur
Where is Chronic Aortic Regurgitation best heard and what is Water-Hammer pulse (Corrigan pulse)?
- high-pitched, decrescendo aortic diastolic murmur along the LSB with NO change during respiration
- exertional dyspnea and fatigue
WHP: rapid rise and fall with an elevated systolic and low diastolic pressure that is best assessed using the brachial or radial pulses (wide pulse pressure with peripheral signs)
What is Atrial Septal Defect and what is a major complication that can develop do to it, especially after age 40?
- loud systolic ejection murmur heard in the 2-3rd intercostal spaces parasternally due to inc. flow through pulmonary valve
- FIXED SPLIT S2
- pts. asymptomatic unless complication occurs and often do NOT manifest a specific murmur
Complication: cardiac arrhythmias (ATRIAL FIBRILLATION) and heart failure
What is Ventricular Septal Defect and what is the difference between small and large shunts?
Small: loud, harsh holosystolic murmur in 3-4th intercostal spaces along sternum (occasionally with mid-diastolic flow murmur)
- the smaller the defect, the LOUDER the murmur
- SYSTOLIC THRILL IS COMMON
Large: right ventricular volume and pressure overload my cause pulmonary hypertension and cyanosis
What is Patent Ductus Arteriosus and what does it sound like?
- CONTINUOUS, harsh, MACHINE murmur usually occurring at S2 below the clavicle due to patent connection between high pressure descending thoracic aorta and pulmonary arteries
Where are these Systolic Murmurs best heard:
- Aortic Stenosis (3)
- Pulmonic Stenosis
- ASD
- Hypertrophic Cardiomyopathy w/obstruction
- Mitral Regurgitation
- Tricuspid Regurgitation
- Ventricular Septal Defect
Abnormal Flow over Outflow Tract/Semilunar Valve
- R base, LLSB, apex
- L base
- L base
- LLSB
Regurgitation from High Pressure –> Low Pressure
- apex
- LLSB
- LLSB
Where are these Diastolic Murmurs best heard:
- Aortic Regurgitation
- Pulmonary Regurgitation
- Mitral Stenosis
- Tricuspid Stenosis
Where is Patent Ductus Arteriosus best heard?
Backward Flow across leaking Semilunar Valve
- LLSB
- L base
Abnormal Forward Flow over Atrioventricular Valve
- apex
- LLSB
- PDA best heard at L base
What is Erb’s Point and why is it important?
- transition point at the 3rd intercostal space
- S2 > S1 ABOVE this point but S1 > S2 BELOW this point
What is the difference between:
- Wide physiologic splitting
- Fixed splitting
- Paradoxical/reversed splitting
- inc. splitting of S2 during inspiration persisting through respiratory cycle
- delayed closing of pulmonic valve or early aortic closure (RBBB)
- wide splitting that does NOT vary with inspiration
- prolonged RV systole, ASD, or RV failure
- splitting that appears on expiration and disappears on inspiration
- LEFT BUNDLE BRANCH BLOCK
- abnormal delayed aortic valve closure
What is S3 heart sound, where is it best heard, what age group is it pathologic in, and what are its two indications?
- low-pitched murmur heard best at APEX with BELL
- follows S2 (normal in kids) and is pathological in ADULTS after age 40
- indicates LV failure and volume overload
What is S4 heart sound, where is it best heard, what does it reflect, and what 4 conditions can it be heard in (AS/HTN/HC/CAD)?
- low-pitched murmur heard best at APEX with BELL
- precedes S1 and reflects atrial contraction into a non-compliant ventricle (inc. ventricular diastolic stiffness)
- found in Aortic Stenosis, Hypertension, Hypertrophic Cardiomyopathy, and Coronary Artery Disease
Where are these Systolic Murmurs heard and what helps identify them:
- Aortic Stenosis
- Ventral Septal Defect
- Tricuspid Regurgitation
- Mitral Valve Prolapse
- RUSB with reduced CAROTID PULSE
- LLSB that does NO get louder (accentuates) with inspiration
- HOLOSYSTOLIC MURMUR
- LLSB that DOES get louder (accentuates) with inspiration
- left midclavicular line (cardiac apex) that presents as systolic CLICK w/ or w/o murmur
- Holosystolic Murmur = Mitral Regurgitation
Where are these Diastolic Murmurs heard:
- Aortic Insufficiency
- Pulmonic Regurgitation
- Mitral Stenosis
- Tricuspid Stenosis
- RUSB or Left Midsternal Border
- best heard with BELL
- LUSB
- RLSB in LEFT LATERAL DECUBITUS POSITION
- LLSB
How are these grades of murmurs differentiated:
Grade 1 Grade 2 Grade 3 Grade 4 Grade 5 Grade 6
- very faint; may not be heard in all positions
- quiet, heard after placing stethoscope on chest
- heard in 1-2 beats
- moderately loud
- loud w/PALPABLE THRILL
- very loud w/THRILL; heard w/stethoscope partly off chest
- very loud w/THRILL; heard w/stethoscope completely off chest
What are the 2 causes of Aortic Stenosis and what is its classical triad?
