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Terms in this set (53)

Noninflammatory diarrhea is caused by the action of enterotoxins on the secretory mechanisms of the mucosa of the small intestine, without invasion. This leads to large volume watery stools in the absence of blood, pus, or severe abdominal pain. Occasionally, profound dehydration may result. The enterotoxins may be either preformed before ingestion or produced in the gut after ingestion. Examples include Vibrio cholerae, enterotoxic Escherichia coli, Clostridium perfringens, Bacillus cereus, [3] Staphylococcus organisms , Giardia lamblia, Cryptosporidium,rotavirus, norovirus (genus Norovirus, previously called Norwalk virus), and adenovirus.

Inflammatory diarrhea is caused by the action of cytotoxins on the mucosa, leading to invasion and destruction. The colon or the distal small bowel commonly is involved. The diarrhea usually is bloody; mucoid and leukocytes are present. Patients are usually febrile and may appear toxic. Dehydration is less likely than with noninflammatory diarrhea because of smaller stool volumes. Fecal leukocytes or a positive stool lactoferrin test indicates an inflammatory process, and sheets of leukocytes indicate colitis.

Sometimes, the organisms penetrate the mucosa and proliferate in the local lymphatic tissue, followed by systemic dissemination. Examples include Campylobacter jejuni, Vibrio parahaemolyticus, enterohemorrhagic and enteroinvasive E coli, Yersinia enterocolitica, Clostridium difficile, Entamoeba histolytica, and Salmonella and Shigella species.

In some types of food poisoning (eg, staphylococci, B cereus), vomiting is caused by a toxin acting on the central nervous system. The clinical syndrome of botulism results from the inhibition of acetylcholine release in nerve endings by the botulinum.

The pathophysiological mechanisms that result in acute GI symptoms produced by some of the noninfectious causes of food poisoning (naturally occurring substances [eg, mushrooms, toadstools] and heavy metals [eg, arsenic, mercury, lead]) are not well known.

A major contributor to seafood contamination with foodborne pathogens appears to be naturally occurring biofilm formation. [4] Vibro and Salmonella species, Aeromonas hydrophila, and Listeria monocytogenes are common seafood bacterial pathogens that form biofilms.Histamine fish poisoning is among the most common toxicities related to fish ingestion, constituting almost 40% of all seafood-related food-borne illnesses reported to the US Centers for Disease Control and Prevention (CDC). [1] Histamine fish poisoning results from the consumption of inadequately preserved and improperly refrigerated fish. It resembles an allergic reaction but is actually caused by bacterially-generated toxins in the fish's tissues. [2]

Previous terms for histamine fish poisoning were scombroid fish poisoning, pseudoallergic fish poisoning, histamine overdose, or mahi-mahi flush. The term scombroid was used because the first fish species implicated in this poisoning were from the suborder Scombridae, which includes mackerel, tuna, marlin, swordfish, albacore, bonito, skipjack, and almost 100 other species (Scombridae is derived from the Greek word scombros, which means mackerel or tunny).Typical manifestations of histamine fish poisoning include skin flushing on the upper half of the body, rash (see the image below), gastrointestinal (GI) complaints, and throbbing headache. [4] (See Presentation.) Generally, the diagnosis is made on clinical grounds; no laboratory tests are necessary. If confirmation is required, histamine levels in uneaten portions of the suspect fish can be measured. In addition, elevated histamine levels can be measured in patients' urine
Hashimoto thyroiditis is part of the spectrum of autoimmune thyroid diseases (AITDs) and is characterized by the destruction of thyroid cells by various cell- and antibody-mediated immune processes. This condition is the most common cause of hypothyroidism in the United States in individuals older than 6 years. CM: Early nonspecific symptoms may include the following: Fatigue, Constipation, Dry skin, Weight gain

More advanced/florid symptoms may include the following:Cold intolerance, Voice hoarseness and pressure symptoms in the neck from thyroid enlargement, Slowed movement and loss of energy, Decreased sweating, Mild nerve deafness, Peripheral neuropathy, Galactorrhea, Depression, dementia, and other psychiatric disturbances, Memory loss, Joint pains and muscle cramps, Hair loss, Menstrual irregularities, Sleep apnea and daytime somnolence
DX and TX: Physical findings are variable and depend on the extent of the hypothyroidism and other factors, such as age. Examination findings may include the following:

