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HESI Pathophysiology Final
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Terms in this set (35)
Normal values — The range of normal values varies among laboratories. In general, normal values for acidity (pH), the partial pressure of carbon dioxide (PaCO2) and bicarbonate concentration (HCO3) are as follows:
●pH - 7.35 to 7.45
●PaCO2 - 35 to 45 mmHg (4.7 to 6 kPa)
●HCO3 - 21 to 27 mEq/L
excess CO2 retention, pH <7.35, HCo3 >45, PaCO2 >45
S/S: anxiety, apprehension, confusion/coma, excessive sweating, headache, restlessness, tachycardia
excess CO2 excretion, pH >7.45, HCO3 <35, PaCO2 <35
S/S: anxiety, fear, lightheadedness, paresthesias, rapid deep breathing, twitching
HCO3 loss and acid retention, pH <7.35, HCO3<22, PaCO2 >35
S/S: coma (in severe cases), drowsiness, fatigue, fruity breath (if DKA), headache, lethargy, nausea, rapid deep breathing, vomiting.
HCO3 retention, acid loss, pH>77.45, HCO3 >28, PaCO2 > 45
S/S: coma (in severe cases), confusion, irritability, hypertonic muscles, mental apathy, restlessness, seizures, slow shallow breathing, tetany, twitching
●An unsalvageable extremity due to critical limb ischemia in patients with vascular disease. Primary amputation may be the only option for patients without an anatomic option for revascularization or those with medical risk factors that contraindicate revascularization.
•Peripheral artery disease.
•Acute arterial thrombosis or thromboembolism.
●Trauma resulting in a mangled extremity or failed attempt at limb salvage.
●Severe infections with extensive soft tissue or bony destruction, or osteomyelitis.
●Locally unresectable malignant tumors of the musculoskeletal system .
●Failed management of acute compartment syndrome.
●Failed management of Charcot's degenerative osteoarthropathy.
●Debilitating extremity paralysis, which can be unilateral but is frequently bilateral (eg, paraplegia), from infection or pressure-related complications.
Amputation Medical Risks
●Myocardial infarction is the most common cause of death following lower extremity amputation in patients with peripheral artery disease
●Pulmonary complications, including atelectasis and pneumonia, complicate 5 percent of major lower extremity amputations
●The incidence of new-onset renal failure after a lower extremity major amputation is 0.6 to 2.6 percent. Renal failure is associated with increased operative and long-term mortality
-Deep vein thrombosis — Deep vein thrombosis (DVT) has been reported in up to 50 percent of patients following major lower extremity amputation without prophylaxis . The incidence of deep vein thrombosis is higher for above-knee amputation compared with below-knee amputation (37.5 versus 21.2 percent, respectively) . This difference may contribute to the increased incidence of sudden death due to thromboembolism in patients with above-knee amputation. Thus, it is important to provide thromboprophylaxis. (See 'Thromboprophylaxis' above and 'Perioperative mortality' below.)
-Stump hematoma — Postoperative bleeding that requires reoperation occurs in 3 to 9 percent of major lower extremity amputations, and stump hematoma may lead to stump wound breakdown [9,48]. Patients on antithrombotic therapy, including DVT prophylaxis, are at a higher risk for stump hematoma. Patients with stump hematoma causing pain and stump swelling with or without drainage should have the wound opened partially, the hematoma evacuated, and the wound washed out and packed with a moist saline dressing.
-Infection — Wound infection following major lower extremity amputation occurs in 13 to 40 percent of patients [26,27,49]. Patients with diabetes, preoperative wound infection, malnutrition, malignancy, advanced age, wound hematoma, and prior prosthetic bypass grafts have an increased risk for stump wound infection. In patients with prior lower extremity bypass graft, stump infection rates are reduced by complete removal of synthetic graft material .
-Superficial wound infections are treated by removing the skin sutures and initiating broad-spectrum antibiotics, which are adapted to reflect the results of wound culture and sensitivities. Deeper wound infection requires operative management with removal of skin and fascial sutures, drainage and washout of the wound, and debridement of any nonviable tissue (picture 1).