What does it sound like and where?
- calcific valve degeneration (>75 years old)
- congenital bicuspid aortic valve (40-70 yo)
Triad: heart failure, angina, syncope
- carotid pulse with dec. amplitude and upstroke (parvus et tardus) and systolic crescendo-decrescendo murmur at RUSB or suprasternal notch that radiates to neck
- LOUDER WITH SQUATTING
- systolic thrill over upper precordium
Aortic Stenosis
What are pts at a higher risk of developing, what is the S:ASH mneumonic, and why is treatment with vasodilators cautioned?
- pts. at higher risk of developing CAD (1/3 - 40-60 yo and 2/3 - 60+ yo)
S:ASH =median survival without surgical intervention
A - angina = 5 yr survival
S - syncope = 3 yr survival
H - heart failure = 1 yr survival
- aortic stenosis has WORST prognosis of all valvular lesions and medical therapy ALONE is not effective
What is the difference between Acute and Chronic Aortic Regurgitation?
What does a Chronic Aortic Regurgitation sound like and what kind of pulses does it have?
Acute: severe pulmonary edema and low CO
- pts need immediate Aortic Valve Replacement
- no bounding arterial pulse, murmur is SHORT
Chronic: due to valve deformity or abnormal aortic root
- causes LV volume overload (LV dilation)
- decrescendo, high-pitched blowing murmur at LSB (3rd space) or RSB
- wide/bounding Corrigan pulse 2nd to elevated systolic/low diastolic BP
How is Aortic Regurgitation diagnosed and how is it treated?
Dx: aortic angiography, though echocardiogram is more frequently used (follows LV size and function)
Severe AR: vasodilators
- not recommended for NONSEVERE AR
- use ACEI/ARB, along with diuretics, to treat symptoms
Tricuspid Regurgitation
Where is it heard and what does it present with?
- holosystolic murmur along the LLSB that INCREASES with inspiration and does NOT radiate to the axilla
- large, jugular V waves present that reflect the backflow through the tricuspid valve during ventricular contraction
- often result of RV dilation
Mitral Stenosis
What is it commonly caused by and what is a complication it can lead to?
What does it sound like and where?
- almost always due to Rheumatic Fever and can lead to Atrial Fibrillation
- diastolic murmur with OPENING SNAP caused by chordae tendineae and stenotic leaflets that is best heard at the APEX
- time between S2 and OS INVERSELY related to severity (more severe = earlier OS)
What Triad is seen on CXR of a patient with Mitral Stenosis?
- prominent pulmonary artery vascularity
- enlarged left atrium
- normal-sized LV
Atrial Septal Defect
What is it, what are two findings on ECG, and what kind of murmur is it?
What are patients at inc. risk of developing?
- secundum atrial septal defect; is the most common form of congenital heart disease, except for bicuspid aortic valve
ECG: right axis deviation and RBBB
- systolic ejection murmur at LSB with FIXED SPLIT S2
- patients often develop ATRIAL FIBRILLATION
Ventricular Septal Defect
What is it and what does it sound like?
- most common congenital defect in children
- holosystolic murmur at the LLSB (large VSD cause SOFT murmur while small VSD cause LOUD murmur)
Patent Ductus Arteriosus
What does it sound like and where, and what does it present with?
- continuous, MACHINE-like murmur at LUSB (more common in FEMALES)
- usually asymptomatic, but HF/Infective Endocarditis can occur
- see differential cyanosis with pulmonary HTN; CXR show calcification of ductus arteriosus
What is the correct way to measure Blood Pressure?
- avoid caffeine, tobacco, EtOH for 30 min prior
- rest quietly for 5 min; feet flat/back supported/arm at LEVEL OF HEART
What are 3 concerns that garner collecting Orthostatic Vital Signs?
