And the winner is no surprise here: Pathophysiology Made Incredibly Visual! Well, as you can see, Pathophysiology Made Incredibly Visual has swept The Visual Awards! Selected references Assessment made incredibly easy (4th ed.). () Rubin's pathology: Clinicopathologic foundations of medicine (5th ed.). pathophysiology? Gain confidence, with the newly updated Pathophysiology Made Incredibly Easy!®, 6th Edition. Jumpstarts. ▽. Home > Books > Pathophysiology Made Incredibly Easy! Pathophysiology Made Incredibly Easy! View PDF. Jan 4, Pathophysiology made incredibly Easy 5th Edition PDF Free Download Pathophysiology made incredibly Easy 5th Edition PDF Free Download If.
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Pathophysiology made incredibly easy!.—5th ed. p. ; cm. Includes bibliographical references It will make you smile as it enhances your knowledge and skills. One of the top-selling titles from the Incredibly Easy series, the fully updated 5th edition of Pathophysiology Made Incredibly Easy presents. download Pathophysiology Made Incredibly Easy! Series®) 5th Edition, Kindle Edition We're sorry, the Kindle Edition of this title is not currently available for.
Enter your mobile number or email address below and we'll send you a link to download the free Kindle App. Then you can start reading Kindle books on your smartphone, tablet, or computer - no Kindle device required. To get the free app, enter your mobile phone number. Would you like to tell us about a lower price? It presents vital information needed by nurses and student nurses on the difficult topic of pathophysiology in an easy-to-learn, easy-to-remember approach -- as only Incredibly Easy titles can do!
There were many topics that were missing from the book. As one might guess given it's small size compared to a patho text book. I got an A in patho and all I can say is know causes, manifestations, and the reasons why those are what they are. Know this inside and out and you will be okay.
downloadd this book as a resource for my graduate level Pathophysiology book. I truly don;t even think it would be any help to a beginning student. The book contains nothing more than headings you would find in a patho text. There is no explanation and no explaining of information. The content is truly what you would find in the summary bullet points at the end of a chapter.
This is not a book I would recommend on any level, save your money for sure. This is an awesome book. I am a nurse practitioner student who's taking advanced pathophysiology, but haven't had pathophysiology.
This book is an excellent bridge between the two. Colorful and easy reading. An excellent resource. Helped me understand the class versus just memorizing material. Would recommend for anyone having issues with patho or anyone who needs more in depth explinations.
I love this book, it really made a difference in nursing school. It's better than other nursing book series as it's very concise but has enough detail that it helps you understand everything. A must have for a nursing student. Kindle Edition Verified download. Very helpful for my pathophysiology class in nursing school!! Covers the most important topics! Must have for visual learners!! See all reviews. site Giveaway allows you to run promotional giveaways in order to create buzz, reward your audience, and attract new followers and customers.
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Deals and Shenanigans. PillPack Pharmacy Simplified. site Renewed Refurbished products with a warranty. Amy R. Hospital Susan A. It all makes me vant to return to my cell, er, coffin. Large groups of individual cells form tissues, such as muscle, blood, and bone. Tissues form the organs such as the brain, heart, and liver , which are integrated into body systems such as the central nervous system [CNS], cardiovascular system, and digestive system. I combine protein and other material the cell needs.
I protect the cell and transport material in and out of the cell. This occurs during the growth phase, called interphase. Chromatin, the small, slender rods of the nucleus that give it its granular appearance, begins to form.
Replication and duplication of deoxyribonucleic acid occurs during the four phases of mitosis. The centromeres then align themselves in the middle of the spindle. During prophase, the chromosomes coil and shorten, and the nuclear membrane dissolves. Each chromosome is made up of a pair of strands called chromatids, which are connected by a spindle of fibers called a centromere. The spindle fibers disappear, cytokinesis occurs, and the cytoplasm divides, producing two identical new daughter cells.
At the onset of anaphase, the centromeres begin to separate and pull the newly replicated chromosomes toward opposite sides of the cell.
By the end of anaphase, 46 chromosomes are present on each side of the cell. Cells generally continue to function despite changing conditions or stressors. However, severe or prolonged stress or changes may injure or even destroy cells. When cell integrity is threatened, the cell reacts by drawing on its reserves to keep functioning by adaptive changes or by cellular dysfunction.
Adaptive cell changes Normal cells Atrophy Atrophy is a reversible reduction in the size of the cell. It occurs as a result of disuse, insufficient blood flow, malnutrition, denervation, or reduced endocrine stimulation. Hypertrophy Hypertrophy is an enlargement of a cell due to an increased workload. It can result from normal physiologic conditions or abnormal pathologic conditions. Cell adaptation 7 Hyperplasia Hyperplasia is an increase in the number of cells caused by increased workload, hormonal stimulation, or decreased tissue.
I can better handle stress. Metaplasia Metaplasia is the replacement of one adult cell with another adult cell that can better endure the change or stress. Dysplasia In dysplasia, deranged cell growth of specific tissue results in abnormal size, shape, and appearance.
Although dysplastic cell changes are adaptive and potentially reversible, they can precede cancerous changes. Cell injury may result from any of several intrinsic or extrinsic causes and may be classified as toxic, infectious, physical, or deficit.
Toxic injury Deficit injury Toxic injuries may be caused by factors inside the body endogenous factors or outside the body exogenous factors. Common endogenous factors include genetically determined metabolic errors, gross malformations, and hypersensitivity reactions.
Exogenous factors include alcohol, lead, carbon monoxide, and drugs that alter cellular function, such as chemotherapeutic agents or immunosuppressive drugs. A lack of just one of these basic requirements can cause cell disruption or death.