-Need for re-amputation — The rate of revision following major amputation remains high despite the availability of a variety of methods to select amputation level.
-Phantom limb pain — True phantom limb pain is a complex, poorly understood pain syndrome that is described as burning, aching, or electric-type pain in the amputated limb . There is no clear consensus on the mechanisms of this disorder and no standard treatment . The diagnosis of phantom pain should only be made after other causes of stump pain have been eliminated, including ischemia, infection, neuroma, and pressure-related wounds. (See 'Stump pain' above.)
-Flexion contracture — Flexion contracture at the hip or knee joint (15° limitation) occurs in 3 to 5 percent of major lower extremity amputations. Although up to 15° hip contracture can be accommodated with prosthetic alignment, a more than 25° contracture will cause compensatory lumbar lordosis, leading to low back pain. Contractures are more likely to develop in older patients, particularly those with dementia or prior ipsilateral stroke. Failure to provide adequate postoperative analgesia may also result in flexion contracture. Once a significant contracture develops, it may not be possible to correct it with physical therapy or surgery .
Hip flexion contracture can be retarded with prone positioning; however, patients may not tolerate this position.
◾The major elements of the neurologic examination include mental status, cranial nerves, motor, reflex, and sensory examinations. A screening neurologic examination assesses general aspects of these five spheres and can be performed in five minutes or less
◾Mental status — Test patients for orientation to person, place, and time. Make sure they can follow at least one complicated command, taking care not to give them any nonverbal cues. If their responses are appropriate and they are able to relate a detailed and coherent medical history, no further mental status testing is necessary
◾Cranial nerves — Test visual fields in one eye, both pupillary responses to light, eye movements in all directions, facial strength, and hearing to finger rub.
◾Motor system — Test strength in the following muscles bilaterally: deltoids, triceps, wrist extensors, hand interossei, iliopsoas, hamstrings, ankle dorsiflexors. Test for a pronator drift. Test finger tapping, finger-to-nose, and heel-knee-shin performance. Test tandem gait and walking on the heels.
◾Reflexes — Test plantar responses and biceps, triceps, patellar, and ankle reflexes bilaterally.
◾Sensation — Test light touch sensation in all four distal limbs, including double simultaneous stimulation. Test vibration sense at the great toes.
Mental Status Exam
◾Level of consciousness (arousal)
◾Attention and concentration
◾Memory (immediate, recent, and remote)
◾Visual spatial perception
◾Mood and thought content
is a common clinical condition characterized by -cough, with or without sputum production, which lasts for at least five days. It is typically self-limited, resolving within one to three weeks. Symptoms result from inflammation of the lower respiratory tract and are most frequently due to viral infection.
-Viruses are the most commonly identified pathogens in patients with acute bronchitis
Bronchitis Clinical Features
Cough is the cardinal symptom in patients presenting with acute bronchitis. By definition, the cough lasts at least 5 days, although, in most patients, it persists for 1 to 3 weeks, with a median duration of 18 days [3,12,26]. The cough may be associated with either purulent or nonpurulent sputum production [3,27]. The presence of purulent sputum is a nonspecific finding and does not appear to be predictive of bacterial infection or response to antibiotics [28,29].
Upper respiratory tract infection (eg, common cold) can precede the onset of acute bronchitis. During the first few days of illness, symptoms associated with these two conditions such as headache, nasal congestion, and sore throat can overlap [3,27]. With involvement of the lower respiratory tract, cough becomes the predominant symptom.
Wheezing and mild dyspnea may accompany the cough. Both wheezing and rhonchi may be auscultated on physical examination; rhonchi usually clear with coughing. Although pulmonary function testing is typically not indicated in clinical practice, bronchospasm, evidenced by reduced FEV1, has been reported in 40 percent of patients in a small case series , and bronchial hyperreactivity can be demonstrated with provocative testing . Bronchial hyperresponsiveness is typically transient, resolving in six weeks, and is believed to be the mechanism that underlies the persistent cough [7,30].