How are Orthostatic Vital Signs obtained?
- dehydration, blood loss, syncope/near syncope
- lay pt. down for at LEAST 5 minutes and obtain pulse/BP; assist pt. to seated position and after 1-2 minutes recheck pulse/BP
- if (+) in seated position –> do NOT have them stand
What are the two positive findings of Orthostatic Vital Signs?
How long should normal capillary refill take to return to baseline and what three problems would increased time point to?
- pulse INCREASE of 10 bpm or greater between laying down and sitting up
- BP DECREASE of 20 mmHg or greater between laying down and sitting up
- normal capillary refill should return to baseline in LESS than 2 seconds
- > 2 seconds = dec. circulating vol, dec. CO, PVD
Where are the Dorsalis Pedis, Posterior Tibial, and Carotid Pulses located?
DP: anterior medial foot
- use index/middle/ring fingers to help ID pulse
PT: behind medial malleolus
C: anterior to the SCM
What is the Pulse Grading Scale?
0 1 2 3 4
0 = absent, not palpable
1 = diminished, difficult to palpate, weak
2 = expected, easy to palpate (NORMAL)
3 = full, increased
4 = bounding, strong
Who should have their Carotid pulse listened to?
Who should have an Abdominal Aorta ultrasound
- anyone over the age of 50 yo due to increased risk of atherosclerosis (inc. risk of vascular disease)
- use the BELL of the stethoscope
U/S: anyone 50 yo+ with a HISTORY of smoking needs to be checked for Abdominal Aortic Aneurysm
- smoking associated with 3-5x inc. for prevalence
What is the normal value for Jugular Venous Pressure?
6-8 cm (measured from R sternal notch to JV); assesses central venous pressure (judges hearts efficiency as a pump)
What does the Pitting Edema grading scale reflect:
+1
+2
+3
+4
pitting edema graded 1-4 after 5 seconds of pressure
\+1 = 2 mm indention \+2 = 4 mm indention \+3 = 6 mm indention \+4 = 8 mm indention
What is the difference between Acute and Chronic Peripheral Arterial Disease?
Acute: severe pallor
Chronic: claudication –> progressive pain/heaviness with walking that eases with rest
What are the 6 P’s of arterial occlusion and what can they lead to if no emergent intervention is obtained?
How do areas affected by them feel?
6 Ps = paresthesia, perishing cold, pulselessness, pain, paralysis, pallor
- reflects loss of BLOOD FLOW
- can lead to AMPUTATION in severe cases
- extremities affected by arterial occlusion feel WAXY upon palpation
What is the difference between Vascular and Neurogenic claudication?
What test is used to evaluate PAD?
Vascular
- unchanged after walking
- palliative: stopping activity
- provocative: walking UPHILL, inc. metabolics
- pulses: ABSENT
Neurogenic
- inc. weakness after walking
- palliative: bending over or sitting
- provocative: walking DOWNHILL, inc. lordosis
- pulses: PRESENT
- PAD is evaluated using Ankle Brachial Index
How is ABI calculated and what do these ranges indicate:
- > 1.4
- 1.0-1.4
- 0.9-1.0
- 0.8-0.9
- 0.5-0.8
- < 0.5
Right ABI = higher pressure in RIGHT foot/highest pressure in BOTH arms (pick the highest one)
- calcification/vessel hardening (see specialist)
- normal
- acceptable
- some arterial disease (treat risk factors)
- moderate arterial disease (see specialist)
- severe arterial disease (see specialist)
What are Varicosities?
What is Stasis Dermatitis?
- small, irregular dark blue lines that indicate VENOUS CONGESTION
- valves in veins don’t close properly, causing backflow and dilation of vessels (can lead to EDEMA)
SD: reddish, purplish, brownish discoloration in skin develops overtime due to HEMOSIDERIN deposits staining the skin (RBC breakdown)
- occurs with dec. flow or stasis on venous side of circulation
- “BRAWNY EDEMA” = swollen and super thick skin
- skin ulcerations over medial malleolus
What is Cellulitis?
- skin and SubQ tissue inflammation most commonly due to infections
- marked erythema, inc. warmth and swelling, with occasional “skin weeping” without apparent open sores (yellow-clear serous fluid)
What are Janeway Lesions, Osler Nodes, and Splinter Hemorrhage and what are they signs of?
all signs of BACTERIAL ENDOCARDITIS
JL: irregular macules on soles/palms (non-tender)
- occur days-wks after insult
OD: nodules 1 mm-1 cm on fingers, toes, thenar/hypothenar eminence (TENDER)
- occur hours-days after insult
SH: microemboli from valvular pathology at the periphery of nail beds
- more likely from nail trauma if isolated
What is Lymphadema?
