PATHOPHYSIOLOGY – FINAL EXAM STUDY GUIDE (Verified Answers, Download to Score A)

PATHOPHYSIOLOGY – FINAL EXAM STUDY GUIDE (Verified Answers, Download to Score A) PATHOPHYSIOLOGY – FINAL EXAM STUDY GUIDE NEURO – TERMS TO KNOW CONSCIOUSNESS • The state of being aware, or perceiving physical facts or mental concepts; a state of general wakefulness and responsiveness to environment; a functioning sensorium. [L. conscio, to know, to be aware of] • totally aware of surrounding activities and incoming stimuli • oriented to time, place, and people • person can respond quickly and appropriately to questions, commands, or events. • Various levels of reduced consciousness may present as o Lethargy o Confusion o Disorientation o memory loss o unresponsiveness to verbal stimuli o difficulty in arousal • Glasgow Coma Scale o Used for assessing LOC • Coma o Most serious level of loss of consciousness o Affected person does not respond to stimuli (pain, or verbal) o Some reflexes may still be present • Deep coma o Loss of all reflexes o Fixed and dilated pupils o Slow and irregular pulse and respirations AROUSAL • Reticular Activating System • determines the degree of arousal or awareness of the cerebral cortex • The pons and medulla influence the brain's awareness of the incoming pain stimuli o PONS – composed of bundles of both afferent (incoming) and efferent (outgoing) fibers o MEDULLA  contains vital control centers that regulate respiratory and cardiovascular function  contains the coordinating centers that govern coughing, swallowing, vomiting VEGETATIVE STATE • Loss of awareness and mental capabilities • Results from diffuse brain damage AMNESIA • Loss of memory CONVULSION • sudden, involuntary movement with loss of awareness, caused by uncontrolled neuronal discharge in the brain. TONIC • In a state of continuous unremitting action; denoting especially a muscular contraction. 2. Invigorating; increasing physical or mental tone or strength. CLONIC/CLONIC STATE/CLONIC SPASM • Relating to or characterized by clonus • Movement marked by repetitive muscle contractions and relaxations in rapid succession. • Alternate involuntary contraction and relaxation of a muscle DYSPHASIA • Difficulty comprehending language or speaking; partial impairment of communicating ability • Less severe form of aphasia • Caused by damage to the brain APHASIA • Inability to comprehend or express language; total loss of communicating ability • Receptive—damage to Wernicke’s area • Expressive—damage to Broca’s area • Mixed, global—damage to both areas or to the fibers and tracts between them PARESIS • Muscle weakness • Mild paralysis OTORRHEA • Leaking of CSF from the ear • Occurs with fractures • Tearing of meninges o Allows CSF to pass out of the subarachnoid space SEIZURES Seizures (look up types of seizures) ● Generalized o Absence seizures (petit mal) ▪ Lapses of awareness lasting only a few seconds ▪ Appear without warning/end abruptly ▪ More common in children ▪ Are frequently so brief, they go undetected o Tonic-clonic (grand mal) ▪ Most common ▪ Begin with stiffening of limbs (tonic phase) ▪ Followed by jerking of the limbs/face (clonic phase) o Myoclonic ▪ Rapid, brief contractions of bodily muscles ▪ Occur at the same time on both sides of body ▪ Usually involve one arm or a foot ▪ “sudden jerk” movements or “clumsiness” o Atonic (akinetic, astatic, or drop attacks) ▪ Abrupt loss of muscle tone ▪ Can produce head drops, loss of posture, or sudden collapse ▪ Appear without warning ▪ Can result in injuries to head and face ▪ Seizures are resistance to Rx therapy ▪ Protective headgear recommended o Lennox-Gastaut Syndrome (febrile seizures) ▪ Form of severe epilepsy ▪ Begins in childhood ▪ Characterized by multiple types of seizures and intellectual disability ▪ Child experiences frequent seizures (mixed type seizures) ▪ Interrupts neurological development  resulting in learning disabilities  delayed motor development ▪ Difficult to control, even with Rx medication ● Partial o Simple partial ▪ one area of the body is experiencing spasm/twitch ▪ person does not lose consciousness during seizure ▪ while fully aware, person may not be able to speak/move until seizure is over ▪ person may feel odd or altered sensations (affects all five senses) ▪ nausea may be present ▪ emotions may also be affected o Complex partial (psychomotor) ▪ Affect larger area of brain ▪ Affect consciousness; person may appear to altered state of consciousness ▪ During a seizure, person cannot interact normally ▪ Actions are typically unorganized, confused, and unfocused ▪ Unable to control body movements, speech, and actions ▪ Unaware of actions ▪ Does not remember what happened during seizure ▪ “temporal lobe epilepsy” ● Continuous seizures (status epilepticus) o in/out of seizures every second – constant/continuous state of seizure o Increased metabolism of glucose and oxygen o May be life-threatening o primary focus = PATIENT SAFETY ▪ cannot stop a seizure ▪ ABCs + safety o Death or brain damage from status seizures (as opposed to death from the underlying cause) is most likely to result from: ▪ Direct damage to the brain caused by the injury that causes the seizures ▪ Stress on the system from repeated generalized tonic clonic seizures ▪ Injury from repeated electrical discharge in the brain ALZHEIMER’S DISEASE (AD) (tends to be more psychosocial)(can be considered primary) ● Progressive cortical atrophy o Neurofibrillary tangles and plagues o ACh deficit caused by loss of neurons ● No definite diagnostic tests available o Exclusion of other disorders o Careful medical and psychological history ● Specific cause unknown o Repetitive DNA sequences on different chromosomes have been associated with AD. ● Five stages o Pre-clinical stage o Early stage o Mild stage o Moderate stage o Severe stage ● The five “A”s o Anomia – inability to remember names of things o Apraxia – misuse of objects due to failure to identify them o Agnosia – inability to recognize familiar objects, tastes, sounds, and other sensations o Amnesia – memory loss o Aphasia – inability to express language ALZHEIMER’S DISEASE (AD) - Signs and symptoms ● Extend over 10 to 20 years ● Behavioral changes o Irritability, hostility, mood swings ● Gradual loss of memory and lack of concentration ● Impaired learning, poor judgment ● Decline of cognitive function, memory, language ● Change in food intake ● Inability to recognize family, lack of environmental awareness, incontinence, inability to function INCREASED INTRACRANIAL PRESSURE ● Brain is encased in rigid, nonexpendable skull. ● Fluids, blood, and CSF are not compressible. ● Increase in fluid or additional mass causes increase in pressure in the brain o Ischemia and eventual infarction of brain tissue ● Increased ICP is common in many neurological problems. o Brain hemorrhage, trauma, cerebral edema, infection, tumors, abnormal circulation of CSF ● LOC change o may be alert, but not oriented o changes in pulse ▪ could be rapid or slow o changes in BP ▪ wide pulse pressure o Cushing’s Triad ▪ Hypertension (with widening pulse pressure) ▪ Bradycardia ▪ Respiratory depression • Early signs—if cause is not removed o Decreasing level of consciousness or decreased responsiveness (lethargy) o Decreased pupillary responses  Pupils – fixed and dilated o Severe headache  From stretching of dura and walls of