CLINICAL PATHOPHYSIOLOGY made ridiculously simple™ / Клинична патофизиология направена изключително лесна: CHAPTER 1. THE CARDIOVASCULAR SYSTEM

Английски оригинал Перевод на български

volume)

#251

#252

----? increased blood

#253

Increased cortisol, also known as Cushing's syn­ drome (when in excess, cortisol can stimulate aldos­

#254

terone receptors)

#255

#256

cardiacHyperthyroidismoutput) (excess thyroid hormone increases

#257

#258

aryIncreasedto pheochromocytomaepinephrine/norepinephrine,( epinephrine/norepineph­e.g., second­

#259

rine increase heart rate and arterial resistance.)

#260

Changes in the arteries themselves that can lead to hypertension include aortic coarctation and vasculitis.

#261

Consequences of Hypertension

#262

Hypertension was discussed above as a cause of car­ diac hypertrophy and myocardial infarction. Hyper­ tension can also cause kidney damage (nephropathy), retinopathy, stroke, intracranial hemorrhage, aortic aneurysm, and aortic dissection.

#263

Treatment of Hypertension

#264

Lifestyle modifications such as exercise, weight loss, and dietary changes (such as sodium reduction) are an important component of managing hypertension.

#265

Fig. 1-23. Pharmacologic treatment of hypertension. Pharmacologic treatment of hypertension aims to ei­ ther decrease blood volume (diuretics) or decrease ar­ terial resistance. Decreasing arterial resistance can be accomplished by direct vasodilation (e.g., hydralazine, nitrates) or inhibition of vasoconstriction. Inhibition of vasoconstriction can be accomplished by blocking the sympathetic system (alpha blockers), blocking calcium-activated smooth muscle contraction (calcium channel blockers), blocking aldosterone (aldosterone antagonists, e.g., spironolactone), and/or blocking the renin-angiotensin system (ACE-inhibitors, angioten­ sin receptor blockers (ARBs)).

#266

CARDIAC INFECTION, INFLAMMATION, AND NE OPLASIA

#267

Fig. l-24. Sites of cardiac inflammation. Infection and inflammation of the heart can affect any of its three layers: endocardium, myocardium, pericardium.

#268

Endocarditis

#269

Endocarditis, inflammation of the endocardium, can result from noninfectious or infectious causes. Nonin­ fectious causes of endocarditis include hypercoagulable states (which can lead to thrombus formation on valves) and inflammatory conditions such as systemic lupus erythematosis. Lupus-induced endocarditis is called Lib man-Sacks endocarditis.

#270

Infection can occur on a native valve or a prosthetic valve. Any valvular disease can predispose to infectious endocarditis. Common bacterial causes of endocarditis include Streptococcus viridans and Staphylococcus au­ reus. The course of infective endocarditis can be acute or subacute, and symptoms generally include fever and a new heart murmur. Infectious emboli can form and lead to a pulmonary embolus (if the embolus comes from the right heart), or stroke, renal dysfunction, and/or periph­ eral vasculitic lesions (if the embolus comes from the left side). Blood cultures and echocardiography are used to confirm the diagnosis, demonstrating bacteremia and vegetations on the valve, respectively.

#271

IV drug abuse is a common cause of endocarditis. On which valve would you expect an IV drug abuser to have endocarditis? Drugs injected into the venous sys­ tem can cause infectious material to travel to the right heart, infecting the tricuspid (and/or more rarely the pulmonary) valve. Staphylococcus aureus is the most common cause of IV drug-related endocarditis.

#272

Treatment of infective endocarditis involves ex­ tended IV antibiotic therapy. If the damage to the valve is enough to induce heart failure, surgical re­ placement of the valve may be necessary.

#273

If a patient is known to have valvular pathology that could predispose to endocarditis (e.g., congenital lesion, rheumatic heart disease, prosthetic valve), an­ tibiotic prophylaxis is given prior to any procedure that could induce transient bacteremia (e.g., dental work, surgery).

#274

Rheumatic Fever and Rheumatic Heart Disease

#275

Acute rheumatic fever is a complication of Group A streptococcus infection of the upper respiratory tract. Due to what is thought to be an autoimmune response triggered by the bacterium, an inflammatory response occurs that can affect the heart, central nervous sys­ tem, skin, and joints. Acute rheumatic fever manifests as fever, joint pain, subcutaneous nodules, chorea (un­ controllable purposeless movements), and/or other motor disturbances occurring a few weeks after a sore throat. The long-term effects of the inflammation in the heart can include mitral stenosis and/or regurgi­ tation as well as aortic stenosis and/or regurgitation (rheumatic heart disease).

#276

Myocarditis

#277

Myocarditis can be caused by infection (Coxsackie B virus is the most common viral cause, though various other viruses, bacteria, and parasites can cause my­ ocarditis), inflammatory disease (e.g., lupus, dermato­ myositis), or toxins (e.g., drugs, radiation). Depending on the severity, any symptom/sign of congestive heart failure may be present. Treatment is directed toward the underlying cause and alleviating heart failure symptoms/signs if present.

