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PATHO HESI 5/8/17
Get Quizlet's official HESI A2 - 1 term, 1 practice question, 1 full practice test
Terms in this set (53)
acid base analysis - patho
Metabolic acidosis: Decreased pH, decreased HCO 3 -
Metabolic alkalosis: Increased pH, increased HCO 3 -
Respiratory acidosis: Decreased pH, increased CO 2
Respiratory alkalosis: Increased pH, decreased CO 2 pH: 7.35-7.45 HCO3: 22-29 CO2: 35-45
APN neuro exam
bronchitis - patho r/t dx
defined as hypersecretion of mucus and chronic productive cough that continues for at least 3 months of the year for 2 consecutive years. PATHO: inspired irritants result in airway inflammation with infiltration of neutrophils, macrophages, and injures airway epithelial cells. causes edema and increase size and number of mucous glands and goblet cells in the airway epithelium. the thick mucus and hypertrophied bronchial smooth muscle narrow the airways and lead to obstruction, particularly during expiration when the airway in constricted. obstruction eventually leads to ventilation perfusion mismatch with hypoxemia. the airways collapse early in expiration trapping expands the thorax putting the respiratory muscles at a mechanical disadvantage. leads to decreased tidal volume, hypoventilation and hypercapnia. CM: decreased exercise tolerance, wheezing, SOB, productive cough,FVC reduced. TX: dx based on symptoms and physical exam, chest xray, PFT, blood gas analyses. bronchodilators, oxygen
chronic infection - patho
The most common CM of portal hypertension is vomiting of blood from bleeding esophageal varices. bleeding is usually from varices that have developed slowly over a period of years. slow chronic bleeding from varices causes anemia or melena. acute rupture of esophageal varices causes hemorrhage and voluminous vomiting of dark blood. rupture is caused by a combination of erosion by gastric acid and elevated venous pressure. Portal HTN is abnormally high BP in the portal venous system primarily caused by resistance to portal blood flow, pressure is increased to 10mmhg from 3. it is caused by disorders that obstruct or impede blood flow through any component of the hepatic portal system. intrahepatic causes reslts from vascular remodeling with intrahepatic shunts, thrombosis, inflammation, or fibrosis as occurs in cirrhosis of the liver, viral hepatitis. posthepatic causes occur from hepatic vein thrombosis or cardiac disorders that impair the pumping ability of the right side of the heart this causes blood to back up and increase pressure in the portal system. Varices are distended tortuous collateral veins. prolonged elevation of pressure in the hepatic portal vein causes collateral veins to open between the portal vein and systemic veins and their transformation into varices particularly in the lower esophagus and stomach but also over the abdominal wall.
food poisoning - fish
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,  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.  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).  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. 
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.  (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
Food poisoning is defined as an illness caused by the consumption of food or water contaminated with bacteria and/or their toxins, or with parasites, viruses, or chemicals. The symptoms, varying in degree and combination, include abdominal pain, vomiting, diarrhea, and headache; more serious cases can result in life-threatening neurologic, hepatic, and renal syndromes leading to permanent disability or death.
Most of the illnesses are mild and improve without any specific treatment. Some patients have severe disease and require hospitalization, aggressive hydration, and antibiotic treatment. 
A food-borne disease outbreak is defined by the following 2 criteria:
Similar illness, often GI, in a minimum of 2 people
Evidence of food as the source
inflammation lab -patho
Erythrocyte sedimentation rate (ESR)
A blood sample is taken and put in a tube that contains a chemical to stop the blood from clotting. The tube is left to stand upright. The red blood cells (erythrocytes) gradually fall to the bottom of the tube (as a sediment). The clear liquid plasma is left at the top. The ESR measures the rate at which the red blood cells separate from the plasma and fall to the bottom of a test tube. The rate is measured in millimetres per hour (mm/hr). This is easy to measure as there will be a number of millimetres of clear liquid at the top of the red blood after one hour.
If certain proteins cover red cells, these will stick to each other and cause the red cells to fall more quickly. So, a high ESR indicates that you have some inflammation, somewhere in the body.