large blood vessels o Vomiting  Often projectile, not associated with food intake  Result of pressure stimulating the emetic center in the medulla o Papilledema  Caused by increased ICP and swelling of the optic disc HUNTINGTON’S DISEASE • Inherited disease o Autosomal dominant gene  Carried on chromosome 4 • Does not usually manifest until individual is older than 40 years • Progressive atrophy of brain o Particularly in basal ganglia (nuclei) and frontal cortex • Depletion of gamma-aminobutyric acid (GABA) in the basal nuclei • Levels of ACh in brain appear to be reduced • Signs and symptoms o Mood swings, personality changes o Restlessness, choreiform (rapid, jerky) movements in arms and face o Decreased ability to concentrate • Diagnostic tests o DNA analysis • Treatment o Currently no therapy to slow progression of disease o Symptomatic therapy only PARKINSON’S DISEASE • Progressive degenerative disorder • Dysfunction of the extrapyramidal motor system o Progressive degeneration in basal nuclei with deficit of dopamine o Imbalance between excitation and inhibition in basal nuclei o Excess stimulation affects movement and posture.  Resting tremors  Muscular rigidity  Difficulty initiating movement  Postural instability • Primary or idiopathic Parkinson’s disease o Usually develops after age 60 • Secondary parkinsonism caused by: o Encephalitis o Trauma (e.g., sports injury) o Vascular disease o Drug-induced (e.g., phenothiazine tranquilizers) • Early signs and symptoms o Fatigue o Muscle weakness, muscle aching, o Decreased flexibility o Less spontaneous changes in facial expression o Tremors in the hands at rest, repetitive pill-rolling motions of hands • Later signs and symptoms o Tremors affect hands, feet, face, tongue, lips o Increased muscle rigidity o Difficulty initiating movements o Slow movements o Lack of associated involuntary movements o Characteristic standing posture is stooped, leaning forward o Propulsive gait o Complex activities become slow and difficult. • Other functions affected o Low voice, devoid of inflection o Dysarthria o Chewing and swallowing become difficult.  Prolonging eating time  Recurrent drooling o Face might resemble a mask  Blinking of eyelids reduced  Blank, staring face  Impairs communication o Autonomic dysfunction  Urinary retention  Constipation o Orthostatic hypotension  Threat of falls increases o Urinary tract and respiratory tract infections are common complications. o Dementia develops late in course of disease • Treatment o Removal of cause, if known o Dopamine replacement therapy  Levodopa—dopamine precursor o Anticholinergic drugs o Speech and language pathologist o Physical therapy o Occupational therapy o Improves balance, coordination o Monitoring and treatment of respiratory and urinary tract infections Transient Ischemic Attacks (TIAs) = “small strokes” - precursor to CVA ● May occur singly or in a series ● Result from temporary localized reduction of blood flow in the brain o Partial occlusion of an artery o Atherosclerosis o Small embolus ▪ clump that broke off from another part of the body ▪ can be blood, fat, protein o Vascular spasm o Local loss of autoregulation ● Signs and symptoms o Difficult to diagnose after the attack o Directly related to location of ischemia o Intermittent short episodes of impaired function ▪ e.g., muscle weakness in arm or leg o Visual disturbances o Numbness and paresthesia in face o Transient aphasia or confusion may develop. ▪ Repeated attacks may be a warning sign for obstruction related to atherosclerosis. CEREBROVASCULAR ACCIDENT (CVA) • A CVA (stroke) is an infarction of brain tissue that results from lack of blood. o Occlusion of a cerebral blood vessel o Rupture of cerebral vessel • 5 minutes of ischemia causes irreversible nerve cell damage. o Central area of necrosis develops o All function lost o Surrounded by an area of inflammation. this zone will regain function following healing. LEFT HEMISPHERE CVA • Right sided weakness/hemiplegia • Aphasia • Slow performance • Visual field deficits RIGHT HEMISPHERE • Left sided weakness/hemiplegia • Spatial-perceptual deficits o Increased vulnerability to accidents • Tends to minimize problems • Short attention span • Impaired judgement • Impaired time concept TYPES OF CVAs • Occlusion of an artery by an atheroma o Atheroma = fatty deposits and scarring that leads to tissue breakdown of the artery walls o Often develop in large arteries o Can trigger the formation of thrombosis (THROMBUS)(blood clot) o Onset is gradual o May be preceded by transient ischemic attacks (TIAs) • Sudden obstruction caused by an embolus (EMBOLUS) o Lodging in a cerebral artery o Localized unless multiple emboli are present • Intracerebral hemorrhage (HEMORRHAGE) o Caused by rupture of a cerebral artery in patient with severe hypertension  Effects are evident in both hemispheres.  Complicated by secondary effects of bleeding Types of CVAs ISCHEMIC ● thrombus ● embolus ● this patient can usually talk ● watch for mental health status changes HEMORRHAGIC ● hemorrhage ● bleeding in the brain ● this patient is going to unconscious ● likely to code STROKE RECOGNITION • Ask the person to smile and stick their tongue out • Ask the person to make a complete sentence • Ask the person to raise both arms • IF PERSON CANNOT PERFORM THESE THREE TASKS, CALL 911/SEEK MEDICAL ATTENTION INTRACRANIAL (CEREBRAL) ANEURYSM • Localized weakness in the wall of an artery • Cerebral aneurysms frequently multiple. o Usually at the points of bifurcation on the circle of Willis  Berry aneurysms o Often aggravated by hypertension o Initially small and asymptomatic o Slow bleed causes vascular type headache. o Rupture leads to sudden fatal increase in ICP and death. • Signs and symptoms o Loss of visual field or visual disturbances o Headache and photophobia o Intermittent periods of dysfunction o Nuchal rigidity caused by meningeal irritation o Vomiting, seizures, loss of consciousness in case of massive rupture; rapidly followed by death o Treatment  Surgical treatment before rupture  Antihypertensive drugs Infections – BACTERIAL MENINGITIS ● Different age groups are susceptible to infection by different causative organisms. o May be secondary to other infections ● Children and young adults o Neisseria meningitis or meningococci o Classic meningitis pathogen o Frequently carried in the nasopharynx of asymptomatic carriers o Spread by respiratory droplets o Occurs more frequently in late winter and early spring ● Signs and symptoms o Sudden onset is common. o Severe headache o Back pain o Photophobia o Nuchal rigidity (neck stiffness) o Kernig sign ▪ Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees. o Brudzinski sign ▪ Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed. o Vomiting, irritability, lethargy, fever, chills with leukocytosis o Progression to stupor or seizures ● AUTOMATIC PRECAUTIONS o only way to confirm Dx is through CSF analysis Patient with meningitis will still be able to communicate through discomfort Encephalitis (on the brain tissue)(can be seen on a CAT scan) ● Infection of the parenchymal or connective tissue in the brain and spinal cord o Necrosis and inflammation develop in brain tissue. ▪ Result in some permanent damage ● Infection may include meninges. ● Usually of viral origin o May be caused by other organisms ● Early signs o Severe