Your carbon monoxide emissions are way beyond healthy. Frostbite can d-ddamage cells and cause ph-phphysical injury and p-p-pain. Infectious injury Physical injury Physical injury results from a disruption in the cell or in the relationships of the intracellular organelles such as mitochondria, nuclei, lysosomes, and ribosomes. Two major types of physical injury are thermal electrical or radiation and mechanical trauma or surgery. Viral, fungal, protozoal, and bacterial organisms can cause cell injury or death.
These organisms affect cell integrity, usually by interfering with cell synthesis, producing mutant cells. We can do a lot of damage by interfering with cell synthesis, producing mutant cells. A maladaptive response to stress may result in disease. The underlying stressor may be real or perceived. In the alarm stage, the body senses stress, and the CNS is aroused.
The body releases chemicals to mobilize the fight-or-flight response. This release is the adrenaline rush associated with panic or aggression. Hans Selye, a pioneer in the study of stress and disease, described stages of adaptation to a stressful event: The stress response is controlled by actions taking place in the nervous and endocrine systems.
In the resistance stage, the body either adapts and achieves homeostasis or fails to adapt and enters the exhaustion stage, resulting in disease.
Able to label? Golgi apparatus Show and tell 1. Show and tell 5. Label the parts of a cell indicated in this illustration. Signs and symptoms of atypical chest pain include: An aneurysm generally occurs between renal arteries and iliac branches. In a saccular aneurysm, an outpouching occurs in the arterial wall. In fusiform aneurysms, the outpouching appears spindleshaped and encompasses the entire aortic circumference.
In a false aneurysm, the outpouching occurs when the entire vessel wall is injured and leads to a sac formation affecting the artery or heart. How it happens 1 2 3 Degenerative changes create a focal weakness in the muscular layer of the aorta. Types of aneurysms Saccular aneurysm Fusiform aneurysm False aneurysm The inner and outer layers stretch outward to create a bulge, called an aneurysm.
Pressure from the blood pulsing through the aorta weakens the vessel wall and enlarges the aneurysm. Descending AAs may occur in young patients after a traumatic chest injury or after infection but are most common in elderly men with hypertension.
Cardiac tamponade Cardiac tamponade is a rapid, unchecked increase in pressure in the pericardial sac. This compresses the heart, impairs diastolic filling, and reduces cardiac output.
How it happens Cardiac tamponade usually results from blood or fluid that accumulates in the pericardial sac and compresses the heart. This compression obstructs blood flow to the ventricles and reduces the amount of blood pumped out of the heart with each contraction. It can result from any condition that causes significant left ventricular dysfunction and reduced cardiac output, with the most common cause being acute MI.
Decreased cardiac output How it happens Dilated cardiomyopathy results from damage to cardiac muscle fibers. The resulting loss of muscle tone grossly dilates all four chambers of the heart, giving the heart a globular shape. The damage is done 1 The left ventricle and interventricular septum hypertrophy and become stiff, noncompliant, and unable to relax during ventricular filling.
Good enough reason for me to take a break! Early closure of the outflow tract results because of the decreasing ejection fraction. How it happens Stiffness of the ventricle is caused by left ventricular hypertrophy and endocardial fibrosis and thickening. The rigid myocardium fails to contract completely during systole.
Left ventricular hypertrophy Decreased ventricular chamber size As a result, cardiac output falls. Hold on, I think this list could be important! This buildup, called atherosclerosis, causes the vessels to narrow or become obstructed. Coronary arteries Coronary arteries supply blood to heart tissue. They originate from the aorta.
Normal coronary artery How it happens Aorta Coronary artery disease CAD results when atherosclerotic plaque fills the lumens of the coronary arteries and obstructs blood flow to the heart, diminishing the supply of oxygen and nutrients to the heart tissue. Inadequate control of hypertension, diabetes, and obesity; diet, exercise, and lifestyle changes are key to regaining control.
Sex—CAD is more common in men until after age Kinfolk—Heredity is a nonmodifiable risk factor.
Smoking—The sooner stopped, the better. Feel OK? Last week Yerss. Can you give me a lift to the diseased valve tissues? You and your bacteria buddies have formed growths on all the heart valves. Heart failure may be classified as right-sided or left-sided. How it happens To the left! The backed-up blood causes pressure and congestion in the vena cava and systemic circulation.
To the right! As the liver and spleen become engorged, their function is impaired. Therefore, treatment guidelines are directed toward the specific cause.
Hyperlipidemia, also called hyperproteinemia or lipid disorder, can be primary or secondary and occurs when excess levels of cholesterol, triglycerides, and lipoproteins are present in the blood. A closer look How it happens Cholesterol transport in the blood 1 2 Primary Very-low-density lipoprotein VLDL travels through the bloodstream, attaching to the lining of the capillaries. There, its fatty core of cholesterol is drawn out. Hypertension occurs as essential primary hypertension or as secondary hypertension.
How it happens What to look for Several theories exist. Abnormally increased tone in the sympathetic nervous system causes increased TPR. Abnormal renin release results in formation of angiotensin II, which constricts the arterioles and increases blood volume. Age-old story Age and systolic hypertension Elderly people may have isolated systolic hypertension, in which just the systolic blood pressure is elevated, because atherosclerosis causes a loss of elasticity in large arteries.
As you get older, you lose elasticity—in your face and in your arteries! Retained sodium and water increase blood volume. Aldosterone 4 Angiotensin II causes arteriolar constriction and aldosterone secretion.
Third-space fluid shift, which can occur in the abdominal cavity ascites , pleural cavity, or pericardial sac, can also cause hypovolemic shock.
