• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/403

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

403 Cards in this Set

  • Front
  • Back
What are the functions of the pericardium?
limit cardiac dilatation
maintain normal ventricular compliance
reduce friction to cardiac movement
barrier to inflammation
limit cardiac displacement
What causes acute pericarditis?
Idiopathic
Infections (viral, tuberculosis, fungal)
Uremia
Acute myocardial infarction (acute, delayed)
Neoplasm
Post-cardiac injury syndrome (trauma, CT Surgery)
Systemic autoimmune disease (systemic lupus erythematosus, rheumatoid arthritis, ankylosing sponduylitis, periarteritis nodosa, Reiter’s syndrome)
After mediastinal radiation
What is the presentation of acute pericarditits?
sharp chest pain w/ possible radiation to neck/back/arm, exacerbated by inspiration and lying supine, relieved with leaning forward
friction rub (scratching high pitched rub throughout all cycles)
What does the ECG look like for acute pericarditis?
diffuse ST elevations
What is the Tx for acute pericarditis?
underlying cause (uremia = dialysis), NSAIDS, try to avoid corticosteroids
Chronic Relapsing Pericarditis
steroid dependency requiring gradual tapering over 3-12 months; NSAIDs, analgesics, and colchicine may be beneficial
pericardiectomy for relief of symptoms is not always effective
Dressler’s Syndrome
What is it? tx?
fever, pericarditis, pleuritis (typically with a low grade fever and a pericardial friction rub)
occurs in the first few days to several weeks following MI or heart surgery
incidence of 6-25%
treat with high-dose aspirin
Bacterial Pericarditis
Cause? Why is the idagnosis missed?
Typically arises from contiguous spread of intrathoracic infection (pneumonia, empyema, mediastinitis, endocarditis, trauma, surgery)
Usually fatal without adequate treatment
Diagnosis frequently missed
Often lacks characteristic features of acute pericarditis
Tuberculous Pericarditis
What are the physical findings? What is normally positive and negative? What is the definitive test?
Physical findings: fever, pericardial friction rub, hepatomegaly
TB skin test usually positive
Fluid smear for TB often negative
Pericardial biopsy more definitive
What is the differential for acute pericarditis?
Acute myocardial infarction
Pulmonary embolism
Pneumonia
Aortic dissection
What NSAID is used for treating acute pericarditits? What combination is used?
indomethacin

ASA plus colchicine
What is the gold standard for dx pericardial effusion? What is seen?
Why is CXR not the standard?
echocardiogram

a posterior echo-free space present only during systolic phase
echo-free space persist throughout the cardiac cycle (> 25 cc)
large effusion with a “swinging” heart


cannot distinguish between pericardial effusion and cardiomegly
What is seen in the CXR w/ pericardial effusion?
water jug heart similar to cardiomegaly
What is the cause of diffuse low voltage, electrical alternans ECG?
pericardial effusion
What is Beck's triad and what is ti associated with?
hypotension, JVD, and distant heart sounds
pericardial tamponade
What is pulsus paradoxus and what is it TYPICALLY associated with?
> 10 mmHg decrease in systolic with inspiration
pericardial tamponade
What is Kussmauls sign and what is it associated with?
jugular venous pressure rises w/ inspiration (normal is inspiration forces jugular blood into R atrium and decreases pressure)

tamponade (normally negative) and constrictive pericarditis
What is the pathophysiology of cardiac tamponade?
increased intracardiac pressure
progressive limitation of ventricular diastolic filling
reduction of stroke volume and cardiac output
What are Sx of pericardial tamponade?
dyspnea, fatigue, agitation and restlessness, syncope, shock, anuria
How do you dx pericardial tamponade w/ echo?
RA and RV diastolic collapse !
reduced chamber size
distension of the inferior vena cava
exaggerated respiratory variation of the mitral and tricuspid valve flow velocities
What are the tx of pericardial tamponade?
pericardiocentesis
pericardial window
pericardiectomy
What is Constrictive Pericarditis?
the encasement of the heart by a rigid, nonpliable pericardium
What are possible etiologies of constrictive pericarditits?
idiopathic, post-surgical, radiotherapy, infectious, drugs, trauma
What is included on differential diagnosis of constrictive pericarditits?
restrictive cardiomyopathy !
right ventricular failure
mitral and tricuspid valve disease
cardiac tamponade
What is the presentation of constrictive pericarditits?
• Presentation: symptoms of dyspnea, fatigue, edema (heart failure symptoms!)
o Exam: JVD, Kussmaul’s sign, pulsus paradoxus rare, diastolic pericardial knock
What are dx tests of constrictive pericarditits?
o ECG: low voltage
o Imaging: CXR (pericardial calcification), CT/MRI (pericardial thickening)
o Hemodynamic studies: looking at pressures in the heart
What are the steps of cardiovascular disease?
risk --> endothelial dysfunction --> atherosclerosis --> CAD --> myocardial ischemia --> thrombosis --> MI --> remodeling --> CHF
4 "stages" of progressive development of atherosclerosis
Endothelial dysfunction
Initial lesion (fatty streak)
characteristic lesion (atheroma)
Complicated lesion
What do injured endothelium secrete?
↓vasodilatory substances, ↑vasoconstrictor substances (thromboxanes, endothelins).
↓amounts of antithrombotic and anti-adhesion substances (prostacyclin, nitric oxide)
↑adhesion molecules
What are fatty streaks?
oxidized lipid in foam cells
How do fatty streaks further their own development?
free radicals and inflammatory cytokines which further damage the vessel wall
What is a Fibro fatty Plaque?
atheroma
What attracts smc to atheromas?
macrophage cytokines
What released by endothelium inactivates platelets; inhibits smooth muscle cell migration and proliferation?
Endothelial derived relaxing factor (EDRF) or nitric oxide
Atherosclerotic arteries are deficient in
_________.
EDRF (nitric oxide) which increase likelihood of a mural thrombus
ischemic cascade
stiffening of the left ventricle
results in decreased diastolic filling (diastolic dysfunction)
impaired systolic emptying
hypokinesis, akinesis, dyskinesis
What EKG changes are due to myocardial ischemia?
ST segment depression
ST segment elevation
T wave inversion
ventricular arrhythmias
What are the 2 types of MI?
transmural infarction - Q wave
subendocardial infarction - non Q wave
What are treatments for atherosclerosis?
Change in dietary habits to lower plasma cholesterol by reducing
intake of saturated fats
Weight reduction and physical exercise
Quit smoking
Lipid lowering drugs (fibrates, statins)
Oral anticoagulants and anti-inflammatory drugs (aspirin)
Control of primary disorders such as hypertension and diabetes
What is CABG? What is the problem?
Used in patients with advanced coronary artery disease for whom balloon angioplasty is not suitable.
Left internal mammary artery or the Saphenous Vein are grafted around the obstructed vessel to re-route blood to the affected area.
20-30% grafts fail within 5 years due to atherosclerosis
What does endothelium secrete that helps w/ collateral development?
VEGF
What drugs are suitable for chronic angina?
aspirin, B-blockers, and nitrates
What 2 techniques are used for revascularization?
percutaneous transluminal coronary angiography
CABG
What enzymes i used to diagnose reinfarction?
CKMB
What is Tx post MI?
modify risk, MONA, improve mortality: aspiring, B-blockers, ACE-I, heparin, lytics, PTCA
What are the 3 theories on etiology of atherosclerosis?
Injury (Hypoxia, HTN, Shear Forces, Chemical, & Immunologic)
Lipid (Cholesterol --> SMC)
Monoclonal (Benign SMC + Mutagens)
What are possible consequences of PVD emboli?
Stroke
Retinal Infarct
Renal Infarcts
Distal Embolization
Digital Embolization
What possible drugs are used to treat PVD?
Pentoxyphyllin, Cilostazol
When does stenosis indicate need to treat even when below 60% occluded?
CAD
Extra Cranial Carotid Disease
What is the presentation of peripheral arterial disease?
o Intermittent claudication: reproducible leg pain that occurs with exertion and always relieved with rest
o Rest pain: leg pain that is present at rest and worse when lying flat, usually improving with letting the legs hang down
o Ulceration/gangrene: a result of critical limb ischemia due to poor perfusion
o May also have muscle atrophy, pallor, hair loss, distal cyanosis
What are common location for peripheral arterial disease?
o Aortoiliac: Leriche’s syndrome (claudication of buttocks, male impotence)
Rule out OA of back, pseudoclaudication (lumbar spine compression)
o Femoropopliteal disease: leg/calf claudication
How do you diagnose peripehral arterial disease?
o Clinical diagnosis, poor distal pulses, auscultation of bruits
o Ankle-brachial index (ABI): ratio of ankle to brachial systolic BP, normal 0.9-1.0
o Doppler ultrasound: measures flow
o Angiography
What is the tx for peripheral arterial disease?
o Risk factor modification: smoking cessation, exercise (develop collaterals), diet
o Medical therapy: ASA, Pentoxyphyllin, Cilostazol
β-blockers may worsen symptoms
o Interventional therapy: percutaneous transluminal angioplasty, stenting, bypass graft, endarterectomy, amputation
Note: only indicated if symptoms causes significant disability
What is the typical pathophysiology and presentation for acute peripheral arterial disease?
• Pathophysiology: embolization from heart or cholesterol atheroembolism, usually affecting distal digits
• Presentation: 6 P’s – pain, pallor, pulselessness, paralysis, paresthesia, poikilothermia
• Diagnosis/Treatment: similar to above, but may be more aggressive
What are alba dolens and cerulia dolens of Peripehrla venous disease?
Alba Dolens – milk leg of pregnancy/puerperal phlebitis
Cerulia Dolens – severe pain, swelling, cyanosis and circulatory collapse
What should not be used to prevent DVTs?
TED stockings
What are the causes of chronic venous insufficiency/stasis?
obstruction, thrombosis, valvular dysfunction, pressure dysfunction
What is the pathophysiology behind obstruction, thrombosis, valvular dysfunction, and pressure dysfunction in chronic venous insufficiency?
Obstruction, Thrombosis, Valvular dysfunction, Pressure dysfunction
What is the presentation of chronic venous insufficiency?
swelling, dry itchy skin, reddish brown discoloration (hemosiderin staining), weeping of transudate, ulcers
How do you diagnose chronic venous insufficiency?
o Palpable cord if varicose veins
o Trendelenberg test: looks at filling of veins with and after a tourniquet is placed
o Doppler ultrasound, Venography, CT/MR imaging
What is the treatment of chronic venous insufficiency?
elevation, NSAIDs/analgesics, compression stockings, surgery
How does Virchow's Triad cause DVTs?
o Stasis: long trips, bed rest, incompetent valves
o Endothelial injury: injury to lower extremities
o Hypercoaguable state: malignancy, pregnancy, OCP, genetic abnormalities (Protein C/S deficiency, Factor V Leiden, Antithrombin III mutation, hyperhomocysteinemia, prothrombin mutation)
What are is the presentation of DVTs and what are 2 possible complications?
pain, swelling, erythema
o Pulmonary embolus (SOB, fever, pleuritic pain, tachy, hemoptysis)
o Stroke if PFO
How do you diagnose DVTs?
o Physical exam: palpation of calves, Homan’s sign (50% sensitivity/specificity)
o Doppler ultrasound
o Spiral CT or V/Q scan if suspect PE
What is the TX of DVTs?
anticoagulation, elevation/compression, IVC filter if anticoagulation is contraindicated
How do you prevent DVTs, what do you not use?
early ambulation > Heparin/LMWH > pneumatic compression