headache, stiff neck, lethargy, vomiting, seizures, fever ● Patient will be completely shut down ● Western equine encephalitis o Arboviral infection spread by mosquitoes o More frequent in summer months o Common in young children ● St. Louis encephalitis o Affects older persons more seriously than younger individuals ● West Nile fever o Caused by a flavivirus o Spread by mosquitoes ● Neuroborreliosis (Lyme disease) o Caused by Borrelia burgdorferi o Transmitted by ticks o Typical bull’s-eye lesion—sore throat, dry cough, fever, headache, cardiac arrhythmias, neurological abnormalities o Antimicrobial therapy ● Herpes simplex encephalitis o Occurs occasionally o Spread from herpes simplex I o Extensive necrosis and hemorrhage in the brain Multiple Sclerosis (MS) ● Progressive demyelination of neurons in the brain, spinal cord, and cranial nerves ● Disease progresses in stages (4-5 stages) ● Progressive, intermittent lost of motor function ● Different types of MS o Variation in effects, severity, and progression ● Loss of myelin interferes with conduction of impulses in affected fibers o May affect motor, sensory, and autonomic fibers o Occurs in diffuse patches in the nervous system o Early symptoms include: ▪ Numbness ▪ Weakness in legs ▪ Visual problems Amyotrophic Lateral Sclerosis (ALS) ● Also referred to as Lou Gehrig’s disease ● No identified cause o Genes on various chromosomes have been linked to the disease. ● Progressive degenerative disease affecting upper motor neurons in the cerebral cortex and lower motor neurons in brainstem and spinal cord ● No indication of inflammation around the nerves ● Cognition unimpaired ● Descending progression (from the brain and works down the body) Guillain-Barre syndrome • Postinfection polyneuritis, acute idiopathic polyneuropathy, acute infectious polyradiculoneuritis • Inflammatory condition of the PNS • Exact cause unknown • Local inflammation with accumulated lymphocytes, demyelination, axon destruction • Changes cause impaired nerve conduction. • Critical period develops. o Ascending paralysis involves diaphragm and respiratory muscles • Progressive muscle weakness, lack of reflex response, ascending flaccid paralysis, pain, general muscle aching o Paralysis may move upward—vision and speech may be impaired. o Process may occur rapidly over a few hours or several days. o Life-threatening situation may develop. • Treatment primarily supportive HEAD INJURIES • May involve skull fractures • Hemorrhage and edema • Direct injury to brain tissue • Injury may be mild. o Bruising of the tissue • Can be severe and life-threatening o Destruction of brain tissue o Massive swelling of the brain ● Hit to parietal lobe - loss of consciousness ● Hit to temporal lobe - excessive dizziness Types of Head Injuries ● Concussion (minimal brain trauma) o Reversible interference with brain function ▪ Causes sudden excessive movement of the brain o Result of mild blow to the head or whiplash-type injury o Amnesia and headaches may follow o Avoid sleep; NEED TO KEEP AN EYE ON THE LOC ● Contusion o Bruising of brain tissue, rupture of small blood vessels, and edema o Bruising of brain on CAT scan = can be white o Contusion will stay in hospital overnight for observation ▪ observing for bleeding ▪ observing for bruised area to revasculate Primary brain injuries ● Direct injuries ● Laceration or compression of brain tissue ● Rupture or compression of cerebral blood vessels ● Damage because of rough or irregular inner surface of the skull ● Movement of lobes against each other Secondary injuries ● Result from additional effects of cerebral edema, hemorrhage, hematoma, cerebral vasospasm, infection, ischemia related to systemic factors COUP/CONTRACOUP • Coup – direct impact site • Contracoup – secondary injury on the opposite side away from primary injury BRAIN TUMORS (CANCER) • Space-occupying lesions that cause increased ICP • Benign and malignant tumors can be life-threatening. o Unless accessible and removable • Gliomas form the largest category of primary malignant tumors. o Classified according to cell derivation and location of the tumor • Tumors in the meninges or pituitary gland cause similar neurological effects. • Primary malignant tumors rarely metastasize outside the CNS. • Secondary brain tumors o Metastasize from breast or lung tumors o Cause effects similar to those of primary brain tumors • Pathophysiology o Primary malignant brain tumors  Usually no well-defined margins  Invasive and have irregular projections into adjacent tissue  Difficult to remove completely o Usually inflammation around the tumor • Occurrence o Brainstem and cerebellar tumors common in young children o Adults—occur more frequently in the cerebral hemispheres • Signs and symptoms o Site of tumor determines focal signs o Seizures often first sign  Surrounding inflammation stimulates neurons to discharge spontaneously o Headaches (increased ICP), vomiting, lethargy, irritability, personality and behavioral changes, possible unilateral facial paralysis or visual problems o Do not cause systemic signs of malignancy  Will cause death before they cause general effects • Treatment—may cause damage to normal CNS tissue o Surgery if tumor is accessible o Chemotherapy and radiation (many are radioresistant) Rabies • Viral—transmitted by: o Bite of rabid animal o Transplantation of contaminated tissues • Virus travels along peripheral nerves to CNS • Headache and fever, nervous hyperirritability, sensitivity to touch, seizures • Virus also travels to salivary glands o Difficulty swallowing o Fear of fluids • Respiratory failure, death Herpes zoster (shingles) • Caused by varicella-zoster virus in adults o Can occur years after primary infection of varicella (chickenpox) • Usually affects cranial nerve or one dermatome • Pain, paresthesia, vesicular rash o If antiviral drugs started within 48 hours of onset, pain is significantly reduced • Lesions and pain persist for several weeks. o Postherpetic pain may persist for months to years in some cases. • Vaccine available for those 60 years or older GASTROINTESTINAL SYSTEM DISORDERS MELENA • Passage of tarry stools, due to the presence of blood altered by the intestinal juices. • results from significant bleeding that has occurred higher in the digestive tract; the hemoglobin has been acted on by intestinal bacteria, causing the dark color. HEMATEMESIS • Vomiting blood that resembles “coffee grounds” • a brown, granular material resulting from the partial digestion in the stomach of protein in the blood • bright red blood = coming from upper GI • yellow/green vomit = bile (enzymes and hormones) HEMATOCHEZIA • Passage of bloody stools (in contradistinction to melena, or tarry stools) • Fresh blood (bright red) in the stool Gastroesophageal Reflux Disease ● Periodic reflux of gastric contents into distal esophagus causes erosion and inflammation. ● Often seen in conjunction with hiatal hernia ● Severity depends on competence of the lower esophageal sphincter. ● Delayed gastric emptying may be a factor. ● Avoidance of: o Caffeine, fatty and spicy foods, alcohol, smoking, certain drugs ● Use of medication may reduce reflux and inflammation ACUTE GASTRITIS • Gastric mucosa is inflamed. • May be ulcerated and bleeding • May result from o Infection by microorganisms o Allergies to foods o Spicy or irritating foods o