How it happens 1 Blood pressure declines. Oxygen and nutrient delivery to cells decreases. Myocarditis is focal or diffuse inflammation of the cardiac muscle myocardium. It may be acute or chronic and can occur at any age. How it happens Damage to the myocardium occurs when an infectious organism triggers an autoimmune, cellular, and humoral reaction. The resulting inflammation may lead to hypertrophy, fibrosis, and inflammatory changes of the myocardium and conduction system.
The heart muscle weakens and contractility is reduced. The heart muscle becomes flabby and dilated, and pinpoint hemorrhages may develop. Acute pericarditis can be fibrinous or effusive, with purulent, serous, or hemorrhagic exudate. Chronic constrictive pericarditis is characterized by dense, fibrous pericardial thickening. Common symptoms of pericarditis are pain at the sternum and shallow, rapid respirations.
Macrophages, neutrophils, and monocytes in the tissue begin to phagocytose the invading bacteria. These products are eventually reabsorbed into healthy tissue. I think someone forgot to shut off the aortic valve! Aortic insufficiency is the incomplete closure of the aortic valve.
It can be acute or chronic and is usually caused by scarring or retraction of valve leaflets. In aortic insufficiency, blood flows back into the left ventricle during diastole, causing fluid overload in the ventricle, which dilates and hypertrophies.
The excess volume causes fluid overload in the left atrium and, finally, in the pulmonary system. Left-sided heart failure and pulmonary edema eventually result. It may be classified as: A R cquired heumatic. Increased left ventricular pressure tries to overcome the resistance of the narrowed valvular opening.
The added workload increases the demand for oxygen, and diminished cardiac output causes poor coronary artery perfusion, ischemia of the left ventricle, and left-sided heart failure. How it happens Aortic stenosis can occur as a result of: Blood from the left ventricle flows back into the left atrium during systole, causing the atrium to enlarge to accommodate the backflow.
As a result, the left ventricle also dilates to accommodate the increased blood volume from the atrium and to compensate for diminishing cardiac output.
Ventricular hypertrophy and increased end-diastolic pressure result in increased pulmonary artery pressure, eventually leading to left-sided and right-sided heart failure. How it happens Mitral insufficiency can occur as a result of: It occurs more frequently in women than in men. How it happens What to look for Mitral valve prolapse can occur as a result of: Mitral valve prolapse A view of the mitral valve from the left atrium shows redundant and deformed leaflets that billow into the left atrial cavity.
Dizziness, syncope, palpitations, chest pain, and heart murmur? Just as I suspected— mitral prolapse, I presume. To help you remember them, just think SIP: Stenosis Insufficiency Prolapse. Inflammation of the pericardium 2. An infection of the endocardium, heart valves, or cardiac prosthesis 3.
An abnormal dilation in the aortic arterial wall 4. An unchecked increase in pressure in the pericardial sac 5. Narrowing of the aortic valve 6. A disease of heart muscle fibers A. Cardiomyopathy Aortic stenosis Cardiac tamponade Endocarditis Aortic aneurysm Pericarditis Rebus riddle Solve the riddle to find an important fact about coronary artery disease. Matchmaker 1. A Rebus riddle Fatty deposits that accumulate in the arteries are called plaque. Ventricular fibrillation or standstill may occur.
A closer look 1 Phase In phase 1, injury reduces normal blood flow to the lungs. Platelets aggregate and release histamine H , serotonin S , and bradykinin B. Fluids then shift into the interstitial space. Trauma-related factors, such as fat emboli, pulmonary contusions, and multiple transfusions, may increase the likelihood that microemboli will develop.
As a result, alveoli collapse, impeding gas exchange and decreasing lung compliance. Oxygen O2 and CO2 levels decrease in the blood. Use the abbreviation for ARDS to remember key treatments. It causes episodic airway obstruction resulting from bronchospasms, increased mucus secretion, and mucosal edema.
Asthma is one type of chronic obstructive pulmonary disease COPD , a long-term pulmonary disease characterized by airflow resistance. Cases of asthma continue to rise. It currently affects an estimated 17 million Americans; children account for 4. A case of exposure How it happens Allergens 2 Allergens are absorbed into the tissues. Immune cell 1st exposure 1 Allergens may enter through the nose and mouth. One-third of patients develop asthma from ages 10 to 30, and the incidence is the same in both sexes in this agegroup.
Immediate tightening, swelling, and increased mucus secretion occurs. Mast cell Allergens reenter the nose and mouth. Preformed mediators Newly formed mediators 6 Allergens attach to IgE antibodies, causing mast cells to release mediators.
Best to keep those lungs and heart healthy! Left ventricle Age-old story Age and cor pulmonale In children, cor pulmonale may be a complication of cystic fibrosis, hemosiderosis, upper-airway obstruction, scleroderma, extensive bronchiectasis, neuromuscular diseases that affect respiratory muscles, or abnormalities of the respiratory control area.
Obstruction results from tissue changes, rather than mucus production, as occurs in asthma and chronic bronchitis. The distinguishing characteristic of emphysema is airflow limitation caused by a lack of elastic recoil in the lungs.
How it happens Emphysema may be caused by a deficiency of alpha1protease inhibitor or by cigarette smoking. In emphysema, recurrent inflammation is associated with the release of proteolytic enzymes enzymes that promote protein splitting by peptide bond hydrolysis from lung cells. This causes irreversible enlargement of the air spaces distal to the terminal bronchioles. Enlargement of air spaces destroys the alveolar walls, which results in a breakdown of elasticity and the loss of fibrous and muscle tissues, making the lungs less compliant.