TED stockings
What are risk factors aortic aneurysm?
Age
CT disorders in younger cases
Hypertension
Hypercholesterolemia
Smoking
What is the borderline for elective surgery of arotic dissection?
5.5 cm
What is medical therapy for aortic aneurysms under 5.5 cm?
SMOKING CESSATION
ß blockade
Other antihypertensive?
Statin therapy
Who should be screened for aortic aneurysm?
Men 65-75 y/o who have smoked
Men 65-75 with a relative with AAA
Patients with family history of connective tissue disorder and prior aneurysm
What are complications of aortic dissection?
Proximal propagation --> aortic valve, coronary arteries and pericardium (including tamponade)

Distal propagation--> aortic arch, carotid or subclavian vessels, descending aorta and branch vessels. Consequences include infarction from branch occlusion to pulse deficit.
What inflammatory diseases are associated with aortic disease?
Giant Cell Arteritis
Syphylis
Mycotic aneurysm due to endocarditis
Takayasu
Rheumatoid and Psoriatic arthritis
What are the 3 locations of aortic aneurysm?
o Ascending: Marfan’s (root)
o Arch: Syphilis (tree bark)
o Descending/Abdominal: often associated with atherosclerosis (HTN, smoking, hypercholesterolemia)
Majority below the renal arteries (no vasa vasorum = no blood supply resulting in a weaker aorta)
What is the presentation of AAA?
usually asymptomatic; AAA – pulsatile abdominal mass, abdominal bruit
o If AAA rupture: hypotension, tearing abdominal pain, pulsatile abdominal mass
What are the associations of aortic dissection?
o Most often associated with severe HTN (one of your hypertensive emergencies)
o Other risks: inflammatory vasculitis, connective tissue d/o, aortic valve dysfunction, trauma, cocaine
What are the 2 types of aortic dissection and the recommended treatment?
o Ascending: SURGICAL EMERGENCY. AHHHHH!!!
o Descending: medical management for BP control (Labetolol, Nitroprusside, IV B-blockers)
What is the treatment for CHF?
Class I- Loop/ACE-I
Class II- Above + BB
Class III/IV- above + spironolactone and digoxin (symptomatic)

MONA (angina)
statin (CAD)
anticoag (a. fib)
ICD (ventricular arrythmia)
Marfan Syndrome in aortic disease leads to what and who are particularly affected?
Aneurysmal dilation of root leads to aortic insufficiency
Dissection begins just above the coronary ostia
Pregnant women are at particularly increased risk
Aortic involvement independent of occular and skeletal manifestations
FBN-1 mutations are found in patients without Marfan syndrome
How does the heart attempt to maintain CO in CHF?
RAAS, SNS (vasoconstriction [blood pressure and preload] and HR), Frank-Starling
What is CO?
HR * SVR
What causes decompensation in CHF?
- increased PVR and intravascular volume -->pulmonary and systemic congestion
- Annular Dilation --> Tricuspid and mitral regurgitation
- Atrial fibrillation
- Bundle branch block (cardiac asynchrony)
- Intracardiac thrombi
How does CHF cause mitral regurg?
DILATED LV, PAPILLARY MUSCLE DYSFUNCTION
What are the consequences of ELEVATED CENTRAL VENOUS PRESSURE in CHF?
JVD, HEPATOMEGALY, PERIPHERAL EDEMA
How does CHF cause TRICUSPID REGURGITATION?
DILATED RV
What can cause diastolic failure?
Hypertrophic cardiomyopathy Restrictive cardiomyopathy Pericardial or cardiac tamponade
What can cause systolic HF?
Myocarditis Dilated cardiomyopathy Malnutrition Ischemia
Besides typical drug therapy (CHF/BB/SPIRONOLACTONE), how do you manage CHF
Anticoagulation for EF <30%, history of thromboemoli, presence of mural thrombi, or atrial fibrillation
Intravenous nesiritide, dopamine, dobutamine and/or phosphodiesterase inhibitors
EP therapy (AICD, CRT)
Cardiac transplantation/VAD’s
What are surgical approaches to tx of CHF?
Revascularization
Coronary Artery Bypass
TMLR

Left Ventricular Remodeling
Batista Procedure
Dor Procedure
Myosplint

Support Devices
Acorn Cardiac Support Device
Mitral Valve Repair
Left-Ventricular Assist Device (LVAD)
This is a mechanical pump that can be implanted in your chest. It temporarily assists the heart's pumping. This is used to maintain patients awaiting heart transplants.
Cardiomyoplasty
This is a surgical procedure in which a muscle from the back is removed and wrapped around the heart. A mechanical device stimulates the transplanted muscle to squeeze the heart, thus assisting the heart's pumping action.
What does the PV loop of systolic HF look like?
o Decreased inotropy (force of contraction) results in decrease in height of curve
o Decreased stroke volume results in decrease in width of curve
o Higher volume requirements to achieve the same pressure results in shift to right
What does the PV loop of diastolic HF look like?
o Decreased compliance results in higher resting pressure during diastole
o Decreased ability to fill (decreased volume) results in shift to left
o Decreased stroke volume results in decrease in width of curve (note: ejection fraction is still the same, even though stroke volume is less)
What are Sx of left HF?
• Dyspnea (SOB): pump dysfunction & ↓compliance --> pulmonary edema/congestion
• Orthopnea: dyspnea when lying flat due to redistribution of fluid towards lungs
• Paroxysmal nocturnal dyspnea: acute SOB awakening the patient (same mechanism)
• Rales: fluid in the alveoli; crackling sounds auscultated as alveoli open
• Dullness to percussion: fluid in lower lung fields
• S3 heart sound: during early diastole, blood hits against the high volume in an overfilled ventricle (thus more associated with systolic heart failure & dilated cardiomyopathy)
• S4 heart sound: during late diastole, atrial push tries to get volume into a poorly compliant ventricle (thus diastolic heart failure & hypertrophic cardiomyopathy)
• Fatigue: decreased tissue perfusion to body, brain
• Tachycardia: decreased cardiac output & blood pressure leads to reflex tachycardia
What are Sx of right HF?
• Peripheral pitting edema: volume overload & increased hydrostatic pressure in periphery
• Jugular venous distension (JVD): blood backed up behind the pump
• Hepatomegaly/hepatojugular reflux: blood backed up to liver
• Nocturia: increased venous return when legs are elevated
How do you dx CHF w/ CXR?
• Acute exacerbation: pleural effusion, prominent interstitial markings, Kerley B lines
• Chronic CHF: cardiomegaly
How do you dx CHF w/ BNP?
Elevated in CHF exacerbation & not useful for following progression of known CHF. May be useful in differentiating between acute dyspnea caused by CHF and COPD, but clinical assessment is still better. This is because BNP is also elevated by other disease including pulmonary embolus, pulmonary HTN, kidney failure.
How do you dx CHF w/ echo?
Test of choice. Differentiates between systolic/diastolic & evaluates for causes of CHF. Estimates ejection fraction & shows dilation and/or hypertrophy.
How do you dx CHF w/ cath and stress test?
Cath evaluates for CAD as an underlying cause of CHF. Stress test can assess for ischemia as a result of CHF.
What are the 3 types of cardiomyopathies?
Dilatated (congestive, DCM, IDC)
ventricular enlargement and syst dysfunction
Hypertrophic (IHSS, HCM, HOCM)
inappropriate myocardial hypertrophy in the absence of HTN or aortic stenosis
Restrictive (infiltrative)
abnormal filling and diastolic function
Which cardiomyopathies have normal EJ?
hypertrophic and constrictive
What is the etiology of dilated cardiomyopathy?
idiopathic (majority), infection (Coxsackievirus) peripartum, EtOH, connective tissue disorders, cocaine, nutrition deficiency (wet beriberi)
What is a dilated heart like in dilated myopathy?
Heart is enlarged, increased cardiac mass
Marked 4 chamber enlargement
Chamber dilatation out of proportion to any hypertrophy
Myocyte degeneraton
Interstitial and perivascular fibrosis
Besides left HF, what other Sx are in dilated cardiomyopathy?
arrythmia and embolic phenomenon
What heart sound is associated with dilated cardiomyopathy?
S3
What do yiou find on exam with dilated cardiomyopathy?
Decreased C.O.
Tachycardia
decreased BP and/or narrow pulse pressure
cool extremities (vasoconstriction)
Pulsus Alternans
Pulmonary venous congestion:
rales
pleural effusions
Cardiac:
laterally displaced PMI
S3
mitral regurgitation murmur
Systemic congestion
increased JVD
enlarged liver
ascites
peripheral edema
What lab results help dx dilated cardiomyopathy?
o CXR: enlarged cardiac shadow, pulmonary congestion
o Echo: enlarged 4 chambers
o ECG/Holter if arrhythmias suspected
Who qualifies for a cardiac catheterization in dilated cardiomyopathy?
age >40, ischemic history, high risk profile, abnormal ECG
What is not predictive of prognosis of cardiomyopathy?
age, virus, and duration
What is the prognosis of dilated cardiomyopathy?
worsens as Sx worsen. Complete recovery rare. 5 year mortality 40-80%
What is the pathophysiology of hypertrophic cardiomyopathy?
results in a small LV, assymetrical septal hypertrophy and systolic anterior motion of the mitral valve
o During systole: anterior leaflet of mitral valve obstructs the outflow tract
o During diastole: small ventricle is non compliant, resulting in impaired filling
What is the presentation of hypertrophic cardiomyopathy and the accompanying heart sound?
o History: Syncope, angina, palpatations, fatigue
o Classic picture: athlete presenting with sudden death during activity
o S4: stiff, noncompliant ventricle with increased atrial kick
What is the murmur heard with hypertrophic cardiomyopathy? How do you differentiate from aortic stenosis?
o Systolic crescendo-decrecendo murmur can be differentiated from aortic stenosis
Obstruction increases with decreased preload = ↑murmur with valsalva
Obstruction decreases with increased afterload = ↓murmur with hand grip
What is the effect of decreased afterload on LVO obstruction?
increased obstruction
What is the tx for HOCM?
o Avoid strenuous activity
o Beta-blockers, Calcium channel blockers to decrease heart rate and promote filling of ventricle
o Antiarrythmics as needed
o Surgery to trim down septum, mitral leaflet.
How do you increase/decrease murmur with HOCM?
increase w/ valsalva, standing radiate to carotids
decrease w/ squatting, handgrip , passive leg elevation
What do you see with echo on HOCM?
asymmetrically thickened left ventricular wall
What are causes of restrictive cardiomyopathy?
1. Non-infiltrative
Idiopathic
Scleroderma
2. Infiltrative
Amyloid
Sarcoid
Gaucher disease
Hurler disease
3. Storage Disease
Hemochromatosis
Fabry disease
Glycogen storage
Endomyocardial
endomyocardial fibrosis
Hypereosinophilic synd
Carcinoid
metastatic malignancies
radiation, anthracycline
How is restrictive cardiomyopathy different from constrictive pericarditits?
pericardial knock & friction rub sometimes w/ constrictive
Which cardiomyopathy has right sided failure Sx?
restrictive (diastolic problems --> venous congestion)
What is the difference in histories between restrictive cardiomyopathy and constrictive pericarditis?
Constrictive pericarditis
history of TB, trauma, pericarditis, collagen vascular disorders