Puffy face and periorbital edema typical of hypothyroid facies
Cold, dry skin, which may be rough and scaly
Peripheral edema of hands and feet, typically nonpitting
Thickened and brittle nails (may appear ridged)
Bradycardia
Elevated blood pressure (typically diastolic hypertension)
Diminished deep tendon reflexes and the classic prolonged relaxation phase
Macroglossia
Slow speech
Ataxia

Testing

Laboratory studies and potential results for patients with suspected Hashimoto thyroiditis include the following:

Serum thyroid-stimulating hormone (TSH) levels: Sensitive test of thyroid function; levels are invariably raised in hypothyroidism due to Hashimoto thyroiditis and in primary hypothyroidism from any cause
Free T4 levels: Needed to correctly interpret the TSH in some clinical settings; low total T4 or free T4 level in the presence of an elevated TSH level further confirms diagnosis of primary hypothyroidism
T3 levels: Low T3 level and high reverse T3 level may aid in the diagnosis of nonthyroidal illness
Thyroid autoantibodies: Presence of typically anti-TPO (anti-thyroid peroxidase) and anti-Tg (anti-thyroglobulin) antibodies delineates the cause of hypothyroidism as Hashimoto thyroiditis or its variant; however, 10-15% of patients with Hashimoto thyroiditis may be antibody negative

The following tests are not necessary for the diagnosis of primary hypothyroidism but may be used to evaluate complications of hypothyroidism in some patients, as indicated:

Complete blood count: Anemia in 30-40% of patients with hypothyroidism
Total and fractionated lipid profile: Possibly elevated total cholesterol, LDL, and triglyceride levels in hypothyroidism
Basic metabolic panel: Decreased glomerular filtration rate, renal plasma flow, and renal free water clearance in hypothyroidism; may result in hyponatremia
Creatine kinase levels: Frequently elevated in severe hypothyroidism
Prolactin levels: May be elevated in primary hypothyroidism
Pharmacotherapy

The treatment of choice for Hashimoto thyroiditis (or hypothyroidism from any cause) is thyroid hormone replacement. The drug of choice is individually tailored and titrated levothyroxine sodium administered orally, usually for life.

Surgery

Indications for surgery include the following:

A large goiter with obstructive symptoms, such as dysphagia, voice hoarseness, and stridor, caused by extrinsic obstruction of airflow
Presence of a malignant nodule, as demonstrated by cytologic examination
Presence of a lymphoma diagnosed on fine-needle aspiration
Cosmetic reasons (eg, large, unsightly goiters)
Patients with venous leg ulcers commonly complain of swelling and aching of the legs that is worse at the end of the day and improves with leg elevation. The medial lower leg is the most common site. The borders of venous ulcers are typically saucer-shaped, initially with a shallow wound base. The surrounding skin often exhibits pitting edema, induration, hemosiderosis, varicosities, lipodermatosclerosis, atrophie blanche, and/or stasis dermatitis. Venous (or stasis) ulceration is initiated by venous hypertension that develops because of inadequate calf muscle pump action and after the onset of either primary (with no obvious underlying etiology) or secondary (as seen after deep venous thrombosis) valvular incompetence. Two hypotheses have been proposed to explain venous ulceration once venous hypertension develops.

The first states that distention of the capillary beds occurs because of increased stasis. This leads to leakage of fibrinogen into the surrounding dermis. Over time, a fibrinous pericapillary cuff is formed, impeding the delivery of oxygen and other nutrients or growth factors to the affected tissue. The resulting hypoxic injury leads to fibrosis and then ulceration.

The other hypothesis suggests that the endothelium is damaged by increased venous pressure and leukocyte activation. Proteolytic enzymes and free radicals are released, escape through the leaky vessel walls, and damage the surrounding tissue, leading to injury and ulceration.

In addition, studies have shown a relationship between obesity, chronic venous disease, and popliteal venous compression (PVC). [5] This syndrome may clarify the previously unexplained venous presentations. Other explanations of increased incidence of vascular ulcers in obese patients could be the direct result of intra-abdominal venous compression.

