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