Restrictive cardiomyopathy
amyloidosis, hemochromatosis

Mixed
mediastinal radiation, cardiac surgery
What is the tx for restrictive cardiomyopathy?
o Treat the underlying cause
o Drug therapy is not too effective, but may use diuretics/vasdodilators as needed for symptoms of CHF, antiarrythmics as needed
What are the dx tests for restrictive cardiomyopathy?
o ECHO or cardiac catheterization
o Lab tests, possible biopsy looking for etiology
What is the presentation of restrictive cardiomyopathy?
o Heart failure symptoms, R > L
How do you diagnose aortic stenosis
2D echo, doppler, cardiac catheterization
What is the tx for aortic valve dysfunction?
valve replacement, poor prognosis otherwise
What are causes of aortic stenois?
o Unicuspid/Bicuspid valve: early onset of AS
o Elderly: normal valve becomes calcified due to atherosclerosis
What is the pathophysiology of aortic stenosis?
calcified valves difficult to open
o Counterproductive compensatory mechanism: Progressive LVOT obstruction causes increased afterload, resulting in concentric hypertrophy of LV (LaPlace). Pressure backup from from AS surpasses compensation leading to failuire.
What is the murmur of aortic stenosis and how is different from HOCM?
opening click --> systolic ejection CRESCENDO-DECRESCENDO murmur best heard at R base, radiating to carotids
o Murmur decreases with valsalva & increases with hand grip (see HOCM lecture)
What is the most common etiology of mitral stenosis?
chronic rheumatic fever
What is the pathophysiology of mitral stenosis?
2° to rheumatic fever, valve become calcified and difficult to open
o Counterproductive compensatory mechanism: ↑pressure in atria due to stenosis leads to LA hypertrophy with eventual failure
What is the presentation of mitral stenosis?
asymptomatic until compensatory mechanisms fail and LAE occurs
o Pulmonary congestion from ↑hydrostatic P: dyspnea, orthopnea, PND
o Atrial fibirillation (caused by hypertrophy, leading to atrial thrombus)
o Other: infective endocarditis, dysphagia, hoarseness, hemoptysis
What is the murmur in mitral stenosis?
opening snap --> diastolic rumble loudest at apex
o Snap = calcified heavy valve, snapping open after LA pressure overcomes it
o Rumble = blood passing over a stenotic valve during ventricular filling
What does the PV loop of mitral stenosis looks like?
o Decrease in EDV due to impaired filling
o Stroke volume decreases, but EF maintained
What is the Tx for mitral stenosis?
Indication for mitral valve replacement is combination of severe mitral valve stenosis and symptoms with minimal exertion or at rest
Balloon valvuloplasty can be done earlier if morphology of the valve is favorable
What techniques are used to diagnose mitral stenosis?
2d-echo and doppler, TEE
What heart sound is louder than normal in mitral stenosis?
S1
What is the etiology for acute and chronic mitral regurgitation?
o Acute: acute rheumatic fever, acute MI, infective endocarditis
o Chronic: mitral valve prolapse, dilated cardiomyopathy (papillary m displaced)
Acute versus chronic mitral regurgitation
Sudden volume overload
Increased stretch and pressure in LV translates to pressure increase in LA
Pulmonary congestion, edema and dyspnea
Hyperdynamic left ventricle


LV volume overload
Increased LV end-diastolic volume
Increased stroke volume
High ejection fraction
What is the murmur w/ acute and chronic mitral regurgitation?
Short systolic murmur, soft or absent

Loud holosystolic murmur radiating to axilla
When do you tx mitral regurg?
Mitral valve replacement/repair before LV dysfunction develops

acute MR = emergency
What is the etiology of aortic regurgitation?
o Valvular: congenital bicuspid valve, infective endocarditis (acute AR), HTN, rheumatic disease
o Aortic root dilatation: Marfan’s, aortic dissection (acute AR), trauma, aortitis
What is the difference between acute and chronic aortic regurgitation?
Large blood volume abruptly in non-compliant left ventricle
Increased intracardiac pressure
Increased pulmonary venous pressure
Dyspnea
Pulmonary edema


Stretching and elongation of myocardial fibers over time
Dilatation and hypertrophy of LV
Initially increase in LVEF due to LV enlargement
LV dysfunction develops
Increased LV-end systolic volume is an index of myocardial dysfunction
What is the presentation of aortic regurg (named signs only)?
Wide pulse pressure with diastolic pressure less than 60mmHg
Sharp, rapid carotid upstroke with abnormal collapse (Corrigan or water-hammer pulse)
“Pistol shot” sound over femoral artery (Duroziez murmur)
Nodding of head (de Musset sign)
Capillary pulsation in nail beds (Quincke’s sign)
Biphasic bruit during mild compression over femoral artery
What is the tx of aortic regurg?
Vasodilator therapy and endocarditis prophylaxis
Aortic valve replacement
What is the pathophysiology of long term aortic regurg?
damage to valve --> backflow
Counterproductive compensatory mechanism: ↑preload --> LV --> eccentric hypertrophy (dilation + ↑wall thickness) --> failure
What is the murmur of aortic regurgitation?
soft systolic murmur --> high pitched blowing diastolic murmur --> Austin flint murmur (low-pitched diastolic murmur due to regurgitant jet hitting mitral valve)
What is the presentation of aortic regurg?
asymptomatic until late in the disease
o Symptoms: fatigue, left sided heart failure, angina
o Signs: due to HUGE stroke volume with quick run off of regurgitant blood
 Wide pulse pressure (ie BP 200/50)
 Corrigan’s water hammer pulse: rapid rise and fall of peripheral pulses
 deMusset’s sign: head bob occurring with each heartbeat
What is the initiating event for acute coronary syndrome?
rupture of an unstable, lipid-rich plaque in a coronary artery
What is the effect of an angiospasm?
As the clot forms an occlusion, the vessel wall injury causes
smooth muscle spasm which further narrows the vessel
What is generated post MI which can lead to lethal arrhythmias?
Premature Ventricular Contraction
When is a Q wave pathologic?
when it exceeds 0.04 sec
What is the J-point?
End of QRS
What do you compare the ST segment to?
TP segment
What drug should never be used in Pintzmetal angina?
B-blockers (unopposed alpha and neg inotrope)
Wghat drugs are indicated in anti-Mi treatment?
Time is muscle!
open the blocked artery
thrombolytics (“clot busters”)
anti-platelet agents (aspirin, clopidogrel etc.)
angioplasty
anticoagulants
Heparin, low molecular weight heparin etc.
Beta-Blockers
Reduce myocardial Oxygen demand by reducing both Inotropic as well as chronotropic function
Anti-arrhythmic therapy (if necessary)
What are complications of MI?
arrhythmias
ventricular fibrillation soon after MI kills 20-30% of patients
heart block
Ectopic foci (premature ventricular contractions)
heart failure
damage to myocardium
damage to Mitral valvular apparatus
cardiogenic shock
unable to maintain perfusion to vital organs
ventricular rupture
almost always fatal outcome
death
What determines the severity of a Tetrology of Fallot?
pulmonary stenosis/resistane toward pulmonary arteries
What does the heart look like in Tetrology of Fallot? Why?
Booted shaped, RVH
What is the presentation of Tetrology of Fallot?
Tet Spells- cyanotic spells --> squats

squatting compresses femoral arteries --> increased systemic resistance and reverses R to L shunt, sending blood to lungs
What is the mechanism of transposition of the great vessels?
CXR?
TX?
• Mechanism: failure of aorticopulmonary septum to spiral during embryology
• CXR: egg on side appearance
• Treatment: requires surgical correction
Truncus arteriosus
Truncus arteriosus: no division between the aorta and pulmonary arteries
Tricuspid atresia:
Tricuspid atresia: no valve formation, thus no communication between RA and RV, requires multiple protective shunts (ASD/VSD & PDA)
Total anomalous pulmonary venous return
Total anomalous pulmonary venous return: pulmonary veins connect to systemic venous system rather than the L atrium, requires protective shunt (ASD, PFO)
Ventricular septal defect