Excessive alcohol intake o Ingestion of aspirin or other NSAIDs o Ingestion of corrosive or toxic substances o Radiation or chemotherapy Intestinal Obstruction ● Lack of movement of intestinal contents through the intestine o More common in small intestine ● Mechanical obstructions o Result from tumors, adhesions, hernias, other tangible obstructions ● Functional or adynamic obstructions o Result from impairment of peristalsis ▪ Spinal cord injury ▪ Paralytic ileus caused by toxins or electrolyte imbalance ● Gases and fluids accumulate proximal to the blockage, distending the intestine. ● Increasingly strong contractions of proximal intestine o Effort to move contents along ● Pressure increases in lumen. o More secretions enter the intestine. o Compression of veins in wall ▪ Intestinal wall becomes edematous ▪ Prevention of absorption ● Intestinal distention leads to persistent vomiting. o Additional loss of fluid and electrolytes o Hypovolemia can result ● Intestinal wall becomes ischemic and necrotic. o If obstruction is not removed, gangrene ensues. ● Ischemia and necrosis → decreased innervation and cessation of peristalsis ● Paralytic ileus occurs if it is not a cause to begin with. ● Obstruction promotes rapid reproduction of intestinal bacteria. o Some produce endotoxins. o Affected wall becomes necrotic and more permeable o Bacteria and toxins leak into peritoneal cavity (peritonitis) or into blood (bacteremia and septicemia). ● Perforation of the necrotic segment may occur. o Generalized peritonitis and septic shock ● Functional obstructions or paralytic ileus from: o Abdominal surgery (follows surgery) o Spinal shock following spinal cord injuries o Inflammation related to severe ischemia o Pancreatitis, peritonitis, infection in the abdominal cavity o Hypokalemia o Mesenteric thrombosis o Toxemia ● Mechanical obstruction from: o Adhesions that twist or constrict intestine o Hernias o Strictures caused by scar tissue o Masses—tumors or foreign bodies o Intussusception o Volvulus o Hirschsprung’s disease o Gradual obstruction from chronic inflammatory conditions ● Mechanical obstruction of small intestine o Severe colicky abdominal pain o Intermittent bowel sounds can be heard. ● Paralytic ileus o Pain is steady. o Bowel sounds decrease or are absent. ● Vomiting and abdominal distention o Occurs quickly with obstruction of small intestine o Vomiting is recurrent, eventually with bile-stained content ● Obstruction of the small intestine is a medical emergency! ● Obstruction of large intestine o Develops slowly, with mild signs o Constipation o Mild abdominal pain, followed by abdominal distention o Anorexia, vomiting, more severe pain ● Treatment o Treatment of underlying cause o Fluid and electrolyte replacement o Surgery and antimicrobial therapy Gastritis ● Inflammatory disorder of the gastric mucosa ● Acute gastritis ● Chronic gastritis o Chronic fundal gastritis o Chronic antral gastritis Acute Gastritis • Gastric mucosa is inflamed. • May be ulcerated and bleeding • May result from o Infection by microorganisms o Allergies to foods o Spicy or irritating foods o Excessive alcohol intake o Ingestion of aspirin or other NSAIDs o Ingestion of corrosive or toxic substances o Radiation or chemotherapy • Basic signs of gastrointestinal irritation o Anorexia, nausea, vomiting may develop o Hematemesis caused by bleeding o Epigastric pain, cramps or general discomfort o With infection, diarrhea may develop. o Acute gastritis is usually self-limiting. o Complete regeneration of gastric mucosa o Supportive treatment with prolonged vomiting o May require treatment with antimicrobial drugs Chronic Gastritis • Characterized by atrophy of stomach mucosa o Loss of secretory glands o Reduced production of intrinsic factor • Helicobacter pylori infection is often present. • Signs may be vague. o Mild epigastric discomfort, anorexia, intolerance for certain foods • Increased risk of peptic ulcers and gastric carcinoma • Certain autoimmune disorders are associated with one type of chronic gastric atrophy. Gastrititis: Gastroenteritis • Inflammation of stomach and intestine • Usually caused by infection • May also be caused by allergic reactions to food or drugs • Microbes can be transmitted by fecally contaminated food, soil, and/or water o Most infections are self-limiting. o Serious illness may result in compromised host or virulent organisms. o May cause epidemic outbreaks in refugee or disaster settings o Safe sanitation essential for prevention GASTRIC AND DUODENAL ULCERS • Most caused by H. pylori infection • Usually occur in the proximal duodenum (duodenal ulcers) • Also found in the antrum of the stomach (gastric ulcers) o Development begins with breakdown of mucosal barrier o Decreased mucosal defense more common in gastric ulcer development o Increased acid secretion predominant factor in duodenal ulcers • Damage to mucosal barrier predisposes to development of ulcers and is associated with: o Inadequate blood supply  Caused by vasoconstriction (e.g., by stress, smoking, shock, circulatory impairment in older adults, scar tissue, anemia)  Interferes with rapid regeneration of epithelium o Excessive glucocorticoid secretion or medication o Ulcerogenic substances break down mucous layer. o Aspirin, NSAIDs, alcohol o Atrophy of gastric mucosa  Chronic gastritis • Increased acid pepsin secretions o Increased gastrin secretion o Increased vagal stimulation o Increased sensitivity to vagal stimuli o Increased number of acid pepsin secretory cells in the stomach (genetic anomaly) o Increased stimulation of acid pepsin secretion o Alcohol, caffeine, certain foods o Interference with normal feedback mechanisms o Rapid gastric emptying • Complications of peptic ulcer o Hemorrhage  Caused by erosion of blood vessels  Common complication  May be the first sign of a peptic ulcer o Perforation  Ulcer erodes completely through the wall.  Chyme can enter the peritoneal cavity.  Results in chemical peritonitis o Obstruction  May result later because of the formation of scar tissue • 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 • Treatment o Combination of antimicrobial and proton pump inhibitor to eliminate H. pylori o Reduction of exacerbating factors Chronic Inflammatory Bowel Disease ● Crohn’s disease and ulcerative colitis are chronic inflammatory bowel diseases (IBDs). ● Causes unknown ● Genetic factor appears to be involved. ● Crohn’s disease—often during adolescence ● Ulcerative colitis—second or third decade ● Many similarities between Crohn’s disease and ulcerative colitis Crohn’s Disease ● May affect any area of the digestive tract o Usually small intestine affected ● Inflammation occurs in characteristic distribution o “Skip lesions”—affected areas separated by areas of normal tissue ● Progressive inflammation and fibrosis may cause obstructed areas. o Damaged walls impair processing and absorption of food. o Inflammation stimulates intestinal motility. ● Interference with digestion and absorption o Hypoproteinemia, avitaminosis, malnutrition, possibly steatorrhea ● Other complications o Adhesions between loops may form and fistulas may develop. ● Children o Delayed growth and sexual maturation ● Glucocorticoid used in treatment ULCERATIVE COLITIS • Inflammation starts in the rectum • Progresses through the colon • Mucosa and submucosa are inflamed. o