With prolonged coughing, chest wall or substernal musculoskeletal pain can occur [3,27]. Other complications are rare; most common among them are the development of pneumonia or bacterial superinfection. For most patients, acute bronchitis is a self-limited illness that does not require specific diagnostic testing or treatment.
Certain clinical features suggest a specific cause or an alternate diagnosis that may require antimicrobial therapy (table 1). For example, paroxysms of cough accompanied by an inspiratory whoop or posttussive emesis suggest pertussis, particularly during known outbreaks. Fever, or other systemic symptoms, are rare in patients with acute bronchitis. These findings, in addition to cough and sputum production, should raise suspicion for influenza or pneumonia. On physical examination, signs of parenchymal consolidation such as dullness to percussion, decreased or bronchial breath sounds, rales, egophony, or signs of pleural inflammation such as a pleural rub suggest that disease extends beyond the bronchi, and chest imaging should be considered.
Acute bronchitis should be suspected in patients with cough for at least five days (often one to three weeks) who do not have clinical findings suggestive of pneumonia (eg, fever, tachypnea, rales, signs of parenchymal consolidation) and do not have chronic obstructive pulmonary disease. For most patients, the diagnosis can be made based upon the history and physical examination. Testing is generally reserved for cases in which pneumonia is suspected, clinical diagnosis is uncertain, or when results would change management (eg, a positive influenza test result in a patient who meets criteria for antiviral therapy).
Chest radiograph — Chest radiographs are unlikely to change management for most patients with acute cough [31,32]. In patients with acute bronchitis, chest radiographs are either normal or findings are nonspecific, though subtle changes consistent with thickening of the bronchial walls in the lower lobes are occasionally reported .
The primary reason for obtaining a chest radiograph is to exclude pneumonia; reasonable indications for suspecting pneumonia and obtaining imaging include the following [33-39]:
●Abnormal vital signs (pulse >100/minute, respiratory rate >24 breaths/minute, temperature >38°C [100.4°F], or oxygen saturation <95 percent)
●Signs of consolidation on chest examination (rales, egophony, or tactile fremitus)
●Mental status or behavioral changes in patients >75 years old, who may not mount a fever
Additional factors, such as moderate or severe dyspnea, hemoptysis, immunocompromise, older age, and/or dementia, raise the likelihood of pneumonia or other underlying pulmonary disorders. The decision to obtain a chest radiograph or other imaging should always take the full clinical picture into consideration
For most patients with acute bronchitis, symptoms are self-limited, resolving in about one to three weeks. Reassurance and symptom control are the cornerstones of care. Antibiotics are not recommended for routine use [1,50-52].
Patient education — We suggest having a discussion on the expected course of illness and treatment plan with all patients. Reassuring patients that acute bronchitis is a self-limited illness that typically resolves in one to three weeks without specific therapy can help improve patient satisfaction and reduce inappropriate antibiotic use
●Nonpharmacologic therapy - For patients with acute bronchitis who are bothered by cough, offering nonpharmacologic options for cough relief such as throat lozenges, hot tea, honey, and/or smoking cessation or avoidance of secondhand smoke is a reasonable first step. Although these interventions have not been directly evaluated in clinical trials, they may provide some benefit and expected harms are small. (See "Treatment of subacute and chronic cough in adults" and "Overview of smoking cessation management in adults".)
●Pharmacologic therapy - For patients with acute bronchitis who desire medication for cough relief, we suggest offering over-the-counter (OTC) medications, such as dextromethorphan or guaifenesin. Selection of an OTC medication should take into account patient comorbidities and drug interactions. As an example, selective serotonin reuptake inhibitors (SSRIs) may enhance the serotonergic effect of dextromethorphan (eg, precipitate serotonin syndrome). Although the benefits of these medications for symptom improvement in patients with acute bronchitis are uncertain, multiple clinical practice guidelines suggest that offering medications for symptom relief may help reduce requests for antibiotics
Coronary Artery Disease Pathological Risk Factors
●Overweight and obesity
●Diabetes mellitus (considered in some guidelines as a coronary heart disease [CHD] risk equivalent)
In adults, recurrent infections are usually due to an anatomic lesion, a functional disorder, or to a secondary cause of immunosuppression.