Levels of ESR are generally higher in females. Also the level increases with increasing age. C-reactive protein (CRP)
This is sometimes called an acute phase protein. This means that the level of CRP increases when you have certain diseases which cause inflammation. CRP can be measured in a blood sample. The CRP test measures the level of one specific protein, whereas the ESR takes account of many proteins.
oxygen - patho
Oxygen diffuses from capillaries to cells, where it is utilized at the tissue level. Simultaneous exchange of oxygen and carbon dioxide is followed by removal of carbon dioxide from the blood into the alveoli, where this waste gas is ultimately exhaled, completing the normal respiratory cycle.
patho - hashimoto's thyroiditis
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)
Elevated blood pressure (typically diastolic hypertension)
Diminished deep tendon reflexes and the classic prolonged relaxation phase
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
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.
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)
patho - acute pertussis
Pertussis is primarily a toxin-mediated disease. The bacteria attach to the cilia of the respiratory epithelial cells, produce toxins that paralyze the cilia, and cause inflammation of the respiratory tract, which interferes with the clearing of pulmonary secretions. Until recently, it was thought that B. pertussis did not invade the tissues; however, recent studies have suggested that the bacteria are present in alveolar macrophages.
patho - acute sickle PNA
Hb S - sickled RBC lack of oxygen causing pain.
patho - alcoholism - GERI
patho - anemia
pernicious anemia - lack of B12 for erythropoiesis. Folate deficiency amenia - lack of folate for erythropoiesis. Iron deficiency - lack of iron for hemoglobin production. Sideroblastic anemia- dysfunctional iron uptake by erythroblasts and defective porphyrine and heme synthesis. Thalassemia - impaired synthesis of alpha or beta chain of hemoglobin.
patho - antipersonality disorder outcome
patho - cardiac murmur
Heart murmurs are often caused by defective heart valves. A stenotic heart valve has a smaller-than-normal opening and can't open completely. A valve may also be unable to close completely. This leads to regurgitation, which is blood leaking backward through the valve when it should be closed.
Murmurs also can be caused by certain congenital defects and other conditions such as pregnancy, fever, thyrotoxicosis (a diseased condition resulting from an overactive thyroid gland) or anemia.
A murmur that occurs when the heart muscle relaxes between beats is called a diastolic murmur. A systolic murmur is one that occurs when the heart muscle contracts. Systolic murmurs are graded by intensity (loudness) from one to six. A grade 1/6 is very faint, heard only with a special effort. A grade 6/6 is extremely loud. It's heard with a stethoscope slightly removed from the chest.
patho - CHF
patho - chronic alcoholism
causes structural alterations in parctically all organs and tissues in the body especially the liver and stomach. can cause fatty liver, alcoholic, hepatitis, cirrhosis. oxidative stress is associated with cell membrane phospholipid depletion which alters the fluidity and function of cell membranes as well as intercellular transport.
patho - chronic venous pressure ulcer
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).  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.
patho - creatinine and aging
Some elderly patients show gradual increases in creatinine even when hypertension, blood glucose levels, etc., are well controlled. When should these patients be referred to nephrology or come in for a 24-hr urine test? Creatinine levels relate to both muscle mass and to kidney function. As you age, your muscle mass decreases but your kidneys tend to function less effectively. The net result is not much change in creatinine levels in the blood as you get older
patho - cushing disease
With Cushings, one has too many steroids which could be caused by too much ACTH (due to maybe a pituitary tumor) or adrenal gland issues. Right? With Addison's, there is too little steroids, or aldosterone? Because the adrenal glands may not be producing as they should, it may also cause an increase in ACTH due to the the feedback loop being "broken"? So, essentially, both Addisons and Cushings could have too much ACTH? Re: Cushings, you're right, but don't forget you can also have drug-induced cushings occur because of too much exogenous steroid administration.
Re: Addisons, this is also known as primary adrenal insufficiency where a destructive process interferes with hormone synthesis, causing decreased production of adrenocortical hormones (cortisol, aldosterone, and DHEA). This is different from secondary adrenal insufficiency which occurs in patients with pituitary involvement...and if you want to get even more technical, tertiary adrenal insufficiency (seen in patients with hypothalamic involvement). In secondary and tertiary adrenal insufficiency, this is what results in decreased ACTH secretion. Only patients with elevated ACTH levels would be conisdered to have Addisons.
patho - D dimer test
A d-dimer test is a blood test that measures a substance that is released when a blood clot breaks up. Doctors order the d-dimer test, along with other lab tests and imaging scans, to help check for blood-clotting problems. A d-dimer test can also be used to check how well a treatment is working.