Tissue destruction interferes with absorption of fluid and electrolytes in the colon. • Severe acute episodes—toxic megacolon may develop. • Marked diarrhea, with up to 12 stools per day o Contains blood and mucus o Accompanied by cramping pain Diverticulitis • Inflammation of the diverticula • Form at gaps between muscle layers • Congenital weakness of wall may be a factor • Weaker areas bulge when pressure increases. • Many cases are asymptomatic. • Diverticulitis stasis of material in diverticula leads to inflammation and infection. o Cramping, tenderness, nausea, vomiting o Slight fever and elevated white blood cell count o Pain is usually in the lower left quadrant • Treatment of diverticulitis o Antimicrobial drugs o Dietary modifications to prevent stasis Appendicitis: Development ● Obstruction of the appendiceal lumen o By a fecalith, gallstone, or foreign material ● Fluid builds up inside the appendix. o Microorganisms proliferate ● Appendiceal wall becomes inflamed. o Purulent exudate forms o Appendix is swollen. ● Ischemia and necrosis of the wall o Results in increased permeability o Appendicitis – Signs and Symptoms • General periumbilical pain o Related to the inflammation • Nausea and vomiting common • Pain becomes severe and localized in lower right quadrant (LRQ). • LRQ rebound tenderness develops. o Involvement of parietal peritoneum over appendix • After rupture o Pain subsides temporarily. • Pain recurs—severe, generalized abdominal pain and guarding • Low-grade fever and leukocytosis o Development of inflammation • Boardlike abdomen, tachycardia, hypotension o As peritonitis develops, abdominal wall muscles spasm. o Toxins lead to reduced blood pressure ACUTE PANCREATITIS • Inflammation of the pancreas o Results in autodigestion of the tissue • May be acute or chronic o Acute form considered a medical emergency • Pancreas lacks a fibrous capsule o Destruction may progress into tissue surrounding the pancreas o Substances released by necrotic tissue lead to widespread inflammation  Hypovolemia and circulatory collapse may follow • Chemical peritonitis results in bacterial peritonitis. o Septicemia may result. o Adult respiratory distress syndrome and acute renal failure are possible complications. • Causes o Gallstones o Alcohol abuse o Sudden onset may follow intake of large meal or large amount of alcohol ACUTE PANCREATITIS - SIGNS AND SYMPTOMS • Severe epigastric or abdominal pain radiating to the back—primary symptoms • Signs of shock • Caused by o hypovolemia • Low-grade fever until infection develops • Body temperature may then rise significantly. • Abdominal distention and decreased bowel sounds • Decreased peristalsis and paralytic ileus Gallbladder Disorders ● Cholelithiasis o Formation of gallstones o Solid material (calculi) that form in bile ● Cholecystitis o Inflammation of gall bladder and cystic duct Hepatitis ● Inflammation of the liver ● Alcoholic o Fatty liver ● Idiopathic o Fatty liver ● Viral hepatitis o Local infection ● Infection elsewhere in body o Examples—infectious mononucleosis or amebiasis ● Chemical or drug toxicity Hepatitis A ● Hepatitis A can be found in the feces, bile, and sera of infected individuals ● Usually transmitted by the fecal-oral route ● Risk factors: o Crowded, unsanitary conditions o Food and water contamination Hepatitis B ● Transmitted through contact with infected blood, body fluids, or contaminated needles ● Maternal transmission can occur if the mother is infected during the third trimester ● The hepatitis B vaccine prevents transmission and development of hepatitis B Hepatitis C ● Hepatitis C is responsible for most cases of post-transfusion hepatitis ● Also implicated in infections related to IV drug use ● 50% to 80% of hepatitis C cases result in chronic hepatitis Liver Disorders ● Hepatic encephalopathy o A neurologic syndrome of impaired cognitive function, flapping tremor, and EEG changes o The condition develops rapidly during fulminant hepatitis or slowly during chronic liver disease o Cells in the nervous system are vulnerable to neurotoxins absorbed from the GI tract that, because of liver dysfunction circulate to the brain ● Jaundice (icterus) o Obstructive jaundice ▪ Extrahepatic obstruction ▪ Intrahepatic obstruction o Hemolytic jaundice ▪ Prehepatic jaundice ▪ Excessive hemolysis of red blood cells or absorption of a hematoma ASCITES WITH CIRRHOSIS DEVELOPMENT OF ESOPHAGEAL VARICES (enlarged veins in the esophagus) JAUNDICE GASTRIC CANCER • Arises primarily in mucous glands • Mostly in the antrum or pyloric area • Early carcinoma o Confined to mucosa and submucosa • Later stages o Involves muscularis o Eventually invades serosa and spreads to lymph nodes • Asymptomatic in the early stages o Often, prognosis is poor on diagnosis • Diet seems to be a key factor, particularly smoked foods, nitrites, and nitrates. • Genetic influences also play a role. • Symptoms vague until cancer is advanced. o Reason for late diagnosis o Surgery together with chemotherapy and radiation may relieve symptoms. o Survival rate less than 20% COLORECTAL CANCER • Most malignancies develop from adenomatous polyps. • Early diagnosis is essential. • Cancer occurs primarily in persons older than 50 years. • Risk factors o Familial multiple polyposis o Long-term ulcerative colitis o Genetic factors o Environmental factors o Diet low in fiber • Initial signs depend largely on the location of the growth. • General signs • Change in bowel habits • Alternating diarrhea and constipation • Bleeding • Fatigue, weight loss, anemia • Treatment • Surgical removal with radiation and/or chemotherapy Types of Diabetes • Type 1 o Autoimmune destruction of beta cells in pancreas o Insulin replacement required  Person has no ability to produce insulin on their own o Acute onset in children and adolescents o Not linked to obesity o Genetic factors may play a role. o Develops hypoglycemia more frequently • Type 2 o Non–insulin-dependent o Oral hypoglycemic medications may be used. o Caused by decreased production of insulin and/or increased resistance by body cells to insulin o Onset is slow and insidious, usually in those older than 50 years o Associated with obesity o Component of metabolic syndrome o Increasing incidence in teens and young adults General Manifestations • Insulin deficit results in decreased transport and use of glucose in many cells. o Polyphagia o Fatigue • Blood glucose levels rise—hyperglycemia • Excess glucose in urine—glucosuria o the level of glucose in the filtrate exceeds the capacity of the renal tubular transport limits to reabsorb it. o Dehydration results from hyperosmolar filtrate. o Polyuria o Polydipsia KNOW THE THREE “P”s polyphagia = increased hunger polyuria = increased urination (20-30ml) (occurs as a result of osmotic pressure due to glucose) polydipsia = increased thirst (occurs as a result of polyuria, which causes dehydration, which triggers thirst) Diabetes: Diagnostic Tests • Fasting blood glucose level • Glucose tolerance test • Glycosylated hemoglobin test o Clinical and subclinical diabetes o Monitor glucose levels over several months. Diabetes: Treatment Principles • Maintenance of blood glucose levels in normal range o Helps reduce complications • Diet and exercise o Exercise reduces blood glucose level as skeletal muscle uses glucose. • Oral medication o Increase insulin