The alveolar walls then lose their capability of elastic recoil. Collapse then occurs on expiration, as shown here. Normal expiration Impaired expiration Note normal recoil and the open bronchiole. Note decreased elastic recoil and a narrowed bronchiole. Age-old story Age and emphysema Aging is a risk factor for emphysema. Senile emphysema results from degenerative changes; stretching occurs without destruction in the smooth muscle. It involves pulmonary, cerebral, and cutaneous manifestations and occurs 24 to 48 hours after a traumatic injury.
Influenza occurs sporadically or in epidemics appears as early as October; activity peaks in January. Epidemics usually peak in 2 to 3 weeks after initial cases appear and last 2 to 3 months. Influenza results from three types of virus. Type C is endemic and causes only sporadic cases. When someone else breathes in these droplets or gets them on his hands and then touches his own mouth or nose, the virus can enter his body.
The cells in these subtypes differ in size, shape, and chemical makeup and are described here. Although the cancer cells in this type of cancer are small, they can multiply quickly and form large tumors that spread to the lymph nodes and other structures, such as the brain, liver, and bones. Almost all lung cancers start in the epithelium of the lungs.
In normal lungs, the epithelium lines and protects the tissue below it. However, when exposed to irritants or carcinogens, the epithelium continually replaces itself until the cells develop chromosomal changes and become dysplastic altered in size, shape, and organization.
Eventually, the dysplastic cells turn into neoplastic carcinoma and start invading deeper tissues. It occurs in both genders and at all ages. More than 4 million cases of pneumonia occur annually in the United States. The prognosis is good for patients with normal lungs and adequate immune systems. However, bacterial pneumonia is the leading cause of death in debilitated patients. How it happens In bacterial pneumonia, an infection triggers alveolar inflammation and edema.
This produces an area of low ventilation with normal perfusion. Capillaries become engorged with blood, causing stasis. As the alveocapillary membrane breaks down, alveoli fill with blood and exudates, resulting in atelectasis. In viral pneumonia, the virus attacks bronchial epithelial cells, causing inflammation and desquamation. The virus also invades mucous glands and goblet cells, spreading to the alveoli, which fill with blood and fluid.
Bronchopneumonia involves distal airways and alveoli; lobular pneumonia, part of a lobe; and lobar pneumonia, an entire lobe. Location Type Primary pneumonia results from inhalation or aspiration of a pathogen, such as bacteria or a virus, and includes pneumococcal and viral pneumonia; secondary pneumonia may follow lung damage from a noxious chemical or other insult or may result from hematogenous spread of bacteria; aspiration pneumonia results from inhalation of foreign matter, such as vomitus or food particles, into the bronchi.
Respiratory disorders Pneumothorax Pneumothorax is an accumulation of air in the pleural cavity that leads to partial or complete lung collapse. The most common types of pneumothorax are open, closed, and tension.
How it happens tmo en a ctly h w dire ults As x res lows hora ssure f essure.
The air enters the pleural space from the site of pleural rupture, which acts as a one-way valve. More air enters on inspiration, and air pressure begins to exceed barometric pressure. Increasing air pressure pushes against the recoiled lung, causing compression atelectasis. As air continues to accumulate and intrapleural pressures increase, the mediastinum shifts away from the affected side and decreases venous return.
This forces the heart, trachea, esophagus, and great vessels to the unaffected side, compressing the heart and the contralateral lung. This fluid is really accumulating! Pulmonary edema is a common complication of cardiac disorders. It may occur as a chronic condition or develop quickly and rapidly become fatal.
A closer look Normal Capillary Hydrostatic pressure pushes fluids into the interstitial space. Alveolus Interstitial space Plasma oncotic pressure pulls fluids back into the bloodstream. How it happens Pulmonary edema may result from left-sided heart failure caused by arteriosclerotic, cardiomyopathic, hypertensive, or valvular heart disease.
Normally, pulmonary capillary hydrostatic pressure, capillary oncotic pressure, capillary permeability, and lymphatic drainage are in balance. This prevents fluid infiltration to the lungs. When this balance changes, or if the lymphatic drainage system is obstructed, pulmonary edema results.
If colloid osmotic pressure decreases, the hydrostatic force that regulates intravascular fluids is lost because nothing opposes it. Fluid flows freely into the interstitium and alveoli, impairing gas exchange and leading to pulmonary edema. I think this guy needs help ASAP! How a pulmonary embolism develops I must have dislodged. I see the right chambers of the heart, and I seem to be headed right for the pulmonary circulation! Stuck on a branch in the circulatory system.
I fear I may block blood flow distal to where I am. Of those, died. Severe acute respiratory syndrome SARS is a viral respiratory tract infection that can progress to pneumonia and, eventually, death. The disease was first recognized in with outbreaks in China, Canada, Singapore, Taiwan, and Vietnam, with other countries—including the United States—reporting smaller numbers of cases. During the outbreak, SARS was found to be less common among children and to be milder in form in this age-group when it did occur.
The coronavirus that causes SARS is thought to be transmitted by respiratory droplets produced when an infected person coughs or sneezes. The virus can also spread when a person touches a surface or object contaminated with infectious droplets and then touches his mouth, nose, or eyes.
The SARS virion removes the protein coating that protects its genetic material C , replicates D , and matures, and then escapes from the cell by budding from the plasma membrane E. The infection then can spread to other host cells. Tuberculosis 69 Tuberculosis TB is an acute or chronic mycobacterium infection characterized by pulmonary infiltrates and the formation of granulomas with caseation, fibrosis, and cavitation.