It is helpful to consider the following broad categories of etiologies when evaluating an adult with recurrent infections:
●Anatomic lesions, whether congenital or acquired, and disorders affecting the function of specific organs are important causes of recurrent infections in adults (table 1).
●Secondary immune disorders due to other medical conditions or treatments for these conditions are a much more common cause of recurrent infections than primary immunodeficiencies (table 2). (See 'Secondary immunodeficiency' below.)
●Most congenital (primary) immunodeficiencies do not present in adulthood but rather are diagnosed in infancy or childhood, because patients with these disorders often require repeated hospitalizations for serious infections at an early age and may develop growth retardation from chronic and recurrent illnesses [1-4]. However, the number of recognized immunodeficiencies has expanded dramatically in recent decades, and primary immunodeficiency is probably not as rare as previously thought. In addition, there are increasing reports of milder phenotypes of disorders that were previously recognized only in the most severe forms (eg, DiGeorge syndrome).
Chronic Kidney Disease Patho
All patients with renal disease (whether acute or chronic) should undergo an assessment of renal function by estimating the glomerular filtration rate (GFR) from the serum creatinine. This measurement is used clinically to evaluate the degree of renal impairment, to follow the course of the disease, and to assess the response to therapy. An attempt must also be made to obtain a specific diagnosis. The first step in this process is a careful urinalysis, looking for proteinuria, hematuria, and cellular casts. Further evaluation may include quantification of proteinuria, kidney ultrasound, referral to a nephrologist, and a kidney biopsy. Nephrology referral is especially indicated when there is a rapid decline in kidney function, an elevated albumin-to-creatinine ratio (>300 mg/g), or urinary red blood cell casts
Chronic Kidney Disease Lab Values
In routine practice, therefore, individuals who have an eGFR below 60 mL/min per 1.73 m2 are defined as having CKD. These individuals have a significantly increased risk for all-cause and cardiovascular mortality, ESRD, AKI and CKD progression in compared with those whose eGFR is 60 mL/min per 1.73 m2 or higher (figure 2 and figure 3), even if the ACR is normal [12,14-16,24].
GFR — The glomerular filtration rate (GFR; G-stages) follow the original CKD classification scheme
●G1 − GFR >90 mL/min per 1.73 m2
●G2 − GFR 60 to 89 mL/min per 1.73 m2
●G3a − GFR 45 to 59 mL/min per 1.73 m2
●G3b − GFR 30 to 44 mL/min per 1.73 m2
●G4 − GFR 15 to 29 mL/min per 1.73 m2
●G5 − GFR <15 mL/min per 1.73 m2 or treatment by dialysis
Colon Cancer Signs and Symptoms
Typical symptoms/signs associated with CRC include hematochezia or melena, abdominal pain, otherwise unexplained iron deficiency anemia, and/or a change in bowel habits [8-13]. Less common presenting symptoms include abdominal distention, and/or nausea and vomiting, which may be indicators of obstruction.
Colon Cancer Diagnosis
Colonoscopy is the most accurate and versatile diagnostic test for CRC, since it can localize and biopsy lesions throughout the large bowel, detect synchronous neoplasms, and remove polyps
consists of upper-extremity adduction and flexion at the elbows, wrists, and fingers, together with lower-extremity extension, which includes extension and adduction at the hip, extension at the knee, and plantar flexion and inversion at the ankle (figure 2). This occurs with dysfunction at the cerebral cortical level or below and may reflect a "release" of other spinal pathways.
Flexion and extension movements usually represent reflex responses arising from subcortical structures
In general, patients with decorticate posturing in response to pain have a better prognosis than those with decerebrate posturing
are swollen blood vessels in the esophagus and often happen to patients with cirrhosis.
S/S: vomiting blood, dark-colored or black bowl movements, bloody bowel movements or diarrhea, feeling lightheaded, passing out.
DX: upper endoscopy
Treatment: taking beta-blockers, losing weight, avoiding alcohol, taking PPI if variceal band ligation done.