secretion. o Reduce blood glucose levels. • Insulin replacement Type 1 Diabetes • Metabolic changes o Catabolism of fats and proteins  Excessive amounts of fatty acids and metabolites  Ketones in the blood o Ketonuria  Decreased serum bicarbonate  Decrease in pH of body fluids  Ketoacids excreted in urine • Decompensated metabolic acidosis Complications • Complications are directly related to duration and extent of abnormal blood glucose levels. • Many factors lead to fluctuations in serum glucose levels. o Variations in diet and alcohol use o Change in physical activity o Infection o Vomiting • Complications may be acute or chronic. Diabetes: Acute Complications • Hypoglycemia (insulin shock) • More common with insulin replacement treatment • Can occur because of excess oral hypoglycemic drugs • Excess insulin in circulation o Glucose deficit in blood o Can be life-threatening or cause brain damage if untreated o Often follows strenuous exercise o Dosage error o Vomiting o Skipping meal after taking insulin Hypoglycemic Shock: Signs and Symptoms • Disorientation and change in behavior • May appear impaired • Anxiety or decreased responsiveness • Decreased blood glucose level • Decreased BP, increased heart rate • Decreasing level of consciousness • NOTE: Immediate administration of glucose is required to prevent brain damage. • Diabetic ketoacidosis o Occurs in insulin-dependent clients o More commonly seen in type 1 diabetes o Result of insufficient insulin in blood (body is starved for glucose) o High blood glucose levels (but glucose can’t get to the cells) o Mobilization and use of lipids to meet cellular needs result in production of ketoacids  Increased catabolism of fats and proteins instead of glucose o May be initiated by infection or stress o May result from error in dosage, infection, change in diet, alcohol intake, or exercise Signs and Symptoms of Diabetic Ketoacidosis • Dehydration o Thirst, dry, rough oral mucosa o Warm, dry skin • Rapid, deep respiration—acetone breath (“fruity breath”) o Lethargy, decreased responsiveness o Kussmaul’s respirations • Metabolic acidosis o May lead to loss of consciousness • Electrolyte imbalances o Abdominal cramps, nausea, vomiting, lethargy, weakness DEVELOPMENT OF DIABETIC KETOACIDOSIS Acute Complications: HHNK Syndrome • HHNK: HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC • Occurs in type 2 diabetes • Insidious in onset and diagnosis may be missed • Often occurs in older clients and assumed to be cognitive impairment • Results in severe dehydration and electrolyte imbalances HHNK patient is non-insulin dependent; older patient probably dehydrated looks like DKA, but there are no ketones know the difference between DKA and HHNK HHNK Manifestations • Hyperglycemia • Severe dehydration o Increased hematocrit o Loss of turgor o Increased heart rate and respirations • Electrolyte imbalances result in: o Neurologic deficits o Muscle weakness o Difficulties with speech o Abnormal reflexes Antidiuretic Hormone (ADH) • Diabetes insipidus o underproduction of ADH (hyposecretion of ADH or failure to respond to ADH) o Adenoma o May originate in the neurohypophysis  Head injury or surgery  Possible genetic problem  Replacement treatment required o Excess urine output (4-30 liters in a 24-hour period) o Leads to dehydration o Causes include:  Neurogenic  Stroke  Tumor  Infection  Pituitary surgery • Inappropriate ADH syndrome (SIADH) o Excess/overproduction of ADH  May be temporary, triggered by stress; may be secreted by an ectopic source, such as a tumor o Causes the body to retain water (fluid volume excess) o Leads to hyponatremia and water intoxication o Patient will have increased BP, crackles, +JVD o Caused by:  Trauma  Tumors  Infection  Certain medications o Treatment  Diuretics  Sodium supplements IDDM = DKA NIDDM = HHNK (60 + year old patients) DI = diabetes due to tumor in the brain; affects hormone release; in this case, there is a deficit (as in none) of ADH; causes of severe dehydration SIADH = patients experience fluid overload (syndrome of inappropriate ADH) Growth Hormone (GH) • Acromegaly o Excess GH secretion in adults o Often associated with adenoma o Bones become broader and heavier. o Soft tissue grows.  Enlarged hands and feet, change in facial features THYROID DISORDERS • Hyperthyroidism (Graves’ disease) o Related to autoimmune factor o Hypermetabolism and increased stimulation of SNS  Increased body temperature  Heat intolerance  Sweating  Soft silky hair and skin  Reduced BMI  Insomnia  Hyperactivity  Tachycardia o Toxic goiter o Exophthalmos  Presence of protruding, staring eyes, decreased blink and eye movement  “bulging eyes”; appear to be pushing out of the eye socket  Result of increased tissue mass in the orbit  May result in visual impairment • Hypothyroidism o Iodine deficit o Hashimoto’s thyroiditis  Autoimmune disorder o Tumor o Surgical removal or treatment of gland o Cretinism  Results in short stature and severe cognitive deficits  Untreated congenital hypothyroidism  May be related to iodine deficiency during pregnancy Hypothyroidism Manifestations • Goiter if cause is endemic iodine deficiency • Intolerance to cold • Increased BMI • Lethargy and fatigue • Decreased appetite • Myxedema in severe, untreated hypothyroidism o Nonpitting edema in face, thickened tongue o Myxedema coma—acute hypotension, hypoglycemia, and hypothermia result in loss of consciousness; life-threatening if untreated MUSCULOSKELETAL SYSTEM DISORDERS SUBLUXATION • Partial dislocation of a joint • Partial loss of contact between two bone surfaces • Swelling, deformity, and limited movement result DISLOCATION • Complete separation of two bones at a joint with loss of contact between the articulating bone surfaces • one bone is out of position, while the other bone remains in normal position o i.e. humerus @ shoulder joint • Can be caused by: o Trauma; usually a fall o Fracture may occur concurrently with dislocation o Underlying diseases/disorders  Musclular diseases  Rheumatoid arthritis o Damage resulting from torn ligaments Sprains and Strains ● Sprain (ligaments) ● Strain (tendons) ● Avulsion (total pull away/disconnect from the joint) ● Immobilization often used to prevent tissue damage and promote healing ● treat both the same (“R.I.C.E”) ligaments = connect bone to bone tendons = connect muscle to bone BURSITIS • inflammation of the bursae associated with bones, muscles, tendons, and ligaments of various joints • caused by repetitive motions or positions that physically irritate the bursae @ affected joint Bone Disorders—Osteoporosis ● Decrease in bone mass and density ● women are more likely to have this condition ● Occurs in two forms: ● Primary o Idiopathic o Age 50+ years o Decreased sex hormones o Decreased calcium intake o can evaluate blood for osteoblasts/osterclasts ● Secondary o As a complication of another disorder Osteoarthritis ● Degenerative—wear and tear joint disease ● May be the result of increased weight-bearing or lifting ● Incidence increasing ● Genetic component identified in research with mice ● breakdown and erosion of cartilage Rheumatoid Arthritis ● Considered an autoimmune disorder ● Causes chronic systemic inflammatory disease o Systemic inflammatory disorder due to autoimmune reaction ● Higher incidence in women than in men ● Affects all age groups ● presence of