How it happens Multiplication of the bacillus Mycobacterium tuberculosis causes an inflammatory process. A cell-mediated T-cell immune response follows that usually contains the infection within 4 to 6 weeks. The T-cell response results in the formation of granulomas around the bacilli, making them dormant. Bacilli within granulomas may remain viable for many years, resulting in a positive purified protein derivative or other skin tests for TB.
Transmission occurs when an infected person coughs or sneezes, which spreads infected droplets. Upper respiratory tract infection also known as the common cold or acute coryza is an acute, usually afebrile viral infection that causes inflammation of the upper respiratory tract.
Although a cold is benign and self-limiting, it can lead to secondary bacterial infections. How it happens Infection occurs when the offending organism gains entry into the upper respiratory tract, proliferates, and begins an inflammatory reaction.
As a result, acute inflammation of the upper airway structures, including the sinuses, nasopharynx, pharynx, larynx, and trachea, occurs. The presence of the pathogen triggers infiltration of the mucous membranes by inflammatory and infectionfighting cells.
Mucosal swelling and secretion of a serous or mucopurulent exudate result. Solve the word scrambles to uncover terms related to respiratory disorders. Then rearrange the circled letters from those words to answer the question posed. Show and tell Question: What condition discussed in this chapter is considered to be a chronic obstructive pulmonary disease? Identify the types of pneumothorax in these illustrations and describe each. My word! This chapter has all the makings of a great script.
The prognosis for this type of injury is usually excellent; symptoms usually subside when treated. I can just feel it! A wedge-shaped deformity of the bone may be created if the anterior portions of the vertebra are crushed.
A tear in the anterior ligament may pull pieces of bone from the cervical vertebrae. Spinous processes of the vertebrae may be fractured. Intervertebral disks may be compressed posteriorly and torn anteriorly. Vertebral arteries may be stretched, pinched, or torn, causing reduced blood flow to the brain. Nerves of the cervical sympathetic chain may also be injured. Injuries of the neck muscles may range from minor strains and microhemorrhages to severe tears.
Cortical degeneration is most marked in the frontal lobes, but atrophy occurs in all areas of the cortex. The more individuals in a family who have the disease, the greater the risk of others in the family developing it.
Pay attention to the symptoms so you can classify the type. A migraine headache is a throbbing, vascular headache that usually first appears in childhood and commonly recurs throughout adulthood. It may be classified according to the presence of an aura temporary focal neurologic signs, usually visual , such as scotoma an area of lost vision in the visual field , , , , , and colors.
A common migraine may not have an aura, whereas a classic migraine has an aura. Migraine headache is more common in women and has a strong familial incidence. How it happens Prostaglandin, a hormone present in the bloodstream, signals the platelets to aggregate. Platelet aggregation causes the release of serotonin a chemical that transmits signals to nerves.
Many things can affect the level of serotonin in the body, including blood glucose, certain foods, and changes in estrogen levels. In a migraine, serotonin levels in the body are increased. This increase in serotonin causes nerves to signal the blood vessels to vasoconstrict or decrease in diameter, which, in turn, causes a decrease in blood flow ischemia around the brain.
This localized ischemia causes an increase in acid acidosis. The localized acidosis and ischemia cause noninnervated no nerves and innervated blood vessels to dilate. Vasodilation of the innervated arteries results in the headache phase. Inflammation to the surrounding vessels may prolong the headache pain. Platelet aggregation then decreases, lowering the serotonin level, which results in vasodilation. A painful inflammation occurs around the surrounding areas, which can persist.
The structures usually involved are the optic and oculomotor nerves and the spinal nerve tracts. It is characterized by exacerbations and remissions. How it happens The exact cause of MS is unknown. It may be due to a slow-acting viral infection, an autoimmune response of the nervous system, or an allergic response. Other possible causes include trauma, anoxia, toxins, nutritional deficiencies, vascular lesions, and anorexia nervosa, all of which may help destroy axons and the myelin sheath.
In addition, emotional stress, overwork, fatigue, pregnancy, or an acute respiratory tract infection may precede the onset of MS. Genetic factors may also play a part. MS affects the white matter of the brain and spinal cord by creating scattered demyelinated lesions that prevent normal neurologic conduction.
After the myelin is destroyed, neuroglial tissue in the white matter of the CNS proliferates, forming hard yellow plaques of scar tissue. Scar tissue damages the underlying axon fiber, disrupting nerve conduction. This myelin destruction makes transmission of signals along the nerve difficult. These effects are exacerbated by exercise and repeated movement. Myasthenia gravis usually affects muscles in the face, lips, tongue, neck, and throat, which are innervated by the cranial nerves.
However, it can affect any muscle group. Eventually, muscle fibers may degenerate, and weakness especially of the head, neck, trunk, and limb muscles may become irreversible. When the disease involves the respiratory system, it may be life-threatening.
Normal neuromuscular transmission Motor nerve impulses travel to motor nerve terminal. ACh diffuses across synapse. ACh receptor sites in motor end plates depolarize muscle fiber. Depolarization spreads, causing muscle contraction.
ACh is released. Neuromuscular transmission is blocked. Eventually, aspiration pneumonia or some other infection causes death. The extrapyramidal system includes the corpus striatum, globus pallidus, and substantia nigra. The normal balance upset prevents affected brain cells from performing their normal inhibitory function within the CNS and causes most parkinsonian symptoms. That dopamine reduction in the corpus striatum will upset the balance! The prognosis is good if the patient adheres strictly to the prescribed treatment.