A study by Rasmussen et al using near-infrared fluorescence lymphatic imaging found impaired lymphatic function occurring early in the development of venous leg ulcers and revealed bilateral dermal backflow in the presence of chronic venous insufficiency, including in patients without ulcers in the contralateral limb. Venous ulcers

Venous ulceration (see image below) is commonly noted in the "gaiter" region of the legs. This region is located circumferentially around the lower leg from approximately mid calf to just below the medial and lateral malleoli. Larger but shallower than other ulcers, stasis ulcers have a moist granulating base and an irregular border. This base oozes venous blood when manipulated. The tissue surrounding these ulcers may exhibit signs of stasis dermatitis. Patients often report mild pain that is relieved by elevation.
RSV can spread when an infected person coughs or sneezes. You can get infected if you get droplets from the cough or sneeze in your eyes, nose, or mouth, or if you touch a surface that has the virus on it, like a doorknob, and then touch your face before washing your hands. Additionally, it can spread through direct contact with the virus, like kissing the face of a child with RSV.

People infected with RSV are usually contagious for 3 to 8 days. However, some infants, and people with weakened immune systems, can continue to spread the virus even after they stop showing symptoms, for as long as 4 weeks. Children are often exposed to and infected with RSV outside the home, such as in school or child-care centers. They can then transmit the virus to other members of the family.

RSV can survive for many hours on hard surfaces such as tables and crib rails. It typically lives on soft surfaces such as tissues and hands for shorter amounts of time.

People of any age can get another RSV infection, but infections later in life are generally less severe. People at highest risk for severe disease include

premature infants
young children with congenital heart or chronic lung disease
young children with compromised (weakened) immune systems due to a medical condition or medical treatment
adults with compromised immune system
older adults, especially those with underlying heart or lung disease

In the United States and other areas with similar climates, RSV infections generally occur during fall, winter, and spring. The timing and severity of RSV circulation in a given community can vary from year to year. Symptoms of RSV infection usually include

Runny nose
Decrease in appetite
Coughing
Sneezing
Fever
Wheezing
Most RSV infections go away on their own in a week or two. Fever and pain can be managed with over-the-counter fever reducers and pain relievers, such as acetaminophen or ibuprofen, with a healthcare provider's approval. It is important for people with RSV infection to drink enough fluids to prevent dehydration (loss of body fluids). A drug called palivizumab (pah-lih-VIH-zu-mahb) is available to prevent severe RSV illness in certain infants and children who are at high risk. The drug can help prevent development of serious RSV disease, but it cannot help cure or treat children already suffering from serious RSV disease, and it cannot prevent infection with RSV. If your child is at high risk for severe RSV disease, talk to your healthcare provider to see if palivizumab can be used as a preventive measure
Angina pectoris is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand. It is a common presenting symptom (typically, chest pain) among patients with coronary artery disease (CAD). Approximately 9.8 million Americans are estimated to experience angina annually, with 500,000 new cases of angina occurring every year.
Signs and symptoms

Patients should be asked about the frequency of angina, severity of pain, and number of nitroglycerin pills used during episodes. Symptomatology reported by patients with angina commonly includes the following:

Retrosternal chest discomfort (pressure, heaviness, squeezing, burning, or choking sensation) as opposed to frank pain
Pain localized primarily in the epigastrium, back, neck, jaw, or shoulders
Pain precipitated by exertion, eating, exposure to cold, or emotional stress, lasting for about 1-5 minutes and relieved by rest or nitroglycerin
Pain intensity that does not change with respiration, cough, or change in position
Diagnostic studies that may be employed include the following:

Chest radiography: Usually normal in angina pectoris but may show cardiomegaly in patients with previous MI, ischemic cardiomyopathy, pericardial effusion, or acute pulmonary edema
Graded exercise stress testing: This is the most widely used test for the evaluation of patients presenting with chest pain and can be performed alone and in conjunction with echocardiography or myocardial perfusion scintigraphy
Coronary artery calcium (CAC) scoring by fast CT: The primary fast CT methods for this application are electron-beam CT (EBCT) and multidetector CD (MDCT)

Other tests that may be useful include the following:

ECG (including exercise with ECG monitoring and ambulatory ECG monitoring)
Selective coronary angiography (the definitive diagnostic test for evaluating the anatomic extent and severity of CAD)
In high-risk patients, a serum LDL cholesterol level of less than 100 mg/dL is the goal
In very high-risk patients, an LDL cholesterol level goal of less than 70 mg/dL is a therapeutic option
In moderately high-risk persons, the recommended LDL cholesterol level is less than 130 mg/dL, but an LDL cholesterol level of 100 mg/dL is a therapeutic option
Non-high-density lipoprotein (HDL) cholesterol level is a secondary target of therapy in persons with high triglyceride levels (>200 mg/dL); the goal in such persons is a non-HDL cholesterol level 30 mg/dL higher than the LDL cholesterol level goal Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand. This causes myocardial cells to switch from aerobic to anaerobic metabolism, with a progressive impairment of metabolic, mechanical, and electrical functions. Angina pectoris is the most common clinical manifestation of myocardial ischemia. It is caused by chemical and mechanical stimulation of sensory afferent nerve endings in the coronary vessels and myocardium. These nerve fibers extend from the first to fourth thoracic spinal nerves, ascending via the spinal cord to the thalamus, and from there to the cerebral cortex. Studies have shown that adenosine may be the main chemical mediator of anginal pain. During ischemia, ATP is degraded to adenosine, which, after diffusion to the extracellular space, causes arteriolar dilation and anginal pain. Adenosine induces angina mainly by stimulating the A1 receptors in cardiac afferent nerve endings. [6]

Heart rate, myocardial inotropic state, and myocardial wall tension are the major determinants of myocardial metabolic activity and myocardial oxygen demand. Increases in the heart rate and myocardial contractile state result in increased myocardial oxygen demand. Increases in both afterload (ie, aortic pressure) and preload (ie, ventricular end-diastolic volume) result in a proportional elevation of myocardial wall tension and, therefore, increased myocardial oxygen demand. Oxygen supply to any organ system is determined by blood flow and oxygen extraction. Because the resting coronary venous oxygen saturation is already at a relatively low level (approximately 30%), the myocardium has a limited ability to increase its oxygen extraction during episodes of increased demand. Thus, an increase in myocardial oxygen demand (eg, during exercise) must be met by a proportional increase in coronary blood flow.

The ability of the coronary arteries to increase blood flow in response to increased cardiac metabolic demand is referred to as coronary flow reserve (CFR). In healthy people, the maximal coronary blood flow after full dilation of the coronary arteries is roughly 4-6 times the resting coronary blood flow. CFR depends on at least 3 factors: large and small coronary artery resistance, extravascular (ie, myocardial and interstitial) resistance, and blood composition.

Myocardial ischemia can result from (1) a reduction of coronary blood flow caused by fixed and/or dynamic epicardial coronary artery (ie, conductive vessel) stenosis, (2) abnormal constriction or deficient relaxation of coronary microcirculation (ie, resistance vessels), or (3) reduced oxygen-carrying capacity of the blood.

Atherosclerosis is the most common cause of epicardial coronary artery stenosis and, hence, angina pectoris. Patients with a fixed coronary atherosclerotic lesion of at least 50% show myocardial ischemia during increased myocardial metabolic demand as the result of a significant reduction in CFR. These patients are not able to increase their coronary blood flow during stress to match the increased myocardial metabolic demand, thus they experience angina. Fixed atherosclerotic lesions of at least 90% almost completely abolish the flow reserve; patients with these lesions may experience angina at rest.

Coronary spasm can also reduce CFR significantly by causing dynamic stenosis of coronary arteries. Prinzmetal angina is defined as resting angina associated with ST-segment elevation caused by focal coronary artery spasm. Although most patients with Prinzmetal angina have underlying fixed coronary lesions, some have angiographically normal coronary arteries. Several mechanisms have been proposed for Prinzmetal angina: focal deficiency of nitric oxide production, [7] hyperinsulinemia, low intracellular magnesium levels, smoking cigarettes, and using cocaine.