rheumatoid factor ● typical joint involvement includes o bilateral small joints o symmetrical progression to other joints DISTINGUISHING FACTORS ● OA is unilateral (one side) ● RA is bilateral (all over) Articular cartilage is damaged by enzymatic destruction by the pannus (see image below) Synovitis—Inflammation recurs, synovial cells proliferate. Pannus formation—Granulation tissue from the synovium spreads over the articular cartilage. This granulation tissue, called pannus, releases enzymes and inflammatory mediators, destroying the cartilage (Fig. 9-13). Cartilage erosion—Cartilage is eroded by enzymes from the pannus, and in addition, nutrients that are normally supplied by the synovial fluid to the cartilage are cut off by the pannus. Erosion of the cartilage creates an unstable joint. Fibrosis—In time, the pannus between the bone ends becomes fibrotic, limiting movement. This calcifies and the joint space is obliterated. Ankylosis—Joint fixation and deformity develop. Gout ● Also known as gouty arthritis ● Results from deposits of uric acid and crystals in the joint, causing inflammation ● Formation of tophus—large hard nodule of urate crystals ● Tophi cause local inflammation and occur after the first attack of gout. ● very painful ● common in renal failure patients ● common in liver failure patients ● common in pancreatic failure o any patient who has compromised filtration OSTEOMYELITIS • Bone infection caused by bacteria or fungi • Signs and symptoms o Local inflammation and bone pain o Fever and excessive sweating o Chills o General malaise • Treatment o Antibiotics o Surgery may be required. • Often occurs with open fracture • Can be viewed with an X-ray • Long term triple antibiotics required for treatment FRACTURES FRACTURES • A fracture is a break in the integrity of a bone. • Fractures occur because of trauma, neoplasms, or increased stress on bones. • Fractures are charted using the # sign. CLASSIFICATION OF FRACTURES • Complete: bone broken, forming separate pieces • Incomplete: bone only partially broken • Open (compound): skin broken • Closed: skin not broken • Simple: single break, maintaining alignment and position • Comminuted: multiple fractures and bone fragments • Compression: bone crushed or collapsed into small pieces TRAUMA – FRACTURES • Other types: o Impacted—one end forced into adjacent bone o Pathologic—results from weakness; occurs with little stress o Stress—fatigue fractures o Depressed—skull fractured and forced into brain The Five Ps • pain • pulse • pallor • paralysis • paresthesia understand circulation, motor, and sensory as they relate to fractures ● check pulse ● check for tingling/numbness break vs. fracture ● break is a complete separation; surgery required ● fracture is a crack, but bone is still partial intact colles fracture = “boxer’s fracture” (wrist/distal radius fracture) Risk factors for fractures (cited from ) • age – women are more likely to have fractures than men • gender • smoking/tobacco use • alcohol abuse • steroids (corticosteroids) • Rheumatoid arthritis • Chronic disorders o Celiac disease o Crohn’s disease o Ulcerative colitis • Diabetes Type 1 • History of previous low impact fractures • Family history Factors Affecting Bone Healing ● Amount of local damage ● Proximity of bone ends ● Presence of foreign material or infection ● Blood supply to fracture site ● Systemic factors, such as age, nutrition, anemia Complications ● Muscle spasms o occurs due to shift in muscle tissue, blood vessels, and nerves o pain management is difficult ● Infections ● Ischemia ● Fat emboli o requires proactive assessment of respiratory signs o pre-op risk 12-24 hours after injury/prior to surgery o pulmonary embolism = post op ● Nerve damage ● Failure to heal or development of deformity during healing ● Residual effects such as osteoarthritis Treatments of Fractures ● Closed reduction—pressure to restore bone position o requires conscious sedation o used to put bone back into an anatomical position before surgery ● Open reduction—surgery to align and/or Insert pins, screw rods, or plates to align Compartment Syndrome Compartment Syndrome ● Edema within one area of compartment of the limb that is between layers of dense connective tissue (fascia) ● Ischemia and infarction of tissue may occur because of compression of arterial blood supply. ● Dead tissue may become gangrenous, requiring amputation. ● A tight cast can cause compartment syndrome! ● occurs with long bones ● DO NOT PUT ICE ON COMPRESSION SYNDROME o facilitates compartment syndrome ● severe compression ● swelling of the muscle URINARY/RENAL SYSTEM DISORDERS HYDROURETER • Distention of the ureter with urine, due to blockage from any cause. • Obstruction of urine flow in the ureter • i.e. a kidney stone causing backflow HYDRONEPHROSIS • Dilation of the pelvis and calyces of one or both kidneys resulting from obstruction to the flow of urine. • Obstruction of urine flow in the kidney • Secondary problem caused by: o Complication of calculi o Tumors, scar tissue in kidney or ureter o Untreated prostatic enlargement o Developmental abnormalities restricting urine flow • Frequently asymptomatic in early stages • Can be diagnosed with ultrasonography, radionucleotide imaging, CT, or renal scan • If cause is not removed—chronic renal failure RENAL CALCULI/UROLITHIASIS • Can develop anywhere in urinary tract • Stones may be small or very large. • Tend to form with: o Excessive amounts of solutes in filtrate o Insufficient fluid intake—major factor for calculi formation o Urinary tract infection • Manifestations only occur with obstruction of urine flow. o May lead to infection o Hydronephrosis with dilation of calyces o If located in kidney or ureter and atrophy of renal tissue • Calculi composed of calcium salts o High urine calcium levels o Form readily with highly alkaline urine • Uric acid stones o Hyperuricemia  Gout, high-purine diets, cancer chemotherapy o Especially with acidic urine • Struvite and cystine stones • Stone formation depends on predisposing factor. • Stones in kidney or bladder often asymptomatic o Frequent infections may lead to investigation. o Flank pain possible caused by distention of renal capsule • Renal colic caused by obstruction of the ureter o Intense spasms of pain in flank area  Radiating into groin area  Lasts until stone passes or is removed o Possible nausea and vomiting, cool moist skin, rapid pulse o Radiological examination confirms location of calculi. • Treatment o Small stones will be passed eventually. o Extracorporeal shock wave lithotripsy (ESWL) o Laser lithotripsy o Drugs may be used to dissolve stones partially. o Surgery • Prevention o Treatment of underlying condition o Adjustment of urine pH through dietary modifications o Consistent increased fluid intake BLADDER CANCER • Most bladder tumors are malignant and commonly arise from transitional epithelium of the bladder. • Often develops as multiple tumors • Most common in males older than 60 years • Diagnosed by urine cytology and biopsy • Early signs o Hematuria, dysuria o Infection common • Tumor is invasive through wall to adjacent structures. o Metastasizes to pelvic lymph nodes, liver, and bone • Predisposing factors o Working with chemicals in laboratories and industry  Particularly aniline dyes, rubber, aluminum o Cigarette smoking o Recurrent infections