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Final Review in class
Module 3 Not directly relate- more physiology but briefly know list the factors that can effect cardiac output and for each factor write down 1 clinical condition that would effect it o Ex- total peripheral resistance- vasoconstriction o Cardiac output (CO) Blood ejected by a ventricle in 1 minute CO = SV HR (heart rate) o Stroke volume (SV) Volume of blood pumped out of ventricle by each contraction o Preload Amount of blood delivered to heart by venous return o Afterload Force required to eject blood from ventricles o MOST IMPORTANT : o -important in heart failure o Stroke volume- the volume of blood ejected from the ventricle in one heart beat o -perfusion of tissues is directly related to cardiac output o -preload is the amount of blood that is coming back into the right side of the heart, directly related to venous return, the blood that flows into the heart will stretch it and make it contract more o BP in dehydration is decreased because you don’t have enough blood to stretch the heart to make it contract o Afterload is the resistance the left ventricle has to overcome to push blood from left ventricle into the aorta, when this is increased that is what leads to hypertension, directly related to peripheral resistance o What is peripheral resistance related to? Viscosity, diameter of the blood vessels, length of the blood vessels HIGH YEILD- MI diagnostic test, could throw in a lab report- CKMB increases and tryponin increase MI: o Occurs when coronary artery is totally obstructed o Atherosclerosis is most common cause o Thrombus from atheroma may obstruct artery o Vasospasm is cause in a small percentage. o Size and location of the infarct determine the damage. o Feeling of pressure, heaviness, or burning in chest—especially with increased activity o Sudden shortness of breath, weakness, fatigue
o Nausea, indigestion o Anxiety and fear o Pain may occur and, if present, is usually Substernal Crushing Radiating o Diagnostic tests Changes in ECG Serum enzyme and isoenzyme levels Serum levels of myosin and cardiac troponin are elevated. Leukocytosis, elevated CRP and ESR common Arterial blood gas measurements may be altered in severe cases. Pulmonary artery pressure measurements helpful o Complications Sudden death Cardiogenic shock Congestive heart failure Rupture of necrotic heart tissue/cardiac tamponade Thromboembolism causing cerebrovascular accident (CVA; with left ventricular MI) o Know arterial disorders- blood not getting to area (palor about perfusion) o Arteriosclerosis General term for all types of arterial changes Degenerative changes in small arteries and arterioles Loss of elasticity Lumen gradually narrows and may become obstructed-cause increase peripheral resistance Cause of increased BP o Atherosclerosis Presence of atheromas in large arteries- fat in patches along artery Plaques consisting of lipids (LDL), calcium(bc over time they become hard), and possible clots(thrombi) Related to diet, exercise, and stress-risk factors/etiology Venous disorder- blood not getting back to heart (redness) o Varicose veins Irregular, dilated, tortuous areas of superficial veins Familial tendency
Reduced host defenses o Low-grade fever or fatigue o Anorexia, splenomegaly, congestive heart failure in severe cases o Acute endocarditis Sudden, marked onset—spiking fever, chills, drowsiness o Subacute endocarditis Insidious onset—increasing fatigue, anorexia, cough, and dyspnea o Blood culture to identify causative agent Antimicrobial drugs for several weeks, often IV o A patient had been diagnosed with mitral stenosis his ASO titer is high. Explain. o Rheumatic fever Rheumatic Fever o Acute systemic inflammatory condition May result from an abnormal immune reaction Can occur a few weeks after an untreated infection (usually group A -hemolytic Streptococcus ) o Involves heart as well as joints o Usually occurs in children ages 5 to 15 years o Long-term effects Rheumatic heart disease May be complicated by infective endocarditis and heart failure in older adults o Acute stage—inflammation of the heart Pericarditis Myocarditis Endocarditis and incompetent heart valves o Other sites of inflammation Large joints Erythema marginatum Nontender subcutaneous nodules Involuntary jerky movement of the face, arms, legs o Signs and symptoms Low-grade fever, leukocytosis, malaise, anorexia, fatigue, tachycardia o Diagnostic tests Heart function test Electrocardiography ASO titer Differentiate between the forward and backward effects of left and right sided heart failure