Food Poisoning- Fish
As world travel and trade grow, physicians are increasingly likely to encounter patients poisoned by marine toxins. The world's oceans harbor hundreds of different types of marine toxins, and the epidemiology and clinical manifestations of these toxins vary widely. Several of these toxins are produced by dinoflagellates or phytoplankton during algae or marine diatom blooms. Shellfish and pufferfish poisoning arise from consumption of seafood that is contaminated by various toxins (table 1) [1-3]. In most instances the ingested seafood smells, appears, and tastes normal. Clinical features of the most common forms of shellfish or pufferfish poisoning typically develop within minutes to hours of ingestion. A food history that identifies ingestion of seafood commonly associated with the specific toxin, clinical features consistent with the specific poisoning, and detection of elevated levels of the toxin in the ingested seafood provides the diagnosis. Treatment is supportive.
Foodborne Illness Causes
-Salmonella is very common in the intestines of animals and reptiles and often exists in the environment. When food is contaminated from the environment or from contact with animals, it can make humans sick when they subsequently consume that food. Contamination of food can occur on a farm, during food processing, or as a result of cross-contamination (transfer from raw meat to salad) in the home, at a restaurant, or at some other point in the supply chain. Thus, most cases of Salmonella food poisoning are due to either cross-contamination or undercooking of raw meat or poultry products or contamination of fresh produce. However, there have also been large outbreaks of Salmonella from unusual foods, such as peanut butter.
-Escherichia coli — Escherichia coli is a common cause of food poisoning and traveler's diarrhea. Infection with E. coli can occur when food or water becomes contaminated with bacteria from infected feces. Some types of E. coli infection can be very serious, resulting in kidney failure or worse
-Hepatitis A virus is transmitted in foods contaminated by an infected human such as a food handler or from raw shellfish. Symptoms do not usually appear until 15 to 50 days after infection, which can make it difficult to determine the source of infection. In nonimmune individuals, post-exposure administration of passive immune globulin might prevent or mitigate clinical infection
-Norovirus infection is the most common foodborne illness and is often acquired when infected food handlers contaminate the food they are preparing (eg, in restaurants). Norovirus is very infectious and easily passed from person to person. Symptoms usually start 24 to 48 hours after exposure with nausea, vomiting, diarrhea, and abdominal pain. Most cases resolve without medical treatment.
-Listeria monocytogenes — Listeria is a bacteria that has traditionally been found in unpasteurized or contaminated milk, soft cheese, and other dairy products or in contaminated processed/delicatessen meats, hot dogs, and smoked seafood. More recently, Listeria monocytogenes has been found in a variety of other ready-to-eat foods such as hummus, sunflower seeds, and frozen vegetables. Listeria infection may cause gastrointestinal symptoms, which usually develop within 24 hours and include fever, watery diarrhea, nausea, vomiting, headache, and pains in joints and muscles. A much more serious infection, known as listeriosis, may occur one to three weeks later if the bacteria invade the bloodstream. Listeriosis can occur without any of the gastrointestinal symptoms. Listeriosis is usually seen in pregnant women or older adults and the immunocompromised
Food Poisoning Risk Factors
●A weakened immune system - The immune system plays a major role in protecting against a foodborne illness; when your immune system is weakened, you become more vulnerable. A healthcare provider should be able to provide guidance on whether you fall into this group. A few examples of people with a weakened immune system include the very young, older adults, people with chronic disease, pregnant women, and people who take certain types of medication that reduce the ability to fight off foodborne infections.
●Improper food storage or handling, leaving prepared food at room temperature for more than two hours, or improperly cooking or reheating food increase the risk of food poisoning. Use a food thermometer to check internal temperatures of meat, poultry, and seafood before eating them to make sure they are properly cooked. Food should not be left out for more than two hours at room temperature. The "best before" or "use by" dates printed on food are markers of quality, not safety, and should not be used to determine if a food is "safe" to eat. Just because a food looks and smells okay does not mean that it is safe to eat.