A low or normal d-dimer test result means that there is very little of the substance that's released as a blood clot breaks up. Having very little of this substance means that a blood clotting problem isn't likely.
A higher-than-normal d-dimer level might mean that there is a blood-clotting problem. But a higher level might be caused by some other health problem or by a normal healing process.
D-dimer levels are often higher than normal in people who have abnormal blood clotting.
A positive D-dimer result may indicate the presence of an abnormally high level of fibrin degradation products. It indicates that there may be significant blood clot (thrombus) formation and breakdown in the body, but it does not tell the location or cause. For example, it may be due to a venous thromboembolism (VTE) or disseminated intravascular coagulation (DIC). Typically, the D-dimer level is very elevated in DIC.
patho - dietary sodium
recommended less than 2300 daily. but does contain needed iodine. iodine is needed to protect the thyroid.
patho - DM
In autoimmune environmental genetic factors are thought to trigger cell mediated destruction of pancreatic beta cells. Nonimmune type 1 is from a disease. most common in kids. Beta cell defect or failure. T cell mediated disease. Lymphocytes and macrophage infiltration of the islets resulting in inflammation and islet beta cell dealth. Severe insulin deficiency or no insulin secretion at all.
patho - embolic disease
patho - endocrine
patho - glucose tolerance test
DX of diabetes: HbA1C greater than 6.5% OR FPG greater than 126 OR 2hr plasma glucose greater than 200 OR presentation of symptoms. PREDIABETES: FPG 100-125, 2hr PG 75-199, HbA1C 5.7-6.4%
patho - infant fontannels
one diamond shaped anterior fontanel and one triangular shaped posterior fontanel. The posterior fontanel may be open until 2-3 months of age the anterior fontanel normally closes by 18 m.
patho - integumentary
patho - liver disease test results
elevated bilirubin, elevated amonia, low glucose, increased lactate
patho - MI rehabilitation
patho - neuroanatomy
Frontal: personality, emotions and arousal, intelligence, ability to concentrate, make decisions, plan, solve problems, awareness of what is around you, voluntary movement, ability to speak and write, behavior control. Temporal: understand language, hearing, memory, organization. Brain Stem: breathing, HR control, consciousness, swallowing, BP, sweating. Cerebellum: balance, motor, posture, fine motor. Occipital: vision, interpreting what you see. Parietal: sensations, understanding and interpreting size, color and shape, understanding space and distance, math
patho - neuropathology
patho - peds acute
patho - primary hyperthyroidism - lab values
usually a sporadic disease characterized by inappropriate excess secretion of PTH by one or more parathyroid glands. PTH is increased and is not under the usual feedback control mechanism. the calcium level in the blood increases because of increased bone resorption and GI absorption of calcium but fails to inhibit PTH secretion.
patho - RSV precautions
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
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
Decrease in appetite
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
patho - serotonin
A monoamine that works at many areas of the brain and spinal cord. effects are generally inhibitory. is involved with mood, anxiety, and sleep induction. levels of serotonin are elevated in schizophrenia, delusions, hallucinations, withdrawal. also found in the GI system
patho - sleep hygiene
patho - SSRI's
SSRIs ease depression by increasing levels of serotonin in the brain. Serotonin is one of the chemical messengers (neurotransmitters) that carry signals between brain cells. SSRIs block the reabsorption (reuptake) of serotonin in the brain, making more serotonin available. SSRIs are called selective because they seem to primarily affect serotonin, not other neurotransmitters. ex: citalopram, lexapro,fluoxetine, paroxetine, sertraline. Possible side effects of SSRIs may include, among others:
Nervousness, agitation or restlessness
Sexual problems, such as reduced sexual desire or difficulty reaching orgasm or inability to maintain an erection (erectile dysfunction)
patho - stress cycle
patho - TIA
transient episodes of neurologic dysfunction (weakness, numbness, confusion, loss of balance, loss of vision, sudden severe headache). arise from arterial occlusion caused by thrombi formed in the arteries supplying the brain or in the intracranial vessels.