What is the #1 cause world-wide?
- impaired fluid return in lymphatic system due to hereditary or secondary causes (crushing injuries, tropical infections)
- most commonly in US due to axillary LN dissection during mastectomy for breast cancer
- use compression sleeve or support stockings to help control (based on amount of pressure desired in mmHg –> prescribed compression stockings)
worldwide –> FILARIAL INFECTION is most common cause (severe lymphedema)
What are the 5 major modifiable risk factors for stroke?
What two conditions can effective control of modifiable risk factors help prevent?
HTN, DM, smoking, dyslipidemia, physical inactivity
- can prevent ATRIAL FIBRILLATION and CAROTID ARTERTY STENOSIS in pts. that effectively manage their modifiable risk factors (dec. risk of stroke significantly)
What are 4 major unmodifiable risk factors for stroke?
- age (older, usually > 80 yo)
- race (African Americans > Caucasians)
- sex (inc. risk for men)
- family history (also genetic disorders)
What are the 4 goals of the Initial Phase of Stroke Examination?
- ensure medical stability –> ABCs!
- quickly reverse conditions contributing to problems
- determine if IV thrombolytic therapy is needed
- move forward to uncover pathophysiological basis of pts. neurologic symptoms
Neurological Exam for Stroke
What are the 3 most predictive examination findings for the diagnosis of ACUTE STROKE?
- facial paresis
- arm drift/weakness
- abnormal speech (combo of dysarthria and language items from the NIHSS)
National Institutes of Health Stroke Scale (NIHSS) is a very frequently used neurological examination scale
What is Asymptomatic Carotid Artery Stenosis?
- presence of atherosclerotic narrowing of the extracranial internal carotid artery in individuals WITHOUT history of ipsilateral carotid ischemic stroke or TIA
- considered asymptomatic if pt has NOT had ipsilateral carotid ischemic stroke or TIA within the PRIOR 6 months
What is Symptomatic Carotid Artery Stenosis?
What are NOT indicative of carotid stenosis?
- focal neurological symptoms in the distribution of a carotid artery with significant stenosis
- nonspecific neurologic symptoms (dizziness, light-headedness) are NOT indicative of carotid stenosis
- pts with above Sx in isolation should be considered ASYMPTOMATIC even if they have carotid artery stenosis
Should asymptomatic individuals be screened for Carotid Artery Stenosis?
NO –> annual risk for ipsilateral stroke is LOW
- routine duplex U/S would result in many more FALSE-POSITIVES than TRUE-POSITIVE results
What 3 populations should be screened for Carotid Artery Stenosis?
- asymptomatic pts. with carotid BRUITS
- considered in pts who have symptomatic sclerotic disease in ANOTHER VASCULAR BED
- pts. with two+ RISK FACTORS for atherosclerotic disease
What is the Toe-Brachial Index used for?
What would the next step be in a patient suspected of claudication but has an initial NEGATIVE ABI test?
- more reliable indicator of limb perfusion in pts. with diabetes because small vessels of toes are frequently spared from medial calcification
- can impose false ABI readings if done in mid extremities
- next step would be to perform EXERCISE TESTING with post-exercise ABI
What are the 3 cause of VTE (Virchow’s Triad)?
- alterations in blood flow
- vascular endothelial injury
- alterations in the constituents of the blood
What are 5 physical exam findings that could indicate DVT in patients?
- dilated superficial veins (varicose veins)
- unilateral edema/swelling
- unilateral warmth, tenderness, erythema
- pain and tenderness along involved veins
- local or general signs of malignancy
What test is used to help assist risk of DVT in patients?
Well’s Criteria
What would be physical exam findings in patients suffering from PVD?
What does an ABI of < 0.9 and < 0.5 indicate in patients with PVD?
PE: claudication and coldness –> continuous/night pain
- measure ABI symptoms/risk factors associated
- skin pigmentation, pallor, coldness, warm areas (collateral circulation), malnutrition of toenails, ulceration/gangrene
ABI < 0.9 = inc. risk of CV morbidity/mortality
ABI < 0.5 = dec. physical activity than w/claudication
Peripheral Venous Insufficiency
What are the 3 most common symptoms and when is pain worse/better?