●Cross-contamination of food can occur when one contaminated food touches another or when a food comes in contact with a contaminated food preparation surface, such as a counter or cutting board. Keep foods like meat, poultry, and raw fish separate from foods that will not be cooked, such as salads.
●Anyone who handles food should wash their hands before handling food and after using the bathroom, changing diapers, or handling pets. It is easy to pass microbes from the hands into food. Food handlers who fail to wash their hands after using the bathroom can contaminate food with fecal microorganisms.
Food Poisoning S/S
●Diarrhea, which may be watery or bloody
Less commonly, neurologic symptoms develop, such as blurry vision, dizziness, or tingling in the arms. In some instances, the most life-threatening problems occur several days after the start of intestinal symptoms, and these can include kidney failure, meningitis, arthritis, and paralysis, depending on which foodborne microbe you have been exposed to.
Food Poisoning Treatment
In most cases of food poisoning, treatment is primarily supportive. Supportive treatment includes drinking adequate fluids, eating small, low-fat meals, and resting as needed.
Antibiotics are not usually needed or recommended but may be used for some types of food poisoning. In most cases, symptoms resolve quickly and no special treatment is necessary. In people with persistent diarrhea and/or vomiting, intravenous fluids may be needed to prevent dehydration. Antidiarrheal medications (eg, Imodium, Pepto-Bismol) are not generally recommended
caused by glomerular inflammation that results in hematuria, variable degrees of proteinuria (which can sometimes be in the nephrotic range), and leukocyturia in the absence of urinary tract infection. Such patients may also have hypertension, renal insufficiency, and, if the inflammation is not limited to the kidney, findings that suggest involvement of other organ systems (eg, pulmonary hemorrhage, palpable purpura, arthritis). Glomerular inflammation is typically due to one of three major mechanisms
Glomerulonephritis can present in a variety of ways, including a smoldering course characterized by a chronic, slowly progressive rise in serum creatinine and proteinuria (eventually leading to advanced chronic kidney disease and end-stage renal disease), an acute, self-limited course, and a fulminant course with acute, progressive deterioration of kidney function. This last pattern is referred to as "rapidly progressive glomerulonephritis" and is typically associated with extensive crescents on the kidney biopsy.
●Metabolic, genetic, and other factors that result in hyperuricemia (see 'Hyperuricemia and gout' below)
●Physiologic, metabolic, and other characteristics responsible for crystal formation (see 'Hyperuricemia and gout' below and 'Crystals' below)
●Cellular and soluble inflammatory and innate immune processes and characteristics of monosodium urate (MSU) crystals themselves that promote the acute inflammatory response to MSU crystals (see 'Acute inflammation' below and 'Initiation of acute MSU crystal-induced inflammation' below and 'Amplification of acute MSU crystal-induced inflammation' below)
●Immune mechanisms and other factors that mediate the resolution of acute inflammation (see 'Resolution of acute MSU crystal-induced inflammation' below)
●Chronic inflammatory processes and the effects of crystals and immune cells on osteoclasts, osteoblasts, and chondrocytes that contribute to the formation of tophi and to bone erosion, cartilage attrition, and joint injury (see 'The tophus' below and 'Chronic gouty arthropathy' below
Heart Failure Exacerbation causes and precipitating factors
1.Coronary artery disease:
a) Acute coronary syndrome
-Ventricular septal rupture
3. Acute valve syndromes:
•Acute mitral or aortic regurgitation secondary to infective endocarditis, ruptured chordae of a degenerative mitral valve, ischemic papillary muscle rupture, or aortic dissection
•Thrombosed mechanical aortic or mitral valve
•Tear or perforation of a bioprosthetic aortic or mitral valve leaflet
4. Progressive valve disease:
•Severe aortic or mitral valve stenosis, including left atrial myxoma
•Severe aortic or mitral regurgitation
5. Cardiomyopathic states:
•Recent onset dilated cardiomyopathy
•Tachycardia mediated cardiomyopathy
•Stress (takotsubo) cardiomyopathy
6. Poorly controlled hypertension:
•Bilateral renal artery stenosis
Decompensation of chronic HF can occur without known precipitant factors but more often occurs with one or more factors, such as infection, uncontrolled hypertension, rhythm disturbances, and nonadherence with drugs and diet.