o Forward effects (similar with failure on either side) Decreased blood supply to tissues, general hypoxia Fatigue and weakness Dyspnea and shortness of breath o Compensation mechanisms Tachycardia Cutaneous and visceral vasoconstriction Daytime oliguria o Signs of left-sided failure Related to pulmonary congestion Dyspnea and orthopnea Develop as fluid accumulates in the lungs Cough Associated with fluid irritating the respiratory passages Paroxysmal nocturnal dyspnea Indicates the presence of acute pulmonary edema Usually develops during sleep Excess fluid in lungs frequently leads to infections such as pneumonia. o Signs of right-sided failure Dependent edema in feet, legs, or buttocks Increased pressure in jugular veins leads to distention. Hepatomegaly and splenomegaly Digestive disturbances Ascites Complication when fluid accumulates in peritoneal cavity Marked abdominal distention o Acute right-sided failure Flushed face, distended neck veins, headache, visual disturbances Shock- differentiates between the several types of shock cardiogenic, hypovalemic, Vaso/neurogenic (vasodialation shock) o Hypovolemic shock Loss of circulating blood volume o Cardiogenic shock Inability of heart to maintain cardiac output to circulation o Distributive, vasogenic, neurogenic, septic, anaphylactic shock Changes in peripheral resistance leading to pooling of blood in the periphery o Early manifestations Anxiety
o Hypertension – primary and secondary o Predisposing factors Incidence increases with age.- Men affected more frequently and more severely Incidence in women increases after middle age. Genetic factors Sodium intake, excessive alcohol intake, obesity, smoking, prolonged or recurrent stress o Primary hypertension Essential hypertension Blood pressure consistently above 140/90 mm Hg May be adjusted for age Increase in arteriolar vasoconstriction Over long period of time—damage to arterial walls Blood supply to involved area is reduced. Ischemia and necrosis of tissues, with loss of function o Secondary hypertension
Results from renal or endocrine disease, pheochromocytoma (benign tumor of the adrenal medulla) Underlying problem must be treated to reduce blood pressure. o Malignant or resistant hypertension Uncontrollable, severe, and rapidly progressive form with many complications Diastolic pressure is extremely high
Aldosterone, Raas, catecholamines- link to hypetension Emphysema o Destruction of alveolar walls and septae Leads to large, permanently inflated alveolar air spaces o Classified by specific location of changes o Contributing factors Genetic deficiency Genetic tendency Cigarette smoking Pathogenic bacteria o Patho problems that occur: o Breakdown of alveolar wall results in: Loss of surface area for gas exchange Loss of pulmonary capillaries
Intercostal contractions Hyperventilation with prolonged expiratory phase Development of barrel chest Anorexia and fatigue Weight loss Clubbed fingers From chronic hypoxia o Diagnostic tests Chest radiography and pulmonary function tests- such as a barrel chest Bronchitis o Inflammation, obstruction, repeated infection, chronic coughing twice for 3 months or longer in 2 years History of cigarette smoking or living in urban or industrial area o Mucosa inflamed and swollen o Hypertrophy and hyperplasia of mucous glands o Fibrosis and thickening of bronchial wall- narrowing of bronchi- bronchoconstriction-hypoxia o Low oxygen levels o Severe dyspnea and fatigue o Pulmonary hypertension and cor pulmonale o Signs and symptoms Constant productive cough- coughing up sputum Tachypnea and shortness of breath- increased breathing rate Frequent thick and purulent secretions- infection Cough and rhonchi more severe in the morning Hypoxia, cyanosis, hypercapnia Caused by airway obstruction Polycythemia, weight loss, signs of cor pulmonale (heart failure) possible As vascular damage and pulmonary hypertension progress
Asthma- type 1 hypersensativity o Bronchial obstruction Occurs in persons with hypersensitive or hyperresponsive airways o May occur in childhood or have an adult onset o Often family history of allergic conditions o Extrinsic asthma-usually triggered by an allergen- pollen- MOST COMMON