Spread of electrical impulses What to look for Generalized seizures occur as the misfiring signals move across both hemispheres. The patient loses consciousness. A simple-partial seizure begins in one hemisphere of the brain. It interrupts or diminishes oxygen supply, causing serious damage or necrosis in brain tissues. There are two main types: An ischemic stroke is caused by an interruption of blood flow in a cerebral vessel.
A hemorrhagic stroke is caused by bleeding into the cerebral tissue. Age and stroke Although strokes may occur in younger persons, most patients experiencing strokes are older than age In fact, the risk of stroke doubles with each passing decade after age How it happens Bacterial endocarditis Ball thrombus Atrial fibrillation 1 Cardiac thromboses develop as a result of various conditions.
Emboli break away from their site of origin and move from the heart into the general circulation. Plaque can also form in various areas, which can break off, causing an embolus. Depending on the size of the embolus and the vessel affected, the embolus can become stuck in the vessel, causing ischemia in Basilar the brain tissue supplied by the vessel. Cerebral hemorrhage Subarachnoid hemorrhage A cerebral hemorrhage can occur like this one, which produced a hematoma that extended into the ventricle, almost rupturing it.
Hypertension may cause microaneurysms and tiny arterioles to rupture in the brain, creating pressure on adjacent arterioles and causing them to burst, which leads to more bleeding.
Trauma can cause a subarachnoid hemorrhage, which places more pressure on brain tissue. After the pathogen enters the bloodstream, it travels to the brain and causes encephalitis.
Mosquitos serve as the vectors, spreading the virus from bird to bird and from birds to people. In the illustration, label the brain structures. B Able to label? And try not to upset your GI system this time.
Usually, a calculus gallstone becomes lodged in the cystic duct, causing painful gallbladder distention. Cholecystitis may be acute or chronic. Understanding gallstone formation Abnormal metabolism of cholesterol and bile salts plays an important role in gallstone formation. The liver makes bile continuously. The gallbladder concentrates and stores it until the duodenum signals it needs bile to help digest fat. Changes in the composition of bile may allow gallstones to form.
Changes to the absorptive ability of the gallbladder lining may also contribute to gallstone formation. Cholesterol metabolism and bile salts seem to be main culprits at this point.
How it happens Cholecystitis results from the formation of gallstones. Acute cholecystitis may also be due to poor or absent blood flow to the gallbladder. Excessive reabsorption of water and bile salts makes the bile less soluble. Cholesterol, calcium, and bilirubin precipitate into gallstones. Fat entering the duodenum causes the intestinal mucosa to secrete the hormone cholecystokinin, which stimulates the gallbladder to contract and empty.
Obstructing gallstone Age-old story Age and cholecystitis The acute form of cholecystitis is most common during middle age; the chronic form occurs most often in elderly people. This causes scar tissue, fluid accumulation, cirrhosis, portal hypertension, and bleeding.
Bilirubin is absorbed into the blood and causes jaundice.
Biliary narrowing and swelling of the tissue around the stone can also cause irritation and inflammation of the common bile duct. Many causes of chronic liver injury can lead to cirrhosis. The two most common causes of chronic liver injury in the United States are alcoholic liver disease and hepatitis C.
Other causes include: Alcohol is not a friend, especially if the person is male and middle-aged. Nutrition plays a role in nutritional cirrhosis.
This spread would have done a cirrhosis patient some good! It commonly begins as a polyp and is potentially curable if diagnosed early.
Types of colorectal cancer Transverse colon Adenocarcinoma of colon Ascending colon Vermiform appendix How it happens The exact cause of colorectal cancer is unknown. Bacteria have been associated with the conversion of bile acids into carcinogens, and a diet high in refined sugar aids in this process.
How much farther?? It may affect any part of the gastrointestinal GI tract. Inflammation extends through all layers of the intestinal wall and may involve lymph nodes and supporting membranes. Ulcers form as the inflammation extends into the peritoneum. Lymphatic obstruction causes edema, mucosal ulceration, fissures, abscesses and, sometimes, granulomas.
End 6 Eventually, diseased parts of the bowel become thicker, narrower, and shorter and can lead to formation of strictures. Diverticula occur most commonly in the sigmoid colon, but they may develop anywhere, from the proximal end of the pharynx to the anus. Diverticular disease has two clinical forms: How it happens Diverticula probably result from high intraluminal pressure on an area of weakness in the GI wall where blood vessels enter.
Diet may be a contributing factor because insufficient fiber reduces fecal residue, narrows the bowel lumen, and leads to high intra-abdominal pressure during defecation. In diverticulitis, retained undigested food and bacteria accumulate in the diverticular sac.
This hard mass cuts off the blood supply to the thin walls of the sac, making them more susceptible to attack by colonic bacteria.
Inflammation follows and may lead to perforation, abscess, peritonitis, obstruction, or hemorrhage. Occasionally, the inflamed colon segment may adhere to the bladder or other organs and cause a fistula. Age-old story Age and diverticular disease Diverticular disease is most prevalent in men older than age 40 and in people who eat a lowfiber diet.
More than one-half of all people older than age 50 have colonic diverticula. Diverticulosis What to look for Diverticulitis Typically the patient with diverticulosis is asymptomatic and will remain so unless diverticulitis develops. Esophageal varices commonly cause massive hematemesis vomiting of blood , requiring emergency care to control hemorrhage and prevent hypovolemic shock. Esophageal varices can require emergency care if massive hemorrhage occurs. How it happens Portal hypertension occurs when blood meets increased resistance.
As pressure in the portal vein increases, blood backs up into the spleen and flows through collateral channels to the venous system, bypassing the liver. Esophageal varices have two main inflows—the left gastric or coronary vein and the splenic hilus, through the short gastric veins. These collateral veins become dilated and eventually hemorrhage; esophageal varices are very susceptible to bleeding and hemorrhage.