B cells from thyroid tissue of patients with Hashimoto's thyroiditis are activated, as indicated by their ability to secrete thyroid antibodies spontaneously in vitro. T cells in patients with Hashimoto's thyroiditis react with processed thyroid antigens and peptides derived from these antigens. These activated T cells secrete cytokines which themselves activate a variety of other immune cells. T cells have three major roles in this disease: a role in antibody production (a Th2 type of function), a role in the apoptotic destruction of thyroid cells by activating cytotoxic T cells (a Th1 function), and a role in immunoregulation (Treg cells)
most common cause of hypothyroidism in iodine-sufficient areas of the world. Thyroid failure is seen in up to 10 percent of the population, and its prevalence increases with age . It is characterized clinically by gradual thyroid failure, with or without goiter formation, due to autoimmune-mediated destruction of the thyroid gland involving apoptosis of thyroid epithelial cells. Nearly all patients have high serum concentrations of antibodies against one or more thyroid antigens; diffuse lymphocytic infiltration of the thyroid, which includes predominantly thyroid-specific B and T cells; and follicular destruction, which is the characteristic hallmark of thyroiditis.
The cause of Hashimoto's thyroiditis is thought to be a combination of genetic susceptibility and environmental factors. The familial association with Graves' disease and the fact that Graves' disease may sometimes evolve into Hashimoto's thyroiditis (and vice versa) indicate that the two disorders are closely related pathophysiologically, albeit not functionally
Pertussis is caused by the gram-negative coccobacillus B. pertussis, a strict human pathogen with no known animal or environmental reservoir . The organism is fastidious, surviving only a few hours in respiratory secretions and thus requiring special media for culture
Pertussis is a highly contagious respiratory illness. In adolescents and adults, infection may result in a protracted cough and is occasionally associated with substantial morbidity. In children and particularly infants, morbidity is more often substantial, and the disease may be fatal.
The incubation period for B. pertussis ranges from 1 to 3 weeks but is most typically 7 to 10 days. This is in contrast with the shorter incubation period (one to three days) for viral upper respiratory infections associated with cough, such as the common cold
Sickle Cell Disease
Individuals who are homozygous for the gene controlling hemoglobin S. The disease is characterized by the destruction of red blood cells and by episodic blocking of blood vessels by the adherence of sickle cells to the vascular endothelium.
an umbrella term that includes all patients who have the sickle mutation plus a second beta globin gene mutation, the combination of which causes clinical sickling. The other beta globin mutation could be the sickle mutation or a different mutation in the beta globin gene (eg, one associated with beta thalassemia or hemoglobin C disease, or others). Patients with a sickle cell disease exhibit a clinical phenotype, anemia, and laboratory evidence of sickling.
A condition in which the blood is deficient in red blood cells, in hemoglobin, or in total volume.
hemoglobin and HCT typically decrease in parallel. RBC also usually parallels the hemoglobin and HCT, except in cases of extreme microcytosis such as thalassemia, in which the RBC count may be increased despite the presence of anemia
hemoglobin <13.5 g/dL (<135 g/L) or a HCT <41.0 percent represents anemia in men, and a value <12.0 g/dL (<120 g/L) or <36.0 percent, respectively, represents anemia in women
Chronic Heart Failure (CHF)
condition in which the heart is unable to pump sufficient blood to the tissues of the body
Risk factors for HF include coronary heart disease, cigarette smoking, hypertension, overweight, diabetes, and valvular heart disease
Early detection of asymptomatic patients with a left ventricular ejection fraction (LVEF) ≤40 percent is important because effective therapy delays the onset of HF and prolongs life
While signs and symptoms of advanced HF are variable, common manifestations of advanced HF include dyspnea, fatigue, exercise intolerance, unintentional weight loss, refractory volume overload, hypotension, and signs of inadequate perfusion (diminished peripheral pulses or worsening renal function).
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