Approximately 30% of patients with chest pain referred for cardiac catheterization have normal or minimal atherosclerosis of coronary arteries. A subset of these patients demonstrates reduced CFR that is believed to be caused by functional and structural alterations of small coronary arteries and arterioles (ie, resistance vessels). Under normal conditions, resistance vessels are responsible for as much as 95% of coronary artery resistance, with the remaining 5% being from epicardial coronary arteries (ie, conductive vessels). The former is not visualized during regular coronary catheterization. Angina due to dysfunction of small coronary arteries and arterioles is called microvascular angina. Several diseases, such as diabetes mellitus, hypertension, and systemic collagen vascular diseases (eg, systemic lupus erythematosus, polyarteritis nodosa), are believed to cause microvascular abnormalities with subsequent reduction in CFR.

The syndrome that includes angina pectoris, ischemialike ST-segment changes and/or myocardial perfusion defects during stress testing, and angiographically normal coronary arteries is referred to as syndrome X. Most patients with this syndrome are postmenopausal women, and they usually have an excellent prognosis. [8] Syndrome X is believed to be caused by microvascular angina. Multiple mechanisms may be responsible for this syndrome, including (1) impaired endothelial dysfunction, [9] (2) increased release of local vasoconstrictors, (3) fibrosis and medial hypertrophy of the microcirculation, (4) abnormal cardiac adrenergic nerve function, and/or (5) estrogen deficiency. [10]

A number of extravascular forces produced by contraction of adjacent myocardium and intraventricular pressures can influence coronary microcirculation resistance and thus reduce CFR. Extravascular compressive forces are highest in the subendocardium and decrease toward the subepicardium. Left ventricular (LV) hypertrophy together with a higher myocardial oxygen demand (eg, during tachycardia) cause greater susceptibility to ischemia in subendocardial layers.

Myocardial ischemia can also be the result of factors affecting blood composition, such as reduced oxygen-carrying capacity of blood, as is observed with severe anemia (hemoglobin, <8 g/dL), or elevated levels of carboxyhemoglobin. The latter may be the result of inhalation of carbon monoxide in a closed area or of long-term smoking.

Ambulatory ECG monitoring has shown that silent ischemia is a common phenomenon among patients with established coronary artery disease. In one study, as many as 75% of episodes of ischemia (defined as transient ST depression of 1 mm or above persisting for at least 1 min) occurring in patients with stable angina were clinically silent. Silent ischemia occurs most frequently in early morning hours and may result in transient myocardial contractile dysfunction (ie, stunning). The exact mechanism(s) for silent ischemia is not known. However, autonomic dysfunction (especially in patients with diabetes), a higher pain threshold in some individuals, and the production of excessive quantities of endorphins are among the more popular hypotheses. [11]
referred to as trigeminal autonomic cephalagia and occur primarily in men between 20-50. occur in cluster followed by remission. triggers similar to migraines. the rhythmicity of attacks is associated with changes in the inferior posterior hypothalamus. there may be altered serotonergic nerve transmission. sudden onset with unilateral tearing and buring, periorbital and retrobulbar or temporal pain lasting 30 min to 2 hrs. A cluster headache commonly awakens you in the middle of the night with intense pain in or around one eye on one side of your head. A cluster headache strikes quickly, usually without warning, although you might first have migraine-like nausea and aura. Common signs and symptoms during a headache include:

Excruciating pain, generally situated in or around one eye, but may radiate to other areas of your face, head, neck and shoulders
One-sided pain
Restlessness
Excessive tearing
Redness in your eye on the affected side
Stuffy or runny nose on the affected side
Forehead or facial sweating
Pale skin (pallor) or flushing on your face
Swelling around your eye on the affected side
Drooping eyelid
The exact cause of cluster headaches is unknown, but cluster headache patterns suggest that abnormalities in the body's biological clock (hypothalamus) play a role.

Unlike migraine and tension headache, cluster headache generally isn't associated with triggers, such as foods, hormonal changes or stress.

Once a cluster period begins, however, drinking alcohol may quickly trigger a splitting headache. For this reason, many people with cluster headache avoid alcohol during a cluster period.

Other possible triggers include the use of medications such as nitroglycerin, a drug used to treat heart disease.
can treat with calcium channel blocker, corticosteroids, lithium carbonate, melatonin