Murmur and Associations?
• Presentation: muscular defects usually close spontaneously & often asymptomatic, but if they do not, you will hear a harsh holosystolic murmur
• Association: Down’s syndrome, congenital rubella, cri du chat, Edward’s, Patau
Atrial Septal Defect

Murmur?
Associations?
Atrial septal defect (ASD): usually ostium secundum, may be ostium primum or foramen ovale
• Presentation: usually asymptomatic; may give paradoxical emboli; fixed split S2
• Association: Fetal alcohol syndrome, Down’s syndrome
PDA
Open? Close? Murmur?
Patent ductus arteriosus (PDA): during embryology ductus arteriosus is necessary to shunt blood from pulmonary artery to the aorta; PDA when shunt remains
• Keep it Patent with Prostaglandin E2 in those that need the shunt (ie transposition)
• Closed with indomethacin (or any other NSAID that inhibits prostaglandin formation)
• Presentation: Continuous machine like murmur, loudest at time of S2
What is eisenmenger's syndrome?
Eisenmenger’s syndrome: uncorrected L to R shunts (VSD, ASD, PDA), which leads to progressive pulmonary HTN  when pulmonary resistance is higher than systemic resistence, the shunt reverses, resulting in a R to L shunt  late cyanosis, clubbing, polycythemia
What is the presentation, CXR, and infantile/adult types for Coarctation of the Aorta?
Coarctation of the aorta: narrowing of the aorta distal to the L subclavian artery
• Presentation
o Upper extremity HTN (elevated pressures proximal to narrowing), with risk of aortic regurgitation and berry aneurysms
o Lower extremity hypotension (decreased pressures distal), with claudication
• CXR: rib notching (intercostal arteries work as collaterals and hypertrophy)
• Infantile type: associated with Turner’s syndrome; coarctation proximal to insertion of ductus arteriosus
• Adult type: coarctation distal to ductus arteriosus
Anomalous coronary arteries:
Anomalous coronary arteries: defect in origin or drainage of a coronary artery
• Variable presentation and prognosis, depending on the coronary artery involved and the extent of the defect
• Consider in the differential of a young adult presenting with syncope or sudden death, or in a newborn with cyanosis and other defects are ruled out
What is sick sinus syndrome?
SA node dysfunction resulting in sinus brady, pause, arrest
Tachy-brady syndrome:
subset of SSS, with alternating sinus brady & tachy
Vasovagal reaction sinus bradycardia
pain, anxiety, stress --> sympathetic/parasympathetic response
o Increase in parasympathetic vagus nerve --> bradycardia
o Decrease in sympathetic tone --> vasodilation leading to hypotension
Iatrogenic sinus bradycardia
o Drugs: β-blockers, CCBs, parasympathomimetics, digoxin, antiarrhythmics
o Procedures: damage to conducting system can occur during cardiac catheterization, EP studies, other surgery --> scar tissue does not conduct impulses
Ischemia sinus bradycardia
infarct of coronary artery may cause ischemia to SA and AV nodes
o RCA: usually supplies both SA and AV nodes
o LAD: may supply SA node, depending on anatomy
First degree AV Block
: delay across the AV node reflected as PR interval > 0.2s, but every atrial impulse still results in a ventricular beat (1:1 conduction)
Second degree, Mobitz type I (Wenckebach):
Also, where is the block?
PR interval progressively prolongs and then QRS wave drops out
o Block is located in the AV node
Second degree, Mobitz type II
Where is the block?
QRS wave drops out without a graduation of PR interval
o Block is located in His Bundle
Third degree:
no association between atrial impulses and ventricular beats
o Block is located in either AV node or His Bundle
Brugada syndrome
persistent ST elevations in V1-V3 & RBBB ECG pattern. Causes sudden cardiac death, young Asian males are more affected.
Right ventricular outflow track tachycardia
LBBB seen with wide complex QRS tachycardia (ie ventricular tachycardia). Generally asymptomatic and not dangerous, but must be differentiated from other dangerous ventricular tachycardias.
What are causes of SCD?
hypertrophy, myocarditits, long QT, right ventricular dysplasia, anomalous coronary arteries, Brugada, idiopathic VF
Long QT syndrome
This heritable condition gives a long QT due to prolonged ventricular repolarization, and anything that prolongs QT can lead to torsades de point --> sudden cardiac death.
Hypertrophic cardiomyopathy as a cause of arrhythmia
hypertrophy results in stretching of conduction fibers & disorganization, which can lead to lethal arrhythmias
What are the requirements of reentry?
Unidirectional block
Slow conduction in the alternate pathway
Return of the impulse to the original pathway
What is the typical treatment for typical Atrial flutter?
ablative
A patient with palpitations comes in with 150pbm pulse , but the atria is contracting 300.
atrial flutter
What is the EKG seen for atrial flutter?
sawtooth pattern (atrial constractions)
What is atrial fibrillation?
multiple foci in atria fire continuously and in a chaotic pattern, resulting in a quivering atria & irregular rapid ventricle. Impulses commonly originate around the pulmonary veins. Classified as paroxysmal or continuous/refractory.
What is the EKG of atrial fibrillation?
no P waves, irregular QRS waves
What does the EKG of a PVC look like? What is the etiology, presentation, and tx?
wide QRS not opreced by P wave
o Etiology: hypoxia, electrolyte abnormality, hyperthyroidism, stimulants
o Presentation: usually asymptomatic, may feel palpitations
o Treatment: β-blockers if symptomatic, ICD is repetitive PVCs (risk of VFib)
Ventricular tachycardia

What is the etiology, presentation, and tx?
tachycardia originating below bundle of His, defined as a rapid firing of 3+ PVCs in a row at a rate above 100 bpm

o Etiology: CAD, MI, cardiomyopathies, congenital heart defect, congenital QT
o Presentation: asymptomatic if nonsustained. Sustained VT (>30 seconds) usually symptomatic with palpitations, hypotension, angina, syncope; may lead to VFib
o Treatment: antiarrhythmics and/or cardioversion & ICD placement
Torsades de point:

What is the etiology, presentation, and tx?
a type of ventricular tachycardia characterized by polymorphous QRS complexes in a shifting sinusoidal pattern, preceded by a prolonged QT

o Etiology: QT syndrome, class III antiarrhythmics, TCAs, hypocalcemia/kalemia/magnesemis, structural heart disease, ischemia
o Presentation: palpitations, dizziness, syncope, sudden death
o Treatment: Mg+ provides cardiac stabilization, address underlying disorder
Ventricular fibrillation
multiple foci of ventricles fire randomly leading to quivering ventricles and no CO, seen as erratic QRS complexes

o Etiology: ischemic heart disease, torsades, combination of Afib + WPW
o Presentation: syncope, no blood pressure, pulselessness, death
o Treatment: immediate defibrillation and CPR  advanced cardiac life support
What causes increased/abnormal automaticity in SVTs?
a. Increased sympathetic stimulation of SA node
b. Cells outside SA node start to spontaneously depolarize
c. Change in resting membrane potential (ie from ischemia, electrolyte abnormalities) making it easier to depolarize
What is the etiology, presentation, and tx of atrial fibrillation?
• Etiology: HTN, valve disease, CAD, thyrotoxicosis, EtOH (holiday heart syndrome), pericardial disease, COPD, pheochromocytoma, sick sinus syndrome
• Presentation: range from asymptomatic to dyspnea, fatigue, palpitations; irregularly irregular rhythm on physical exam
o Complications: stroke, other embolic disease, angina, hypotension, syncope
• Treatment: rate control & anticoagulation >>> rhythm control & symptoms
o Rate: β-blockers or calcium channel blockers
o Anticoagulation: aspirin for low risk, warfarin for high risk (CHADS score)
o Rhythm: consider anti-arrhythmics, usually amiodarone
o Symptoms usually controlled with rate control, but some still feel symptomatic
 Cardioversion: shock the heart back into sinus rhythm (Note: unless the patient has been on therapeutic warfarin therapy, must do Echo to rule out ventricular thrombus)
 Ablation: ablate around the pulmonary veins; usually last ditch effort
Wolf-Parkinson-White disease
• Description: accessory pathway from atria to ventricles called the Bundle of Kent, located in the atrioventricular valvular rings. Pathway does not share the rate controlling properties of the AV node, allowing early depolarization of part of the ventricle
Tx of Wolf-Parkinson-White disease
• Treatment: risk stratification – look for risk of atrial tachyarrhythmias on top of WPW, which predisposes to sudden death
o Ablation: very successful
o Avoid drugs that slow AV conduction because that may increase conduction through the accessory pathway
What is the ECG of WPW disease?
short PR, delta wave (antidromic only). and widened QRS
What is a delta wave in antidromic WPW?
slurring of the QRS complex is actually the impulse making it through to the ventricles prematurely (across the accessory pathway) without the usual delay experienced in the AV node
Atrioventricular & AV Nodal re-entrant tachycardia
• Description: (1) Sinus beat conducted down both the fast & slow pathways. (2) Premature atrial contraction shoots out of the atria, but the fast pathway is still refractory, giving a unidirectional block. (3) Conduction through the slow pathway results in retrograde conduction via the fast pathway.
o AVRT: pathways located around the valves
o AVNRT: pathways within the AV node
o ECG: note upside down P wave (above); may have narrow or wide QRS depending on which pathways is depolarizing the ventricles
• Etiology: ischemic heart disease, digoxin toxicity, caffeine/alcohol may exacerbate
• Presentation: may feel palpitations, generally not dangerous
• Acute treatment: (1) Maneuvers (Valsalva, carotid massage, breath holding, head immersion in cold water) to stimulate vagus delay of AV conduction. (2) Adenosine decreases AV nodal activity. (3) Electric cardioversion.
• Ablation if episodes are recurrent and symptomatic
What is the difference is FE Na in prerenal and renal failure?
Prerenal – suffering but not failed and trying to compensate – saving Na/volume
FENa is low