Sx: limb discomfort, pain, limb swelling
Better: limb elevation and walking
Worse: standing or seated for prolonged periods of time
pts with PAD experience WORSE pain with elevation of limb and walking, while sitting RELIEVES pain
What are 3 cardinal manifestations of heart failure with reduced ejection fraction?
What are 3 common symptoms that signal congestion?
- Dyspnea (on exertion or at rest)
- air hunger; severity dec. after RV failure develops
- Fatigue
- synergistic with inactivity
- Fluid Retention/Volume Overload
Congestion: cardiomegaly, hepatomegaly, pulmonary HTN
Paroxysmal Nocturnal Dyspnea and HFrEF
Orthopnea and HFrEF
PND: occurs after pt. has been in supine position for some time, waking up with sensation of choking that is relieved in the upright position
- usually precedes orthopnea
O: dyspnea occurring within minutes of patient assuming supine position
- represents more SEVERE cardiac dysfunction
- usually sleep sitting upright
What are 4 physical exam findings of patients with HFrEF? (PR/PE/H/PL)
- pulmonary RALES (crackles) = fluid overload
- symmetric pitting edema
- hepatomegaly (JVP elevation, JVD)
- pulsatile liver (during systole)
What is required for diagnosis of Heart Failure using the Clinical Framingham Heart Study Criteria of Heart Failure?
What are two Major Criteria that typically point towards heart failure?
Dx: requires two major criteria or one major and 2 minor criteria in order to get heart failure diagnosis
- two Major Criteria typically indicative of HF include elevated JVP and S3 murmur
- inc. risk of death and hospitalization for HF
BNP/NT-proBNP/Cardiac Troponins and Heart Failure
- BNP/NT-proBNP are of diagnostic utility in ACUTE HF
- highly sensitive/specific when diagnosis in doubt
- BNP lvls > 100 and NT lvls > 450-900 (younger/50)
may be INACCURATE in AKI, CKD, liver disease
- CT: detected in over half of systolic HF patients (sign of volume overload and elevated LV filling pressure)
What are CXR findings of a patient with Heart Failure?
- cardiac silhouette and cardiomegaly (cardiothoracic ratio > 50%)
- Kerly B-lines (spindle-shaped linear opacities at the periphery of the lung bases)
- pleural effusions
What is an essential diagnostic tool for assessing cardiac structure and function in a patient with heart failure?
Why should a cardiac catheter be obtained in a patient with HF?
ECHOCARDIOGRAPHY
- should be used early to help define the syndrome (systolic vs diastolic)
- get cardiac catheter if suspicious of CAD as etiologic/aggravating factor for HF
- also helps guide therapy rather than make diagnosis
What is the difference between Cardiogenic and Non-Cardiogenic Pulmonary Edema?
C: associated with cardiac dysfunction
- inc. pulmonary venous pressure - interstitial edema
- exertional dyspnea and orthopnea
- prominent vascular markings in upper lung zones
NC: damage to the pulmonary capillary lining
- hypoxemia; normal intracardiac pressures
- normal heart size and diffuse alveolar infiltrates
What are Pleural Effusions, how are they detected, and what do symptomatic transudates/exudates require?
PE: accumulation of fluid within the pleural space
- either transudate or exudate
- detected via physical exam or CXR
- symptomatic transudates and all exudates require thoracentesis, chest tube drainage, pleurectomy
- asymptomatic transudates require no treatment
What is Light’s Critera?
- exudative pleural effusions fulfill at least 1 of the following:
- protein PF/serum protein ratio > 0.5
- pleural LDH > 2/3 ULN for serum LDH
- pleural/serum LDH ratio > 0.6
- transudative PE do not meet any of these criteria
What are the Anterior and Posterior Chapman’s Points for:
- Esophagus, bronchus
- Upper lung
- Lower lung
- Locations
- A: parasternally, between 2-3 ICS
- P: T2
- Locations
- A: parasternally, between 3-4 ICS
- P: T3
- Locations
- A: parasternal, between 4-5 ICS
- P: T4
What is the difference between Bronchitis and Pneumonia?
How is Pneumonia treated in an outpatient setting vs inpatient?