patho - vaginitis
irritation of the vagina that can be caused by a variety of microorganisms, irritants, pathologies or a disruption of the normal flora of the vagina. characterized by an increase in WBC on saline wet prep exam. normal causes are overgrowth of normal flora, STI, low estrogen with menopause. the acidic natur of the baginal secretions during the reproductive years provides protection against STI. changes in pH put pt at risk for infection.
patho - DM Type 2
PATHO: Insulin resistance a suboptimal response of insulin sensitive tissues to insulin. genetic and enviromental. obesity. decreased beta cell mass and function.
patho - arterial plaque
atherosclerosis is the most common cause of CAD. in this condition, fatty, fibrous plaques, possibly including calcium deposits, progressively narrow the coronary artery lumens, which reduces the volume of blood that can flow through them. this can lead to myocardial ischemia and necrosis. Cholesterol-containing deposits (plaque) in your arteries and inflammation are usually to blame for coronary artery disease.When plaque builds up, they narrow your coronary arteries, decreasing blood flow to your heart. Eventually, the decreased blood flow may cause chest pain (angina), shortness of breath, or other coronary artery disease signs and symptoms. A complete blockage can cause a heart attack. Because coronary artery disease often develops over decades, you might not notice a problem until you have a significant blockage or a heart attack. But there's plenty you can do to prevent and treat coronary artery disease. A healthy lifestyle can make a big impact.
patho - Chest pain
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. 
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,  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.  Syndrome X is believed to be caused by microvascular angina. Multiple mechanisms may be responsible for this syndrome, including (1) impaired endothelial dysfunction,  (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. 
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. 
patho - cluster headaches
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
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
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
patho - DKA
INFO: complication of DM. develops when there is an absolute or relative deficiency of insulin and an increase in levels of insulin counterregulatory hormones. More common in DM 1. PATHO:in a state of relative insulin deficiency ther is an increase in the concentrations of insulin counterregulatory hormones including catecholamines, cortisol, glucoagon and GH. hepatic over production of B hydroxybutyrate and acetoacetic acids causes increased ketone concentrations. CM: polyuria, dehydration from osmotic diuresis. deficits of sodium, phosphorus, magnesium are common. potassium can be normal to elevated bc the volume contraction and a shift of potassium out of the cell and into the blood caused by metabbolic acidosis. Kussmaul respiration (hyperventilation to compensate for the acidosis). EVAL and TX: BS about 250, bicarbonate less than 18, pH less than 7.30, ketones in urine. treated with insulin and fluids.
patho - dysplasia
abnormal changes in the size, shape, and organization of mature cells. not considered a true adaptive process but is related to hyperplasia ans is often called atypical hyperplasia. common in the epithelial tissue of the cervix and respiratory tract, wher they are strongly associated with common neoplastic growths and often are found adjacent to cancerous cells.
PE - patho consequence
Kidney function. it is a chemical waste product thats produced by your muscle metabolism and to a smaller extend by eating meat. health kidneys filter creatinine and other wast products from blood. high creatinine means kidneys arent working well. can temporarily increase if dehydrated, low blood volume, or large intake of meat. If levels are low could be from muscle wasting and malnutrition. Normal for men 0.7-1.3 and for women 0.6-1.1
third heart sound PEDI
S3 is a normal finding in children and young adults. caused by sudden limitation of longitudinal expansion of the ventricular wall. brief low pitched sound in mid-diastole; audible in about 6-10% of young people. Murmurs grading: I- barely audible, II- audible, the majority of murmurs, III - stronger than II may have thrill, IV must have thrill, V - audible with on edge of stethoscope on chest VI- audible without stethoscope. Third heart sound is also known as the ventricular gallop occurs just after S2 when the mitral valve open allowing passive filling of the left ventricle.S3 can also be a sign of systolic heart failure because in this setting the myocardium is usually overly compliant, resulting in a dilated LV. S3 is a low pitched sound can be heard with the bell of the stethoscope. best heard at the cardiac apex when pt is in left lateral decubitus position
THIS SET IS OFTEN IN FOLDERS WITH...
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Hesi Pathophysiology Practice Exam
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