ATN – damaged tubules and not compensating – not saving Na (just dumping filtrate)
FENa is high
What is the AKIN criteria for ARF?
Rise in Serum Creatinine > 0.3 mg/dL
Increase in SCr > 50% baseline
Urinary output < 0.5cc/Kg for > 6 hours
What is the formula for FENa?
FENa = UNa*PCr / PNa*UCr (x100)
What is clearance eqn?
Clearance = UCr x V / PCr
v= urine flow
What is creatine? What factors affect level?
Metabolic product of muscle
Dependent on muscle mass
Men have more generation
Older people have less generation
What is the intial response in ARF, how does this lead to CKD?
hyperfiltration of remining nephrons --> wear and tear --> failure
What are the 5 radiography densities?
gas
fat
soft tissue
calcific
metal
What does ultrasound tell you about kidneys?
position, size
cortical echogenicity
cortical thickness
masses
What kind of cysts can you pick up via echo?
cysts
1) anechoic (black)
2) posterior acoustic enhancement (brightness)
3) imperceptible, smooth wall
4) benign - common in elderly
stones
echogenic (white)
acoustic shadowing (darkness)
With KUB X-ray, what is IVP used for?
obstruction or reflux
What is ultrasound primarily used for in renal dysfunction?
cysts, hydronephrosis
What kind of stones are caused by antifreeze?
calcium oxalate
What king od stones are caused by infection with protease producing bacteria and form staghorn calculi that can be a nidus for further UTIs?
struvite
What stones are radiolucent?
uric acid
What causes hyperuricemia --> uric acid stones?
increased cell deth (leukemia, myeloproliferative), alcoholism, gout, Lesch-Nyhan
What causes cystine stones?
congenital cystinuria - defect in amino acid transporter
Phleboliths
incidental/benign calcifications in gonadal veins
How can contrast dye damage kidneys? How do you prevent?
decreased blood flow, direct toxicity, and free radicals

hydration, cautious use, and N-acetylcysteine
What is the deal w/ non-ionic contrast dye?
safer, but more expensive
What is the presentation for transitional cell carcinoma?
50 -70 y.o.
painless hematuria
gross 75%
often clears
hydronephrosis " pyelonephritis
frequency, bladder irritability, dysuria
What is evidence and cause of obstruction in renal radiology?
dilated ureters, hydronephrosis, delayed excreted of dye

stone, tumor, clot, reflux
What is a complication of horseshoe kidney?
infereior poles get caught on inferior mesenteric artery as they ascend during embryo --> ischemic colitis
What is the presentation of adult polycystic disease in renal radiology? Where else can you see cysts?
hypertension, hematuria, proteinuria, pain
stones, infection, cyst rupture, hemorrhage, renal failure

liver/pancreas
How is body water split?
ICF = 2/3 TBW
ECF= 1/3 TBW
Interstitial = 3/4 of ECF or 1/4 of total
Vascular = 1/4 ECF = 1/12 TBW
If an isotonic solution is given to a patient, it will primarily remain in ECF or ICF? How will free water distribute?
ECF
2/3 will go to ICF
1/3 will go to ECF
Which substances are included in osmolarity, but not tonicity?
glucose, BUN. They freely cross the membrane
How do you calculate plasma osmolality?
= 2Na + BUN/2.8 + glucose/18
What causes an osmolality gap?
ethylene glycol, methanol, ethanol
What is psuedohyponatremia?
massive hyperlipidema, hyperproteinemia, or hyperglycemia --> low serum Na, but normal total Na
What are signs of volume overload?
Shortness of breath
Edema
Fatigue
Exercise limitation
JVP elevation
Rales in lungs
Edema
Weight gain
What are signs of volume depletion?
Flat neck veins
Poor skin turgor
Dry mucous membranes
Clear lungs
No edema
Tachycardia
Low blood pressure
orthostasis
Weakness
Lethargy
Dizziness
Drowsiness
Unsteady gait
Fatigue
What are the 4 regulators of volume?
• SNS: vasoconstriction if volume depleted (none if overloaded)
• RAAS: vasoconstriction & Na retention if volume depleted (none if overloaded)
• ADH: water retention if volume depleted (none if overloaded)
• ANP: Na excretion if volume overloaded (none if depleted)
How does the body react to edematous states [VOLUME EXCESS/ UNDERPERFUSION] in context of SNS, RAAS, ADH, ANP?
vasoconstriction, vasoconstriction & Na retention, water retention, Na excretion.
How does the body react to hypervolemic hyponatremia that it can accurately sense (not CHF, edema)?
shutting off ADH --> excretion of dilute urine
How does the body deal with hypernatremia?
turning on ADH --> excretion of concentrated urine
also, thirst stimulated
What is known to cause hypovolemia?
GI loss, 3rd space, polyuria, sepsis, trauma, poor intake, excess insensible loss
What causes hypervolemia?
CHF, nephrotic syndrome, cirrhosis, ESRD, excess intake
What is the point of calculating FENa?
adjusting for urine output by normalizing to SeCr
What are the symptoms of hyperkalemia and HTN?
very general and can be asymptomatic
What is the Cockcroft-Gault formula?
(140 – age) x Wt (Kg) x (.85 women)/ [72 x S.Cr]
What effects the level of SeCr?
Muscle mass
Tubular secretion
Liver disease
Dilution (fluid retention)
What is the pathophysiology of early ARF?
HYPERFILTRATION
Nephron loss (from whatever pathology)
Compensatory increase in filtration of remaining nephrons (increased SNGFR)
Adequate/stable function and excretion
How does the adaptive response lead to progression in later CKD?
Hyperfiltration
Increased glomerular pressures
Increased trophic changes from local vasoactive mediators
-->
Increased wear on remaining nephrons
-->
Progressive loss of function
What is the difference between acute and chronic RF?
chronic = less symptomatic
What is the best test for looking for a urinary tract stone?
CT scan
What has nothing to do with a contrast media reaction?
diarrhea
What is a concern with contrast media?
total: 5-8%
minor: most reactions
nausea / vomiting
minimal hives / mild itching
severe: 0.05%
anaphylaxis / laryngeal swelling / hypotension
cardiorespiratory arrest
death: 1:40,000 - 75,000
What makes a patient more prone to a contrast media reaction? What is the premedication?
Patients at increased risk:
prior contrast media reaction
asthma
Treatment: premedication
beginning 13 hours before the study
oral steroids / Benadryl
What are the serious complications of contrast media?
Kidney failure
impaired renal function
elevated Creatinine
diabetes

sickle cell disease
multiple myeloma
Adult Polycystic Kidney Disease
autosomal dominant
slowly progressive, nearly 100% penetrance
great variation in expressivity
incidence: 1/1000
hypertension, hematuria, proteinuria, pain
stones, infection, cyst rupture, hemorrhage, renal failure
What can cause hydronephrosis?
stone
tumor
blood clot
reflux
Renal Cell Carcinoma
90% of malignant primary kidney tumors
usually > 40 y.o.
risks:
tobacco, phenacetin abuse
hemodialysis
hematuria (56%), flank pain, palpable mass
fever, weight loss
~ 30% found incidentally with imaging
staging accuracy with imaging >90%
Transitional Cell Carcinoma
Transitional cell = urothelium
renal collecting system
ureter
bladder
most common location " most urothelium

Risk factors
tobacco (all kinds)
aniline dyes
textile, printing, plastic, rubber, cable industries
Why should corticosteroids be avoided in pericarditis?
relapse
What do you give to a patient with pericarditis post-MI?
aspirin only
indomethacin causes vasoconstriction
corticosteroids cause relapse
The compartmentalization of the body into the ICF and ECF is possible because of which of the following factors?
semipermeable membranes
Active transport of ions (Na/K)
Energy expenditure (ATP)
All of the above
All of the above
Major ionic composition of the ICF includes all of the following except:
a. Phosphates
b. Proteins
c. Sodium
d. Potassium
Sodium
A tonic fluid would contain which of the following:
Glucose-
Sodium-
Urea-
Lipids-
A tonic fluid would contain which of the following:
Glucose-metabolized and transported, so generates no force
Sodium-correct
Urea-NOT TONIC, BECAUSE IT TRAVERSES ALL MEMBRANES
Lipids-HUGE MOLECULES, in order to be tonic, would need a huge concentration…glucose and lipids, when very excessive, give enough osmolarity that sodium has to go down. Since osmalarity is regulated, if you naturally put “exogenous” stuff (lipids, glucose) in blood, body will compensate by decreasing sodium levels
Your classmate dares you to drink two quarts of saltwater to pass the boredom in Dr.Sankaran’s lecture. But Dr.Sankaran catches you and punishes you by asking what your hormonal profile would be.
a. Increased renin, angiotensin aldosterone
b. Increased epinephrine (SNS)
c. Increased ANP
d. Increased ADH
You are volume overloaded --> ANP