Bronchitis: cough lasting 1-3 weeks
- constitutional symptoms
- mainly caused by VIRUSES
- rhonchi with or without wheezing (clear w/cough)
Pneumonia: cough and dyspnea
- FEVER (>100.4) and TACHYPNEA (> 20 BPM)
- fine/coarse RALES (+ infiltrates later)
- dullness to percussion, egophony, tact. fremitus
Outpatient: macrolides
Inpatient: fluoroquinolone OR macrolide + B-lactam
COPD
Who is at inc. risk of developing it, how is it diagnosed, and what is seen on physical exam?
When should PFT/Spirometry be done?
RF: smoking, occupational exposure
Dx: productive cough with SPUTUM production for > 3 months for 2 consecutive years
PE: inc. AP diameter of chest, prolonged expiration on auscultation, hyper-resonance with percussion
do PFT/spirometry ANNUALLY
Pertussis
What is the difference between Catarrhal, Paroxysmal, and Convalescent phases?
What is the best predictor of pertussis as the cause of prolonged cough in adults?
- Catarrhal - 1-2 wks; nonspecific symptoms
- excessive lacrimation and conjunctival injection
- Paroxysmal - starts during 2nd week
- severe, vigorous coughs w/single expiration
- distinctive “whooping” sound (worse at night)
- vomiting w/cough (post-tussive emesis) is BEST predictor of pertussis as the cause of prolonged cough in adults
- Convalescent - reduction in frequency/severity of cough
- may last up to 3 months
What is CURB/CRB and what are its 4 criteria?
- used to predict mortality in patients with community-acquired pneumonia
Criteria:
- new onset confusion with illness
- severe tachypnea (RR > 30 BPM)
- hypotension (< 90 mmHg S or < 60 mmHg D)
- age > 65 years old
Pertussis
What testing should be done in weeks 1-2, 2-4, and after week 4 in these patients?
How is Pertussis treated and how does immunization help with disease?
Wk 1-2: get culture and PCR
Wk 2-4: get PCR
Wk 4+: only check serology
Tx: antibiotics must be initiated within the 1st 3 weeks (unless underlying chronic disease –> can treat after 3 weeks) as well as treating all household and close contacts
- MACROLIDES are FIRST LINE ANTIBIOTICS
- avoid OPIOD-based cough suppressants
Immunization: immunity wanes after 5-10 yrs, so get Tdap booster for adults and healthcare workers
Asthma
How is it diagnosed, what is seen/heard on physical exam, and what is used to confirm diagnosis?
Dx: episodic/chronic symptoms of wheezing, cough that is worse at night and early morning
PE: prolonged expiration and diffuse wheezing; allergies present with pale swollen nasal mucosa and clear rhinorrhea/allergic shiners (eyes)
- pts need spirometry to confirm diagnosis
- inc/dec. FEV1 of 12% and 200 mL from baseline
- change in peak expiratory flow of 20%
Asthma
How are patients treated, what is the cornerstone of pt. treatment, and when can treatment be dialed down?
Short Term: SABA
Management: ICS + LABA (formoterol)
- patient education and monitoring is the cornerstone of asthma treatment
- teach/review with patient at each visit
- can scale back treatment after pt. has been stable for 3 months
- should check inhaler adherence and treat any modifiable RFs before considering step up in treatment
Asthma Action Plan
What is the difference between Green, Yellow, and Red Zones?
G: > 80% of personal best
- continue current medications
- where you WANT TO/SHOULD BE
Y: 50-79% of personal best
- step up medications
- retest in 20-30 minutes (regain green zone status!)
R: < 50% of personal best
- GET HELP IMMEDIATELY
Acute Respiratory Failure
What is the difference between Types 1 and 2, how do they commonly present, and what do ABG lvls show?
Type 1: hypoxic - patient cannot maintain oxygenation even with supplemental O2
Type 2: hypercarbic - ventilation is impaired such that CO2 is retained
C: confusion/delirium/somnolence, pt in tripod position with pursed-lip breathing
ABG: Type 1: PaO2 < 60 mmHg, SaO2 < 90% or Type 2: PaCO2 > 45 mmHg with respiratory acidosis (< 7.35)
Acute Respiratory Failure
How is it commonly treated, what are NIPPV’s two forms, and what should be done if patient does NOT respond or their condition worsens?
Tx: NIPPV is FIRST LINE (non-invasive positive-pressure ventilation): full face mask or nasal mask delivering oxygen under pressure (first line in patients with COPD)
- either C-PAP (continuous positive airway pressure) or Bi-PAP (bi-level positive airway pressure)
- both inc. oxygenation as well as ventilation
- need tracheal intubation with mechanical ventilation in patients that worsen or fail to improve