o Heavy intake of analgesics • Treatment o Surgical resection of tumor o Chemotherapy and radiation o Photoradiation successful in some early cases URINARY TRACT INFECTION Urinary Tract Infections (UTIs) ● Very common infections ● Urine is an excellent growth medium. ● Lower urinary tract infections (LUTS) o Cystitis ▪ Dysuria (painful urination) ▪ Pyuria (pus) o Urethritis ● Upper urinary tract infections o Pyelonephritis ▪ CAT scan used ● Common causative organism o Escherichia coli o bacteria from anal sphincter makes its way into the urethra LUTS - lower urinary tract infections ● postrenal infection Causes of Infection in the Urinary Tract Pyelonephritis ● ONE OR BOTH KIDNEYS INVOLVED ● FROM URETER INTO KIDNEY ● PURULENT EXUDATE FILLS PELVIS AND CALYCES ● Usually caused by E. coli infection ● RECURRENT OR CHRONIC INFECTION CAN LEAD TO SCAR TISSUE FORMATION. o LOSS OF TUBULE FUNCTION o OBSTRUCTION AND COLLECTION OF FILTRATE → HYDRONEPHROSIS o EVENTUAL CHRONIC RENAL FAILURE IF UNTREATED ● automatic admission to the hospital ● can cause renal failure ● pain in lower back; due to inflammation that stretches the renal capsule PRERENAL - before infection arrives at kidney INTRALRENAL - infection in the kidney POSTRENAL - infection that occurs outside of the kidney Nephrotoxic • pertaining to nephrotoxin • toxic to renal cells Renal Failure AKI =acute kidney injury (follows intense exercise - marathons, stones) ● complains of back pain, hematuria ARF = acute renal failure Acute Renal Failure ● Causes o Acute bilateral kidney diseases o Severe, prolonged circulatory shock or heart failure o Nephrotoxins ▪ Drugs, chemicals, or toxins ▪ Toxic to renal cells o Mechanical obstruction (occasionally) ▪ Calculi, blood clots, tumors ● Block urine flow beyond kidneys ● TPA can be used to bust up clots ● Sudden onset ● Blood tests o Elevated serum urea nitrogen and creatinine levels o Metabolic acidosis and hyperkalemia ● Treatment o Identify and remove or treat primary problem. ▪ To minimize risk of necrosis and permanent kidney damage o Dialysis ▪ To normalize body fluids and maintain homeostasis CAUSES OF RENAL FAILURE: NEPHROTOXINS toxins often get stuck in the loop of henle and never make it out of the distal tubule oliguria = decreased urine output resulting from inflammation and necrosis of the tubules anuric = no urine production micturition = the desire/urge to urinate micturition reflex = Relaxation of the urethral sphincter in response to increased pressure in the bladder CAUSES OF RENAL FAILURE: ISCHEMIA Chronic Renal Failure (irreversible damage) ● Progressive loss of renal function that affects nearly all organ systems ● Associated with HTN, diabetes, intrinsic kidney disease ● Stages: o Normal (GFR >90mL/min) o Mild (GFR 60-89mL/min) o Moderate (GFR 30-59mL/min) o Severe (GFR 15-29mL/min) o End stage (GFR less than 15) End-stage renal failure ● Negligible GFR ● Fluid, electrolytes, and wastes retained in body ● Azotemia, anemia, and acidosis (three As) o Anemia = erythropoitin production affected o Azotemia = toxins in the blood o Acidosis = low pH/low bicarbonate (metabolic) ● All body systems affected ● Marked oliguria or anuria ● Regular dialysis or kidney transplantation o To maintain patient’s life ● Early signs o Increased urinary output o General signs o Anorexia o Nausea o Anemia o Fatigue o Unintended weight loss o Exercise intolerance ● Bone marrow depression and impaired cell function o Caused by increased wastes and altered blood chemistry • Elevated blood pressure ● Complete failure – Uremic signs o Oliguria o Dry, pruritic, hyperpigmented skin, easy bruising o Peripheral neuropathy o Impotence in men, menstrual irregularities in women o Encephalopathy o Congestive heart failure, dysrhythmias o Failure to activate vitamin D (cause of osteodystrophy) o Possible uremic frost on the skin o Systemic infections ● Diagnostic tests o Anemia, acidosis, and azotemia are the key indicators of chronic renal failure. ● Treatment—all body systems are affected. o Difficult to maintain homeostasis of fluids, electrolytes, and acid-base balance o Drugs to stimulate erythropoiesis o Drugs to treat cardiovascular problems o Intake of fluid, electrolytes, protein must be restricted o Dialysis or transplantation RENAL CELL CARCINOMA (KIDNEY CANCER) • Primary tumor arising from the tubule epithelium o More often in renal cortex • Tends to symptomatic in early stages • Often has metastasized to liver, lung, bone, or central nervous system at time of diagnosis • Occurs more frequently in men and smokers • Treatment is removal of kidney. • Immunotherapy may be used in some cases. • Tumor is radioresistant, and chemotherapy is not used in most cases. • Manifestations o Painless hematuria initially o Gross or microscopic o Dull, aching flank pain o Palpable mass o Unexplained weight loss o Anemia or erythrocytosis o Paraneoplastic syndromes  Hypercalcemia or Cushing’s syndrome WILM’S TUMOR • Most common tumor in children • Defects in tumor suppressor genes on chromosome 11 o May occur in conjunction with other congenital disorders • Usually unilateral o Large encapsulated mass • Pulmonary metastases may be present at diagnosis. GLOMERULONEPHRITIS ● Mechanisms of injury o Deposition of circulating soluble antigen-antibody complexes, often with complement fragments (Type III hypersensitivity) o Antibodies reacting in situ against planted antigens within the glomerulus (Type II hypersensitivity–cytotoxic) o Nonimmune (drugs, toxins, ischemia) ● Manifestations o Two major symptoms if severe ▪ Hematuria with red blood cell casts (a complication)(blood in the urine) ▪ Proteinuria exceeding 3 to 5 g/day with albumin (macroalbuminuria) as the major protein (excess protein in the urine) ● lose of protein/”cushion” of osmotic pressure ● edema may not be present, but weight changes will be obvious ● lungs sounds (rales/crackles) will offer clues to this condition o Oliguria (decreased urine output) o Hypertension o Edema (facial and preorbial followed by generalized edema) o Nephrotic sediment (loss in protein) o Nephritic sediment (loss in protein) o Pain in the back or flank due to stretches in the renal capsule Path of Renal Blood Flow (** 1200 ml of blood enters the renal arteries each minute) • Renal Artery • Segmental Arteries • Interlobar Arteries • Arcuate Arteries • Cortical Radiate Arteries • Afferent Arterioles • Glomerular Capillaries • Efferent Arterioles • Peritubular capillaries • Cortical radiate veins • Arcuate veins • Interlobar veins • Renal vein Trace the pathway of a molecule of waste from the time it enters the renal artery until it leaves the body in the urine. Be specific about its pathway through the kidney. Include microscopic structures. • Molecule of waste in renal artery >> • Glomerular Filtration: Glomerular capillaries (glomerulus) >> • Bowman's (Glomerular) Capsule: BECAUSE IT IS A MOLECULE OF WASTE, IT WON'T BE REABSORBED >> • Proximal convoluted tubule >> • Loop of Henle >> • Distal convoluted tubule >> • Collecting duct >> • Minor Calyx >> • Major Calyx >> • Renal Pelvis >> • Ureter >> • Urinary Bladder (by peristalsis) >> • Urethra (after relaxation of internal urethral sphincter) >> • Leaves body in the form of urine (after relaxation of external urethral sphincter) >> • TOILET, FLUSH, WASH, and be on your way! Normal pH of urine = 4.5 – 8.0