Other answers correspond to volume depletion
Your goofball antics get you feeling sick and you get nauseated and have to skip lunch and throw up several times. You feel dizzy and your blood pressure is low. Which would NOT be increased?
a. Renin
b. Aldosterone
c. ADH
d. ANP
volume depletion --> ANP corresponds to volume overload
A 72 year old man with CHF comes in with shortness of breath and ankle edema after his birthday party eating pizza and fries. You would expect.
a. Increased aldosterone
b. Decreased renin, angiotensin
c. Decreased sympathetic activation
d. Decreased ADH
CHF --> hypervolemic hyponatremia = appears volume depleted

Increased aldosterone corresponds to volume depletion
An 50 year old man has the “flu” with watery diarrhea. His BP is normal and he is not orthostatic. His serum Na is 151. You would expect:
a. Decreased ADH
b. Low urine osmolarity
c. Low plasma osmolarity
d. Low urine output
Watery diarrhea = high water loss with low salt loss
A = increases water loss
B & C = opposite would be true due to ratio of water/osmol loss
D= conserves water
Hyponatremia can be related to which of the following conditions?
a. CHF
b. Cirrhosis
c. Nephrotic Syndrome
d. Volume depletion
e. All of the above
All involve hypervolemic hypronatremia
What are the sensors of volume in the body?
Atrial receptors, carotid receptors, chest wall, JGA..when volume depleted is get no stimulation—not a redundant system
What is the test for volume/Na status of the body?
Physical Exam of ECF, there is no test
What is the test for water balance?
Serum Na
What is the main hormonal effector of water balance?
ADH
What substance provided by ingestion of citrate is also lost by diarrhea?
bicarbonate
How does the body resist changes in pH given the daily acid load?
Buffering
bicarbonate buffering system: add/subtract free hydrogen ions from system; regulated by lungs, kidneys
H+/K+ exchanger
Extracellular buffers (bone, PO4, hemoglobin, plasma proteins)
Intracellular buffers (PO4, hemoglobin, intracellular proteins)

Respiratory Compensation (Fast)
Chemoreceptors (medulla), carotid body, aortic body --> sense changes in pCO2 & [H+]. RR either holds onto or blows off CO2.

Renal Compensation (slow): adjustments in kidney excretion of acids. 1. Hold onto HCO3. 2. Excrete NH4+ 3. Titrable acids (PO4), urate) combine w/ free H+ in kidney lumen amking it unavailable for reabsorption
What do you calculate anion gap for? What is it made up of?
metabolic acidosis

Albumin
Sulfates
Phosphates
Other
What causes an increased anion gap metabolic acidosis?
M – Methanol
U – Uremia
D – DKA
P – Paraldehyde
I – INH
L – Lactic Acid
E – Ethylene Glycol
S – Salicylate (Gap Acidosis w/ a Res Alk)
Tx for salicylate (aspirin) intoxication?
alkalinizing the urine with IV sodium bicarbonate and, occasionally, dialysis.
What causes normal anion gap metabolic acidosis?
Hyperalimentation
Acetazolamide
RTA
Diarrhea
Ureterosigmoid fistula
Pancreatic fistula
What causes metabolic alkalosis?
saline sensitive (urine Cl < 10): volume contraction (vomitting, NG, diuretics)

resistant (urine Cl> 20): volume expansion (primary hyperaldosteronism, Cushing's [ glucocorticoid excess])
What causes respiratory alkalosis?
hyperventilation
anxiety, PE, pneumonia, status asthmaticus, sepsis, central hypoxemia, mechanical ventilation, pregnancy (progesterone), salicylate toxicity (CNS hyperventilation)
What causes respiratory acidosis?
hypoventilation

lung disease, airway obstruction, neuromuscular disease, drug induced- morphine, anesthetics, sedatives
What is the normal blood ph?
7.4
What is the normal value for pCO2 and HCO3-
40 and 24
What is the importance of the delta gap?
Delta Gap = Delta Bicarb, then single disorder

Delta Gap > Delta Bicarb, then also a metabolic alkalosis

Delta Gap < Delta Bicarb, then also a metabolic acidosis
What are the major electrolytes of ECF?
Na, Cl, HCO3
What cause K+ shifts that make you think you have total body hyperkalemia?
GI bleed
Tissue Barriers breached
Osmolality: Glucose, mannitol
Acidosis
B-Blockers
Insulin deficiency/resistance
What lowers serum K+ (ECF --> ICF)?
Beta-agonists
Correction of acidosis
Insulin therapy
What two organ system allow significant potassium excretion? Which one is regulated?
GI and renal
renal
Determinants of K+ renal excretion
1. GFR / Protein
2. Intact CCT
3. Distal Na+ delivery (Excretes K+ by taking up Na) amiloride will block Na channel
4. Aldosterone
How do you determine low K+ loss hypokalemia or GI loss?

How do you differentiate renal loss from GI loss in hypokalemia?
Hx

urine K+ is high in renal loss (it should be low to conserve K+) and low in GI loss
What are common causes of hyperkalemia?
Inadequate GFR
Damaged CCT
Volume depletion/drugs*
Aldosterone deficiency/drugs*
Which of these statements about potassium in NOT true?
a. Potassium is the major intracellular ion
b. Can shift from ICF to ECF
c. Movement is not affected by insulin
d. Movement is affected by acidosis
C. insulin causes ECF --> ICF
Factors important to potassium excretion include all of the following EXCEPT?
a. Adequate renal function (GFR)
b. Na+ delivery to the distal nephron
c. Aldosterone secretion
d. ADH secretion
D
What is the cause of increased intake hyperkalemia?
iatrogenic, bolus
What is the cause of decreased output hyperkalemia?
kidney failure in CCT via aldosterone
Volume depletion
Decreased aldosterone- Addison's and iatrogenic from ACE inhibitors and spironolactone/triamterene
What is the presentation of hyperkalemia?
flaccid paralysis, paresthesia, weakness, peak T waves on EKG, arrhythmias and cardiac arrest
What is the treatment for hyperkalemia?
calcium gluconate- stabilize cardiac membrane, will not help with K+
glucose w/ insulin or sodium bicarbonate ( lower K+ to buy time)
kayexalate, dialysis, lasix (lower K+ via stool, blood, or kidneys)
What causes increased renal loss hypokalemia?
K+ wasting diuretics, Mg deficiency, hyperaldosteronism, excessive glycocorticoids (related to ald), and Bartter;s syndrome
What causes increased GI loss hypokalemia?
vomittingand NG drainage, diarrhea, laxative, enemas
What is the presentation of hypokalemia?
muscular weakness, cramps, constipation, arrhythmias, flat/inverted T wave or U wave, exacerbates toxicity
What is the treatment of hypokalemia?
slow replacement and treatment of underlying cause
What is the tx for heavy metal poisoning?
chelation
What are drugs that cause toxic ATN along with
-renal insufficiency
-fluid depletion
-electrolyte depletion (K/Mg)
Aminoglycosides
Cisplatin
Analgesic
Calcineurin Inhibitors
What is the general treatment of drug induced toxic ATN?
Avoidance
Dose Reduction
Monitoring
Reducing Exposure to tubules (Urine flow)
Volume Repletion (avoiding concentration)
What is the mechanism for contrast dye toxic ATN (CIN)? What are risk factors?
Mechanism
Direct tubular toxicity
Ischemia from vasoconstriction
Free radical formation / oxidative injury
Dose Dependent
Risk Factors:
DM, depletion, renal impairment, other
What is the tx for CIN?
Reduce Dose
Using Lower Osmolarity Agents
Volume correction
Salt loading (Isotonic Fluids)
Bicarbonate IV
Mucomyst (Acetylcysteine)
Besides drugs, what can cause TID?
Lithium
Urates
Radiation
MCD (genetic)
Paraproteins (some)
What are the major categories of etiology of tubular necrosis?
Drugs (71%)
Infections (15%)
Idiopathic (8%)
TINU (5%)
Sarcoidosis (1%)
What is the presentation of acute interstitial nephritis?
Fever (27%)
Rash (15%)
Eosinophilia (23%)
Triad (10%)
Eosinophiluria (Hansel’s stain)
Non-glomerular Proteinuria
Biopsy: interstitial inflammation
What drugs cause interstitial disease?
NSAID
Beta-Lactams
Rifampin
Sulfonamides
Quinolones
Cimetidine
Allopurinol
PPI
Indanavir
Aminosalicilate
What infections cause interstitial disease?
Legionella
Leptospirosis
CMV
Streptococci
HIV


Corynebacteria
EBV
Yersinia
Polyoma virus
BK virus
What are autoimmune causes of interstitial disease?
Sarcoidosis
Sjogren’s
Wegener’s
Lupus (SLE)
Goodpastures
TINU
What is tx for interstitial disease?
Remove offending agent
Supportive care (including dialysis)
Steroid therapy
The pathology of tubular diseases includes all of the following EXCEPT:
a. Heavy metal toxicity
b. Anesthetic agents
c. Heavy analgesic use
d. Radiographic contrast
B
What is the presentation of ATN?
oliguric, diuretic, recovery
What is ischemic ATN?
hypoperfusion from shock --> ischemic injury (renal vs. prerenal)
What is renal tubular acidosis?
renal tubular dysfunction --> decrease in H+ excretion --> non anion gap metabolic acidosis and urine alkalosis
Type I, inability to screte H+
Type II- cna't reabsorb HOC3-
Type IV: hypoaldosteronism or renal resistance
I & II- hypokalemia
I has really alkalotic urine pH while II is more proximal and is slightly alkalotic
IV- results in hyperkalemia
The triad of findings commonly associated with Interstitial Nephritis includes:
a. Fever
b. Eosinophilia
c. Heavy proteinuria
d. rash
abd
Which of the following is NOT commonly seen in Tubulointerstitial disease?
a. Acidosis
b. Salt wasting
c. Oliguria (low urine output)
d. Renal insufficiency
C
Auto-immune diseases causing blood vessel damage and multiple clinical manifestations
vasculitis
What are things to associate dwith large, med, and small vessel vasculitis?
large: claudication, poor pulses, and visual loss
medium: internal organ damage
small: organ damage, palpable purpura
Giant cell arterititis?
presentation, association, diagnosis, and tx
elderly with jaw pain (claudications), visual changes, HA, scalp tenderness, enlarged temporal artery, PERMANENT BLINDNESS

polymyalgia rheumatica- shoulder, hip girdle pain, AM stiffness, and ESR

dx: temporal artery biopsy

tx: high dose corticosteroids
Takayasu's arteritis
presentation, association, diagnosis, and tx
Asian women under 40, chronic inflammation of aorta and branches gives limb ischemia, absent pulses, different blood pressures in arms

