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 hypertrophyin 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?
|
SymptomsAnorexiaFatigueMental status changesNausea and vomitingPruritusSeizures (if blood urea nitrogen level is very high)Shortness of breath (if volume overload is present)
Physical findingsAsterixis and myoclonusPericardial or pleural rubPeripheral 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 |