I get totally passed by when portal hypertension occurs. Bad news for the esophagus. This common result of cirrhosis may also stem from mechanical obstruction and occlusion of the hepatic veins Budd-Chiari syndrome. As the pressure in the portal vein rises, blood backs up into the spleen and flows through collateral channels to the venous system, bypassing the liver. Thus, portal hypertension causes: In many patients, the first sign of portal hypertension is bleeding esophageal varices dilated tortuous veins in the submucosa of the lower esophagus.
Esophageal varices commonly cause massive hematemesis, requiring emergency care to control hemorrhage and prevent hypovolemic shock. The sauce was pretty garlicky… Popularly known as heartburn, gastroesophageal reflux disease GERD refers to the backflow of gastric and duodenal contents past the lower esophageal sphincter LES and into the esophagus without associated belching or vomiting. The reflux of gastric contents causes acute epigastric pain, usually after a meal.
The pain may radiate to the chest or arms. Esophagus Diaphragm Typically, the sphincter relaxes after each swallow to allow food into the stomach. Viral hepatitis is a common infection of the liver. In most patients, liver cells hepatocytes damaged by hepatitis eventually regenerate with little or no permanent damage.
However, old age and serious underlying disorders make complications more likely. How it happens The virus causes hepatocyte injury and death, either by directly killing the cells or by activating inflammatory and immune reactions.
The inflammatory and immune reactions, in turn, injure or destroy hepatocytes by causing the infected or neighboring cells to disintegrate. Later, direct antibody attack against the viral antigens causes further destruction of the infected cells. Edema and swelling of the interstitium lead to collapse of capillaries, decreased blood flow, tissue hypoxia, scarring, and fibrosis. Gastrointestinal disorders Intestinal obstruction Intestinal obstruction is the partial or complete blockage of the lumen in the small or large bowel.
Small-bowel obstruction is far more common and usually more serious. Complete obstruction in any part of the small or large bowel, if untreated, can cause death within hours due to shock and vascular collapse.
Intestinal obstruction is most likely to occur after abdominal surgery or in persons with congenital bowel deformities. Obstruction in the small intestine results in metabolic alkalosis from dehydration and loss of gastric hydrochloric acid; lower-bowel obstruction causes slower dehydration and loss of intestinal alkaline fluids, resulting in metabolic acidosis.
Ultimately, intestinal obstruction may lead to ischemia, necrosis, and death. Intestinal obstruction develops in three forms. Simple—Blockage prevents intestinal contents from passing, with no other complications. Strangulated— In addition to blockage of the lumen, blood supply to part or all of the obstructed section is cut off.
Close-looped— Both ends of a bowel section are occluded, isolating it from the rest of the intestine. Hernia inguinal ; the sac of the hernia is a continuation of the peritoneum of the abdomen. The hernial contents are intestine, omentum, or other abdominal contents that pass through the hernial opening into the hernial sac.
How it happens The physiologic effects are similar in all three forms of obstruction. When intestinal obstruction occurs, fluid, air, and gas collect near the obstruction. Peristalsis increases temporarily as the bowel tries to force its contents through the obstruction, injuring intestinal mucosa and causing distention at and above the site of the obstruction.
Distention blocks the flow of venous blood and halts normal absorptive processes; as a result, the bowel wall becomes edematous and begins to secrete water, sodium, and potassium into the fluid pooled in the lumen.
Fluid, gas, and air collect behind obstruction. With no treatment, severe hypovolemia occurs. Gas-forming bacteria collect above obstruction, increasing distention. It invariably begins in the rectum and sigmoid colon, rarely affecting the small intestine, except for the terminal ileum. Ulcerative colitis produces edema leading to mucosal friability and ulcerations. The disease cycles between exacerbation and remission. Age-old story Age and ulcerative colitis Ulcerative colitis occurs primarily in young adults.
Onset of symptoms seems to occur most commonly between ages 15 and 30 and between ages 55 and How it happens Ch-ch-changes…I used to have a normal colon attached, but with the progression of ulcerative colitis, my buddy the colon has gone through some changes… Usually, the disease originates in the rectum and lower colon.
Then it spreads to the entire colon. Abscesses formed in the mucosa drain purulent pus, become necrotic, and ulcerate. Sloughing occurs, causing bloody, mucusfilled stools. Rebus riddle Solve the riddle to find out a way to help avoid many GI disorders, including colorectal cancer. Show and tell 1. Rebus riddle A diet high in fiber helps increase stool bulk.
Anyway, osteosomething: Take 6. Continuous or periodic compression on a nerve can cause damage over time. Certain nerves are located in regions of the body that are especially vulnerable to compression injuries. The carpal tunnel is one such region. Branches of the median nerve Flexor tendons Carpal tunnel How it happens The carpal bones and the transverse carpal ligament form the carpal tunnel.
Inflammation or fibrosis of the tendon sheaths that pass through the carpal tunnel usually causes edema and compression of the median nerve. This compression neuropathy causes sensory and motor changes in the median distribution of the hands, initially impairing sensory transmission to the thumb, index finger, middle second finger, and inner aspect of the ring fourth finger.
Normal median nerve Rheumatoid arthritis Repetitive trauma Systemic disorders, such as diabetes, rheumatoid arthritis, hypothyroidism, and amyloidosis can be a risk factor. Erosion of bone and cartilage Inflamed, swollen synovium Repetitive movements expose the nerve to compression forces and stretching.