Acute episodes triggered by type I hypersensitivity reactions o Intrinsic asthma- can involve an allergen but may not, airways is hyper responsive- can be triggered by cold air Onset during adulthood Hyperresponsive tissue in airway initiates attack. Stimuli include: Respiratory infections Stress Exposure to cold Inhalation of irritants Exercise Drugs o Pathophysiological changes of bronchi and bronchioles Inflammation of the mucosa with edema Bronchoconstriction Caused by contraction of smooth muscle Increased secretion of thick mucus In airways Changes create obstructed airways, partial or total o Signs and symptoms Cough, marked dyspnea, tight feeling in chest Wheezing Rapid and labored breathing Expulsion of thick or sticky mucus Tachycardia- compensatory mechanism, SNS stimulation Might include pulsus paradoxus o Pulse differs on inspiration and expiration Hypoxia- decreased ventilation Respiratory alkalosis Initially caused by hyperventilation Respiratory acidosis- Carbon dioxide trapped in conduction zone Caused by air trapping Severe respiratory distress Hypoventilation leads to hypoxemia and respiratory acidosis. Respiratory failure o Status asthmaticus- when asthma attack wont stop Persistent severe attack of asthma Does not respond to usual therapy Medical emergency! May be fatal because of severe hypoxia and acidosis
Pulmonary embolus - perfusion problem- air getting in but not to the blood o Can be a complication of thrombophlebitis and phlebothrombosis o Blood clot or mass that obstructs pulmonary artery or any of its branches o Effect of embolus depends on material, size, and location o Small pulmonary emboli might be “silent” unless they involve a large area of lung. o Large emboli may cause sudden death. o 90% of pulmonary emboli originate from deep vein thromboses in legs; are preventable o Key point- PULMONARY EMBOLISM TAKES PLACE IN 99% OF CASES FROM A CLOT THAT PASSES THROUGH THE RIGHT SIDE OF THE HEART THEREFOR IT HAS TO COME FROM SOMEWHERE IN THE BODY AND THE MOST COMMON AREA IS DEEP VEINS OF THE LEGS o Signs and symptoms Transient chest pain, cough, dyspnea—small emboli Larger emboli—increased chest pain with coughing or deep breathing; tachypnea and dyspnea develop suddenly. Later—hemoptysis and fever Hypoxia—causes anxiety, restlessness, pallor, tachycardia Massive emboli Severe crushing chest pain, low blood pressure, rapid weak pulse, loss of consciousness- similar to MI o Diagnosis Radiography, lung scan, MRI, pulmonary angiography Iron deficiency anemia o Insufficient iron impairs hemoglobin synthesis. Microcytic (smaller than normal rbc), hypochromic(low in hemoglobin content) RBCs Result of low hemoglobin concentration in cells o Very common Ranges from mild to severe Occurs in all age groups, but more common in women of childbearing age and women with problem with periods, also with chronic blood loss (can be period of GI ulcer) Estimated that one in five women is affected Proportion increases for pregnant women o Frequently sign of an underlying problem o Dietary intake of iron below minimum requirement o Chronic blood loss
As from bleeding, ulcer, hemorrhoids, cancer o Impaired duodenal absorption of iron In many disorders, malabsorption syndromes o Severe liver disease- store house for iron May affect iron absorption as well as storage o Signs and symptoms Pallor of skin and mucous membranes Fatigue, lethargy, cold intolerance Degenerative changes Stomatitis and glossitis Menstrual irregularities Delayed healing Tachycardia, heart palpitations, dyspnea, syncope- compensation mechanism Pernicious anemia: Vitamin b12 deficiency- macrocytic anemia o Basic problem is lack of absorption of vitamin B 12 because of lack of intrinsic factor Intrinsic factor secreted by gastric mucosa Required for intestinal absorption of vitamin B (^12) o Characterized by very large(macrocytic), immature, nucleated erythrocytes Carry less hemoglobin- less oxygen transport Shorter life span- bc larger Bone marrow will become over worked- bone marrow hyperplasia Increase production of bilirubin= jaundice bc faster rate of cell death