#278

Pericarditis

#279

The heart is contained within the pericardia! sac. The visceral pericardium lines the outer surface of the heart and connects to the parietal pericardium, which forms the pericardia! sac.

#280

The pericardium can become inflamed (pericarditis) secondary to infectious or noninfectious causes. Infec­ tion can be caused by viruses (echovirus and Cox­ sackie B are the most common), tuberculosis, or bacteria (e.g., Streptococcus, Staphylococcus, gram negatives). Noninfectious causes of pericarditis in­ clude connective tissue diseases (e.g., lupus, rheuma­ toid arthritis), drugs, malignancy, renal failure, radiation, trauma to the heart, and myocardial infarc­ tion (Dressler's syndrome is the name given to post­ myocardial infarction pericarditis). Pericarditis can also occur idiopathically. Chest pain in pericarditis is pleuritic, meaning that it gets worse with deep inspi­ ration. The pain is often affected by position; it gets better when the patient leans forward and worse when the patient lies down. Patients with pericarditis

#281

are often febrile. On auscultation, one may hear a peri­ cardia[ rub, the sound of the inflamed pericardial lay­ ers rubbing against each other. Treatment depends upon the etiology: viral pericarditis is generally self­ limited, while bacterial pericarditis requires antibi­ otics and, often, drainage of infection from the pericardia! space. Treatment may also include anti-in­ flammatories such as aspirin.

#282

Constrictive pericarditis can be a consequence of any of the above etiologies of pericarditis. In constrictive pericarditis, the pericardium becomes rigid and impairs filling of the chambers of the heart. This leads to backup of flow and impaired forward flow, resulting in signs and symptoms similar to those in left and right heart failure. A classic sign of constrictive pericarditis is Kussmaul's sign: a rise in the JVP during inspiration. During inspi­ ration, the decrease in intrathoracic pressure brings blood into the heart. If constrictive pericarditis inhibits the right heart's ability to accept that blood, it will back up into the venous system, producing Kussmaul's sign. Often the pericardium must be surgically removed for definitive treatment of constrictive pericarditis.

#283

Any cause of pericarditis

#284

effusion, an accumulation of fluid in the pericardia! sac. If

#285

can also result in a pericardia[

#286

this happens rapidly (i.e., cardiac injury leading to bleed­ ing into the sac), it can cause tamponade, severe restric­ tion of cardiac motion, which is often fatal. Signs include hypotension (from decreased forward flow), increased JVP (from increased backup), and distant heart sounds (since the fluid in the pericardium muffles the sounds' transmission to the stethoscope). To treat tamponade, fluid is removed from the pericardia! space by needle as­ piration (pericardiocentesis ).

#287

If pericardia! effusion occurs over a more prolonged time course, gradual stretching of the pericardium can accommodate the effusion. If asymptomatic, the pa­ tient can be observed without intervention, but drainage of the fluid by pericardiocentesis or surgery (pericardia[ window) is necessary if hemodynamic compromise arises.

#288

Cardiac Neoplasia

#289

The most common neoplasias of the heart are metas­ tases. Metastases can affect the heart itself or the pericardium.

#290

Atrial Myxoma

#291

Atrial myxoma is the most common primary cardiac tumor. It is most commonly benign and found in the left atrium. Because these tumors tend to be shaped like a ball on the end of a stalk, they can "bob" around, causing intermittent, position-dependent symptoms (e.g., syncope, dyspnea). Emboli from the tumor can cause vascular occlusion (which could lead to stroke, mesenteric ischemia, renal ischemia, retinal artery occlusion). Constitutional symptoms (e.g., fever, fa­ tigue, weight loss) may also occur.

#292

If the myxoma is in the atrium, what type of mur­ mur would you expect it to cause? Atrial contraction occurs at the end of diastole, so an atrial tumor can cause a diastolic murmur. If the myxoma blocks the mitral valve, a diastolic rumble may be heard. The mo­ tion of the tumor on its pedicle can cause a "tumor plop" sound during diastole. The murmur caused by atrial myxoma can be position-dependent.

#293

Atrial myxomas are treated by surgical removal.

#294

CONG ENITAL HEART DISEASE

#295

The embryological development of the heart is com­ plex, and many errors can occur along the way: 8/1000 births have some type of congenital heart defect.

#296

Fetal Circulation

#297

Fig. 1-25. The fetal circulation. The fetal lungs are nonfunctional and mostly collapsed. After all, the fetus is bathed in fluid, so it would not do much good to have the lungs breathe. So how does the fetus get

#298

oxygenated blood? From the mother via the umbilical vein. It is called the umbilical vein because it is com­

#299

ing towards the baby's heart (remember artery =

#300

← Предишна страница

Следваща страница →

Минутку...