Compressed median nerve Transverse carpal ligament Flexor tendon in synovium Nerve fiber Capillary plexus Degenerated myelin sheath No bones about it… carpal tunnel syndrome can be very painful.
In older patients whose disks have begun to degenerate, even minor trauma may cause herniation. Age-old story Age and herniated disks A herniated disk occurs more frequently in middle-aged and older men. How it happens An intervertebral disk has two parts: The nucleus pulposus acts as a shock absorber, distributing the mechanical stress applied to the spine when the body moves.
Physical stress, usually a twisting motion, can tear or rupture the anulus fibrosus so that the nucleus pulposus herniates into the spinal canal. The vertebrae move closer together and, in turn, exert pressure on the nerve roots as they exit between the vertebrae. Physical stress, from severe trauma or strain, or intervertebral joint degeneration may cause herniation.
Herniation occurs in three stages: Think PESto for your pasta and when you want to remember the three steps in herniation. In extrusion, the nucleus pulposus bulges forcibly through the anulus fibrosus, pushing against the nerve root.
Symptoms appear after age 40; its earliest symptoms generally begin in middle age and may progress with advancing age. The rate of progression varies, and joints may remain stable for years in an early stage of deterioration. With osteoarthritis, the degree of disability depends on the site of involvement and its severity.
I can have minor finger limitation or severe knee disability. How it happens Osteoarthritis is chronic, causing deterioration of the joint cartilage and formation of reactive new bone at the margins and subchondral below the cartilage areas of the joints. This degeneration results from a breakdown of chondrocytes cartilage cells , most commonly in the hips and knees. Articular cartilage Death of chondrocytes Cloning of chondrocytes Synovial fluid Tide mark Calcified cartilage Subchondral bone plate Deep crack through tide mark with underlying neovascularization Osteoblast Marrow 1 Osteoclast Chondrocytes break down in the articular cartilage.
Synovial fluid leaks into crack 3 Cartilage is gradually worn away as a result of the degeneration of the cartilage and leakage of synovial fluid.
Synovial fluid leaks out as the cartilage degenerates. Osteophytes bone spurs form at joint margins as articular cartilage erodes, causing joint enlargement. Fibrocartilage plug Thickened bone Osteoblast 4 No worry of limited movement here! Bone cysts Osteophyte Erosion of cartilage and bone New vessels grow below the tide mark from the epiphysis, and fibrocartilage is formed.
The right side shows more severe disease progression with lost cartilage and osteophyte formation. It commonly results from a combination of local trauma—usually trivial but causing a hematoma—and an acute infection originating elsewhere in the body. It may be chronic or acute. Chronic osteomyelitis, which is rare, is characterized by draining sinus tracts and widespread lesions. The most common pyogenic organism in osteomyelitis is Staphylococcus aureus.
Acute osteomyelitis is usually a blood-borne disease and most commonly affects rapidly growing children. Stages of osteomyelitis Initial infection Although osteomyelitis typically remains localized, it can spread through the bone to the marrow, cortex, and periosteum. Age-old story Age and osteomyelitis Osteomyelitis is more common in children especially boys than in adults— usually as a complication of an acute localized infection.
Typical sites in children are the lower end of the femur and the upper ends of the tibia, humerus, and radius. The most common sites in adults are the pelvis and vertebrae, generally after surgery or trauma.
The result is decreased bone mass. Bones affected by this disease lose calcium and phosphate and become porous, brittle, and abnormally prone to fracture. How it happens In normal bone, the rates of bone formation and resorption are constant; replacement follows resorption immediately, and the amount of bone replaced equals the amount of bone resorbed.
Osteoporosis develops when the remodeling cycle is interrupted and new bone formation falls behind resorption. When bone is resorbed faster than it forms, the bone becomes less dense. Calcium is key to building and maintaining bone mass. Right, Bessie? Bone-forming cells, called osteoblasts, produce the osteoid matrix. The mineral portion, which consists of calcium and other minerals, hardens the osteoid matrix.
Large bone cells reshape mature bones by resorbing the mineral and organic components. However, in osteoporosis, osteoblasts continue to produce bone, but resorption by osteoclasts exceeds bone formation.
Cortical bone Trabecular bone I could have sworn I was taller last year. It most commonly occurs in the extremities of long bones near metaphyseal growth plates. Although it can occur in any bone, it tends to appear most frequently in bones that have the fastest bone growth, such as the lower femur or upper tibia or fibula. The humerus is the second most common site. Femur sectioned How it happens All humerus aside…the lower femur, upper tibia, and fibula and humerus are the fore sites most often affected by osteosarcoma.
These abnormal cells divide uncontrollably, and healthy tissue is replaced with unhealthy tissue. Osteosarcomas grow rapidly and move from the metaphysis of the bone to the periosteal surface. Osteosarcoma Age-old story Age and osteosarcoma Osteosarcoma tumors occur equally in male and female adolescents. In females, they usually occur by age 15; in males, after age Osteosarcoma in the distal femur In the distal femur, osteosarcoma has extended through the cortex of the bone into the soft tissue and the bony epiphysis.
In this illustration, label the parts of the hand involved in carpal tunnel syndrome. Solve the word scrambles to identify parts of the musculoskeletal system. Then rearrange the circled letters to answer the question posed. Please move out of the camera until we finish with the anemia, disseminated intravascular coagulation, and leukemia takes. The prognosis after replacement therapy is favorable. Peripheral blood smear in iron deficiency anemia How it happens Iron deficiency anemia occurs when the supply of iron is too low for optimal RBC formation.
When the body uses up its iron stores, including plasma iron, the concentration of transferrin, which binds with and transports iron, decreases.