Dx: CT or angiography

Tx: corticosteroids and immunosuppressives
Polyarteritis nodisa
presentation, association, diagnosis, and tx
purpuric rash, skin nodules, renal failure, single nerve inflammation, abdominal pain, wrist drop

HBV, HIV, drug reaction, idiopathic

dx: tissue biopsy, Arteriogram of leg showing multiple aneurysms in PAN

tx: corticosteroids and immunosuppressives
Isolated CNS vasculitis
presentation and dx
HA, personality changes, obtundation, weakness, crainial neuropathy

lumbar puncture, MRI, angiography
Kawasaki's disease
children under 5 with fever, cervical lymphadenopathy, conjunctivitis, mucositis, rash, palmar erythema

Complications: coronary arteries and future MI

tx: ASA, IV Ig
What is hypersensitivity vasculitis?
sensitivity to drug, infection, etc --> rash, purpura, petechiae, arthalgias, fever, adenopathy, occasional internal organ involvement
diagnosis: clinical hx, skin biopsy
tx: stop drug, then NSAIDS or low dose corticosteroids
Behcet’s Syndrome
Chronic relapsing inflammatory disease
Most common in middle eastern and Asian populations
Recurrent oral ulcers
multiple
3 or more episodes/yr
Associated systemic vasculitis

Systemic features…
Genital ulcers
Ocular disease (uveitis)
Skin lesions
Palpable purpura
Nodules
Pathergy
Neurologic
Vascular
Venous thrombosis
Arterial aneurysm
Arthritis
Wegener’s Granulomatosis
Clinical features
Triad: sinuses, lungs, and kidneys
Almost pathognomonic: saddle nose
Chronic sinusitis, nasal ulcers, oral ulcers
Pulmonary infiltrates, cough, dyspnea
Renal failure
Purpura
Arthralgias
Eyes: uveitis, episcleritis, conjunctivitis
c-ANCA-positive vasculitis (anti-Proteinase-3 antibody)
Churg-Strauss Syndrome
phases, dx, and tx
skin, lungs, and heart

1. prodromal: asthma, atopic dermatitis, allergic rhinitis
2. eosinophilic: pulmonary opacities, eosinophilia
3. Vasculitis: cutaneous & internal organ vasculitis, w/ granuloma formation

complications: MI, stroke, renal, GI bledding, status asthmaticus

Dx: p-ANCA positivie, biopsy, clinical

Tx: corticosteroids and other immunosuppressives; fatal w/o treatment
Henoch Schönlein Purpura
Palpable purpura (100%)
Arthritis (82%)
Abdominal pain (63%)
Renal disease (40%)
GI bleeding (33%)

Children
50% under 5 years old
Often follows URI
Renal disease more severe in older children and adults

Prognosis
Usually self-limited
Complete recovery >90% patients
Treatment
Observation
Steroids and immunosuppressives for severe renal disease
Cryoglobulinemia
Associated with hepC

Circulating immunoglobulins that precipitate at low temperatures
Decreased blood flow
Raynaud’s phenomenon
Acral cyanosis, ulceration and necrosis
Immune complex deposition
Purpura
Arthralgia
Nephritis
Neuropathy
When to Suspect Vasculitis
Palpable purpura
Ischemic changes in absence of risk factors for atherosclerosis
Glomerulonephritis or pulmonary-renal syndrome
Multisystem disease (especially in a younger patient)
Stroke in a young person
Mononeuritis multiplex
Unexplained constitutional symptoms (weight loss, malaise, fatigue) or fever
Labs for vasculitis
Labs: active inflammatory state (anemia, incr ESR, incr CRP, decr Albumin)
syndrome characterized by a rapid decline in renal function over hours or days resulting in the systemic accumulation of nitrogenous wastes and the development of fluid, electrolyte, and acid-base disturbances.
acute renal failure
What is the result of ARF?
azotemia, accumulation of nitrogenous waters, and development of fluid, electrolyte, acid-base disturbances
What are the 2 major causes of ARF?
acute tubular necrosis (ATN) and prerenal disease
What determines GFR?
starling forces and filtration coefficient (permeability)
What is the etiology of RENAL failure (as opposed to pre and post)?
tubular: ischemic ATN, toxic ATN
glomerular: acute glomerulonephritis
vascular: HTN emergency, vasculitis
interstitium: interstitial nephritis
What is pre-renal failure? What is the etiology?
decreased RBF --> decreased GFR
Renal parenchyma and tubules = undamaged, but --> ATN if persists

Etiology: hypovolemia, CHF, peripheral vasodilaiton (sepsis and & BP meds), renal artery stenosis, cirrhosis, hepatorenal disease
What are signs of hypovolemia?
Orthostatic drop in systolic blood pressure greater than 15 mm Hg with rise in pulse greater than 15 bpm
Hypotension while supine
Decreased skin turgor
Dry mucous membranes
Glomerulotubular balance
After glomerular filtration, the blood in the efferent arteriole and peritubular capillaries have a higher oncotic pressure and draw fluid from the tubular interstitium
Increased filtration of glucose, amino acids, phosphate, and organic ions lead to sodium reabsorption by cotransport
What is glomerulotubular feedback?
SNGFR --> high Na --> renin (-->ATII)--> decreased SNGFR
What diseases have FENa <1%, but are renal rather than prerenal?
Hepatorenal syndrome

Urinary tract obstruction
Acute glomerulonephritis
Radiologic contrast–induced ATN
Myoglobinuric and hemoglobinuric ARF
Renal allograft rejection
Drug-related alterations in renal hemodynamics (eg, captopril, NSAIDs)
- Diseases of the renal parenchyma, specifically involving the renal tubules, glomeruli, interstitium
Intrinsic renal failure
How does TG balance affect ARF?
can't reabsorb Na --> high Na sensed --> angiotensin release --> contraction lowers GFR
What is the BUN/Cr ratio in prerenal and renal?
> 20, < 20
What are some examples of post-renal failure?
Tubular obstruction from crystals (eg, uric acid, calcium oxalate, acyclovir, sulfonamide, methotrexate, myeloma light chains)
Ureteral obstruction - Retroperitoneal tumor, retroperitoneal fibrosis (methysergide, propranolol, hydralazine), urolithiasis, papillary necrosis
Urethral obstruction - Benign prostatic hypertrophy; prostate, cervical, bladder, colorectal carcinoma; bladder hematoma; bladder stone; obstructed Foley catheter; neurogenic bladder; stricture
What are signs and sx of renal failure?
Symptoms Anorexia Fatigue Mental status changes Nausea and vomiting Pruritus Seizures (if blood urea nitrogen level is very high) Shortness of breath (if volume overload is present)
Physical findings Asterixis and myoclonus Pericardial or pleural rub Peripheral edema (if volume overload is present) Pulmonary rales (if volume overload is present) Elevated right atrial pressure (if volume overload is present)
What are the tx of ARF?
Prerenal: Dependent upon the underlying cause
Hydration if hypovolemic or hypotensive
Diuretics and treatment of CHF

Intrinsic: ATN, supportive
Try to convert oliguric to non-oliguric by diuretics, easier fluid management
Other intrinsic causes such as interstitial nephritis and glomerulonephritis may be treated with steroids/immunosuppressives