o B12 is responsible for RBC maturation so if B12 is absent or decreased it will result in immature rbc o Dietary insufficiency o Genetic factors have been implicated. o Often accompanies chronic gastritis o May also be an outcome of gastric surgery o Manifestations in addition to those typical for anemias Tongue is typically enlarged, red, sore, and shiny. Digestive discomfort, often with nausea and diarrhea o Vitamin B 12 is needed for the function and maintenance of neurons. Significant deficit of the vitamin will cause symptoms in the peripheral nerves.- neurological manifestation Feeling of pins and needles, tingling in limbs o Patient may complain with sensory problems- pins and needles
Prenatal DNA analysis- punnett squares, amniocentesis After birth you diagnose by CBC, blood smear, but the confirmation test for any hemoglobin test is hemoglobin electropoeisis- you take blood and lyse is and but it on a membrane and but membrane on electrical field and you will find the hemoglobin will migrate Diff between the different types of acute and chronic leukemia o
o DON’T KNOW LAST 2 o Acute leukemias (ALL and AML) High proportion of immature nonfunctional cells in bone marrow and peripheral circulation Onset usually abrupt , marked signs of complications Occurs primarily in children and younger adults o Chronic leukemias (CLL and CML) Higher proportion of mature cells Insidious onset Mild signs and better prognosis
Common in older adults o Hemophilia - punnett square o Classic hemophilia Deficit or abnormality of factor VIII o Most common inherited clotting disorder X-linked recessive trait Manifested in men, carried by women o Varying degrees of severity o Prolonged bleeding after minor tissue trauma o Spontaneous bleeding into joints o Possible hematuria or blood in feces o Key points- prolonged bleeding= anemia=hypoxia o Diagnostic tests Bleeding time and PT normal- bc they deal with platelets and not clotting factor PTT, activated PTT (aPTT), coagulation time prolonged- bc reflective of clotting factors Serum levels of factor VIII are low. Genetic abnormality o BLEEDING TIME AND PT TIME NORMAL- PROBLEM WITH CLOTTING What would be the lab of hemophilia- the bleeding time will be normal, clotting time elevated (PPT) o Punnett squares : o Duchenne-x-linked recessive o Cf-autosomal recessive o Huntingtons- autosomal dominant o Hemophilia –x linked recessive Module 4 GERD o Periodic reflux of gastric contents into distal esophagus causes erosion and inflammation. o Often seen in conjunction with hiatal hernia o Severity depends on competence of the lower esophageal sphincter. o Delayed gastric emptying may be a factor. o Aggravated by: Caffeine, fatty and spicy foods, alcohol, smoking, certain drugs Use of medication may reduce reflux and inflammation Hiatal hernia o Part of the stomach protrudes into the thoracic cavity. o Sliding hernia More common type
Atrophy of gastric mucosa o Chronic gastritis Signs and symptoms o Epigastric burning or localized pain, usually following stomach emptying Diagnostic tests o Fiberoptic endoscopy o Barium x-ray o Endoscopic biopsy
Gastritis is associated with penecious anemia bc loss of instrinic factor o Gastric mucosa is inflamed. o May be ulcerated and bleeding o May result from Infection by microorganisms Allergies to foods Spicy or irritating foods Excessive alcohol intake Ingestion of aspirin or other NSAIDs Ingestion of corrosive or toxic substances Radiation or chemotherapy o Basic signs of gastrointestinal irritation Anorexia, nausea, vomiting may develop Hematemesis caused by bleeding Epigastric pain, cramps or general discomfort With infection, diarrhea may develop. o Acute gastritis is usually self-limiting. Complete regeneration of gastric mucosa
Supportive treatment with prolonged vomiting May require treatment with antimicrobial drugs o Chronic o
Crohns disease o May affect any area of the digestive tract Usually small intestine affected o Inflammation occurs in characteristic distribution “Skip lesions”—affected areas separated by areas of normal tissue Transmural- through all 3 layers o Progressive inflammation and fibrosis may cause obstructed areas. Damaged walls impair processing and absorption of food. Inflammation stimulates intestinal motility. o Interference with digestion and absorption Hypoproteinemia, avitaminosis, malnutrition, possibly steatorrhea- all associated with malabsorption o Other complications Adhesions between loops may form and fistulas may develop. o Children Delayed growth and sexual maturation because of malabsorption giving rise to malnutrition o Terminal ileum is the main part effected, descending colon and rectum, inflammatory lesion goes through all 3 layers of intestines o Skip lesions Ulcerative colitis