Post renal: Relieve obstruction
Intrarenal: hydrate to promote urine flow
What is White Coat HTN?
HTN in front of doctor only
What is masked HTN?
Some patients may have normal blood pressures in the office but elevated blood pressures out of the office based on 24 hour ambulatory monitoring
What is malignant HTN?
Marked hypertension with end organ damage in particular retinal hemorrhage, exudates, or papilledema
May be associated with hypertensive encephalopathy
Usually associated with diastolic > 120 mmHg
May occur as manifestation of another condition such as preeclampsia or acute glomerulonephritis
Hypertensive Urgency
Severe hypertension with diastolic > 120 mmHg in an asymptomatic patient
No evidence of acute end organ damage
What are possible factors to essential HTN?
Increased sodium retention by the kidneys
Increased sympathetic neural activity and enhanced beta adrenergic responsiveness
Increased angiotensin II activity and mineralocorticoid excess
Genetic factors: Twice as common if one or more parent with hypertension, genetics may account for 30% of variance in the population
Reduced nephron mass may predispose to hypertension and may relate to genetic factors, intrauterine developmental disturbances (drugs, hypoxia, nutritional deficiency) and post natal environment (malnutrition, infection)
Role of the Kidney in blood pressure regulation
Sodium homeostasis and its regulation by the kidneys
Sympathetic nerve innervation and Beta adrenergic effects at the level of the kidneys
Renin release
Hormonal influence
Renin angiotensin aldosterone
Atrial natriuretic peptide
What high intake leads to HTN?
NaCl
What increases NaCl sensitivity?
Increases with age, African-Americans, obesity, metabolic syndrome, and chronic kidney disease
What leads to increased Na excretion?
In volume expansion, increased secretion of Atrial Natriuretic Peptide and reduced Aldosterone lead to diminished collecting duct sodium reabsorption
More pronounced hypervolemia leads to diminished proximal sodium reabsorption
Pressure natriuresis also significant contributor to sodium excretion
Cardiorenal reflex
Increase in pressure in the left side of the heart stimulate volume receptors which leads to reduced sympathetic tone to the kidneys
This enhances renal perfusion by vasodilation
Atrial Natriuretic Peptide (ANP) may also be released contributing to renal vasodilation
What are possible causes of secondary HTN?
Chronic kidney disease
Renovascular disease
Primary aldosteronism
Sleep apnea
Drug induced
Chronic steroid therapy or Cushing’s syndrome
Thyroid or parathyroid disease
Coarctation of the aorta
Pheochromocytoma
Pheochromocytoma
Pheochromocytoma: Paroxysmal blood pressure elevations with pounding headache, sweating, and palpitations
Plasma fractionated metanephrines for high index of suspicion: family history, Multiple Endocrine Neoplasia 2 (MEN2), adrenal mass, prior pheo resection
24 hr urine for catecholamines and metanephrines for low index of suspicion: resistant hypertension, hyperadrenergic spells, adrenal mass uncharacteristic of pheo
Primary hyperaldosteronism
: Hypokalemia from urinary potassium wasting; measure plasma aldosterone to plasma renin activity(PRA); > 30 is suspicious
Follow with 24 hr urine for aldosterone
High index if hypertension with hypokalemia or low diuretic dose hypokalemia, severe or drug resistant hypertension, adrenal incidentaloma, family history of early age hypertension, first degree relatives
PRA usually very low due to excess sodium load; would be high is hypokalemia diuretic induced
Renovascular hypertension
Onset of hypertension before age 30
Onset severe hypertension after age 55
Resistant hypertension despite compliance (3 drugs including diuretic)
Acute rise in BP in previously stable patient
Malignant hypertension
30 % rise in creatinine after initiation of ACEI or ARB
Unilateral renal atrophy > 1.5 cm length differential
Coexisting diffuse atherosclerosis
Obstructive Sleep Apnea
Nocturnal cardiac arrhythmias including bradycardia and asystole
Atrial fibrillation
Pulmonary hypertension
Obesity
Coarctation of aorta
Major cause of hypertension in children, also found in adults
Hypertension in upper extremities, diminished or delayed femoral pulses, low or unobtainable arterial blood pressure in lower extremity
The major risk factor for premature cardiovascular disease
HTN
End Organ Damage caused by HTN
Heart
Left Ventricular Hypertrophy
Angina or prior myocardial infarction
Prior coronary revascularization
Heart failure
Brain
Stroke or transient ischemic attack
Chronic kidney disease
Peripheral arterial disease
Retinopathy
What are tests associated with HTN?
Limited echocardiography to detect left ventricular hypertrophy, more sensitive than electrocardiogram
Uric acid: hyperuricemia may be associated or precede hypertension
Microalbuminuria closely correlates to cardiovascular disease
Plasma renin activity
Renal duplex ultrasound if renovascular hypertension is suspected
HTN monotherapy
Thiazide diuretic for mild hypertension: Chlorthalidone preferred
ACE inhibitor or ARB and beta blockers for young people
Thiazide diuretic or calcium channel blocker for African Americans, elderly
What are indications for specfiic antihypertensives?
ACE inhibitors or ARBs in diabetes mellitus, chronic kidney disease, LV dysfunction or MI
Beta blockers in coronary artery disease, atrial fibrillation
Diuretics for volume control in CHF, nephrotic syndrome
What is the best dual antihypertensive therapy?
DHP CCB w/ ACE-I

if B-Blocker initially, add thiazide or DHP CCB
For HTN (not CHF) what should you be careful of with b-blockers?
ACE inhibitor or ARB less effective with beta blocker since renin secretion and angiotensin II formation is already blocked by beta blocker
Beta blocker use with caution verapamil and to a lesser degree diltiazem
Wha tis the role of angiotensin II on HTN?
sympathetic stimulation of NE release, direct stimulation of Na+ reabsorption, stimulates ald, triggers vasoconstriciton, stimulates ADH, stimulates thirst
Evidence of structural or functional kidney abnormalities (abnormal urinalysis, imaging studies or histology) that persist for at least three months, with or without a decreased glomerular filtration rate (GFR)

- OR -

Decreased GFR (<60 cc/min), with or without evidence of kidney damage
CKD
What is MC manifestaiton of kidney dmage?
albuminuria
What is the result of adaptive hyperfiltration?
glomerulosclerosis
How does the kidney increase filtration in adaptive hyperfiltration?
prostaglandins (dilate afferents) and angioensin II (constricts efferents)
What are the 3 most common etiologies of CKd?
DM, HTN, atherosclerosis
marker for glomerular hypertension and an independent predictor of progressive CKD.
proteinuria
How does limiting protein intake help with CKD?
Low protein diets protects against glomerulosclerosis.
Protein restriction also restricts phosphorus.
How does ACE-I help with CKD? What else can help?
Reduce glomerular hypertension and reduce diabetic nephropathy
B-blockers and diuretics
What drugs can treat CKD?
Drug of choice is an ACE inhibitor (ACE-I): Increases kinin levels which increase efferent arteriolar dilatation, reducing glomerular pressure.
An angiotensin receptor blocker (ARB) is OK, too.

The second drug is a diuretic.

A beta blocker is usually given as well.

Non-dihydropyridine Ca channel blockers have
anti-proteinuric effects (diltiazem, verapamil).
Osteitis fibrosa
Osteitis fibrosa is the high turnover bone disease due to high parathyroid hormone (PTH), leading to bone pain and fractures.
Phosphorus retention due to decreased GFR occurs early and may be the central cause of high PTH.
Decreased calcitriol synthesis (1,25-dihydroxyvitamin D) occurs with GFR < 50. High phosphorus and loss of renal mass can do this. Vit D acts thru the vitamin D receptor (VDR) to regulate PTH levels.
Treatment of Secondary Hyperparathyroidism
Diet to restrict phosphate and give Vit D supplements
Cinacalcet (Sensipar)
increasing the parathyroid tissue CaSR sensitivity to Ca levels. This lowers PTH levels and phosphorus levels.
Anemia of Renal Disease
Tx and reason for possible poor response
normocytic and normochromic, due to deficient erythropoietin (EPO) production by the reduced renal mass

Treated with recombinant EPO since 1989 given subcutaneously or IV.

Poor response may indicate iron deficiency, aluminum toxicity, malnutrition, myelofibrosis, uremia or any inflammatory condition.
What are consequences of metabolic acidosis from CKD?
Bone buffering of excess H ions is associated with release of Ca and phosphate from bone

Increases muscle breakdown reducing muscle mass and leading to muscle weakness
Indications for Dialysis
uremia, Uremic neuropathy , malnutrition, tamponade
CI for renal transplant
1. HIV
2. Active malignancy
Life expectancy less than 1 year, especially
severe ischemic heart disease
4. Inability to comply with medications or appointments
5. Active substance abuse
6. Age > 70 is often a contraindication
7. Cause of CKD is no longer a contraindication
What is the dialysis method with more autonomy?
peritoneal
What are the sx associated with urenia?
pericarditis, anorexia, lethargy, asterixis, seizures, platelet dysfunction, WBC dysfunction
What happens to fluids and electrolytes in CKD?
volume overload, hyperkalemia, hypermagnesemia, hyperphosphatemia, metabolic acidosis, and hypocalcemia
What causes hypocalcemia in CKD? What are the effects of hypocalcemia?
decreased renal production of calcitriol, decreased GI absorption

Increased PTH --? renal osteodystrophy and calciphylaxis
What is the type of hematologic, neurologic, and reproductive sx of ckd?
normocytic anemia due to EPO deficiency, lethargy and tetany, secondary to hypocalcemia, decrease in sex hormones due to hypothalamic-pituitary axis
What is the lifestyle management in CKD?
protein restirction, low salt, K/PO4/Mg restriction
quit smoking, lose weight
control lipids,
control bp, especialy with ACE-I
control diabetes
What conditions should be managed in CKD?
secondary hyperparathyroidism, acidosis, anemia, and dialysis
Why does tubulointerstitial disease cause nocturia?
when people wake up, urine = conc
kidney disease = can't conc urine and have to void during night
What are 3 things that could cause renal hypokalemia?
Diuretics
Hyperaldosterone states (Conn's Syndrome)
Excessive salt intake, urine flow
GI loss from diarrhea
Diuretic induced loss
Hyperaldosteronism
Poor K intake (mild)
Low UK, Low UNa
High UK, High UNa
High UK, Low UNa
Low UK, normal UNa
What is the sg, Uosm, and FENa of prerenal failure?
higher, higher, less than 1%
What are 4 risks for CKD?
1. Hypertension – 23% of ESRD 1996-2000
2. DM – 45% of ESRD 1996-2000
3. CVD – 30% of CVD patients have CKD
4. Family member of ESRD patients
What is associated with progression of CKD?
Systemic hypertension
Protein intake
i. Low protein diets protects against glomerulosclerosis.
Protein restriction also restricts phosphorus.
Diabetes mellitus
Hyperlipidemia – treated patients have a slower decline in GFR compared with controls
Smoking - associated with progression
High Phosphorus level
Obesity
What are characterisitics of nephrotic syndrome?
Proteinuria > 3.5 G / 24 hours
Hypoalbuminuric
Edema
Hyperlipidemic
Hypercoaguable state
Usually not associated with renal insufficiency
What are characterisitics of nephritic syndrome?
Hematuria
Renal insufficiency
Systemic Illness
Active urinary sediment
Minimal Change Disease
90% of cases of nephrotic syndrome in children
In adults in association with NSAIDS or with hematologic malignancies
Normal light microscopy or only some mild mesangial proliferation
EM shows fusion of foot processes
Treated with steroids
Membranous Nephropathy
Common form of nephrotic syndrome in adults
Basement membrane thickening and electron dense deposits across the GBM
Usually idiopathic but also seen with Hepatitis B, autoimmune diseases (SLE), drugs (gold, penicillamine, captopril, NSAIDS) or with solid tumors
Focal/Segmental Nephropathy
FSGS or Focal Sclerosis
Focal areas of segmental sclerosis within glomeruli
Idiopathic
Secondary due to HIV, reflux nephropathy, healed previous glomerular injury, massive obesity
Treat with steroids, or treat underlying cause