Patho 1000 Midterm 2 units 5-7

Question Answer
Average volume of blood in a human body? 5-6 L
Which blood cell accounts for approximately 42%-48% of blood volume? Red Blood Cells
What is the most abundant leukocyte? Neutrophils
Blood composition: liquid component – plasma= proteins 7%/ water 91%
Blood component= Red Blood Cells/ White Blood Cells / platelets
White Blood Cells further break down to cytes/ phils
Cytes: Moncytes, Leukocytes (immune cells), Granuleukocyte.
Phils: Neutrophils, Eosinophils, Basophils
Role of Red Blood Cells Deliver oxygen to the body tissues
Role of red blood cells Hemeglobin found within RBC combines with O2 Out number white blood cells 1000:1
Hemeglobin is made up of Heme pigment & globin protein
Any alteration in quantity or structure of the erythrocyte Leads to altered cellular oxygen
O2 transport depends on The amount of RBC’s available
O2 transport depends on Functional cardiovascular system
Red blood cell disorders etiology (anemia) Decreased production leads to Decreased hemoglobin
Red blood cell disorders etiology (anemia) Increased destruction (hemolysis)
Red blood cell disorders etiology (anemia) Increased blood loss
Anemia A deficient number or concentration of erythrocytesOutcome -> blood cannot carry as much O2 as required
Anemia- Decreased production Fe Deficency
Anemia- Decreased production Vitamin B12/ Folic acid deficiency
Anemia- Decreased production Erythropoietin deficiency
Anemia- Decreased production Decreased bone marrow production
Anemia- Decreased production Chronic Disease
Anemia- Increased destruction Infections
Anemia- Increased destruction Genetics
Anemia- Increased destruction Transfusion reaction
Anemia- Increased Blood loss Hemorrhage- not just acute, can be chronic such as GI bleeds or cancer.
Microcytic:Macrocytic: larger than normal erythrocytesNormocytic: normal erythrocytes Abnormally small erythrocytes
‘cytic’ ending refers to Size
‘chromic’ ending refers to Color
Hypochromic: Insufficent hemoglobin content
Normochromic: normal levels of hemoglobin Normal levels of hemoglobin
Due to decreased oxygen carrying capacity:Rationale for Clinical manifestations:Lack of oxygen: fatigue Causes fatigue
Due to decreased oxygen carrying capacity:Rationale for Clinical manifestations:Short of breathe: Causes hyperventilation, to compensation to oxygenate blood
Due to decreased oxygen carrying capacity:Rationale for Clinical manifestations:Dizziness: due to shortness of breathe Caused by shortness of breathe
Due to decreased oxygen carrying capacity:Rationale for Clinical manifestations:Pallor (skin, mucous membranes, nails) Lack of Iron (Fe)
Due to decreased oxygen carrying capacity:Rationale for Clinical manifestations:Increased heart rate Compensation to help oxygenate blood
Iron Deficiency Anemia -> (Microcytic- Hypochromic) Anemia caused by insufficient iron Leads to v hemoglobin synthesisMost common type of anemia in the world
Iron deficiency AnemiaDecreased Fe leads to Decreased hemeglobin synthesis leads to decreased O2 in blood
Fe is obtained through diet recycling of old RBC
Iron deficient AnemiaCells appear microcytic & hypochromic
Iron deficient AnemiaYou must be Must be iron deficient before becoming anemic
Iron deficient AnemiaChronic Hemorrhage causes Excessive/prolonged menstrual bleedingIntestinal bleedingMalabsportion: celiaic flattened villia
Iron deficient AnemiaChronic Hemorrhage causes Low/ insufficient iron intake (rare) * dietary deficiency (vegetarian)May occur in pregnancy
Anemia occurs when Demand for Fe exceeds supply
Fe Deficient Anemia occurs in 3 stages:Stage 1 Body iron stores are depleted
Fe Deficient Anemia occurs in 3 stages:Stage 2 Iron transport to bone marrow is decreased leading to iron deficient erythropoiesis
Fe Deficient Anemia occurs in 3 stages:Stage 3 Small Hemeglobin (Hb) deficient cells enter circulation. Clinical manifestation will appear at this stage
Fe deficient anemia Clinical Mainifestations Symptoms start gradually & can be non-specificWeakness & fatigueSyncope: faintingPallor: iron gives them colorTachycardiaSOBStomatitis: Sores in mouth (late stage)
ThalassemiaEtiology: Inherited Inherited Autosomal recessive disorder
ThalassemiaEtiology: Classified as either minor or major
ThalassemiaEtiology: Affects Alpha or Beta chain synthesis
ThalassemiaEtiology: Beta-Thalasssemia is more common than Alpha
ThalassemiaEtiology: Beta minor is usually asymptomatic
Beta-Thalassemia majorClinical manifestations Severe anemiaCHFSplenomegalyHepatomegalyBone marrow hyperplasia
Beta-Thalassemia majorClinical manifestations May have enlarged spleen. May need many blood transfusions which causes symptoms.Getting rid of red blood cells and heme molecule.Liver tries to rid access iron from transfusionsLivers over working and spleen is over working
Megaloblastic Anemia (Macrocytic-Normochromic) Deficiency of B12 and folic acid causing impaired DNA synthesis
Megaloblastic Anemia decrease/ deficiency vitamin B12 or deficient/ decreased folic acid –> Decreased rate of RBC production
Megaloblastic Anemia Result in large immature erythrocytes (megaloblasts)
Megaloblastic Anemia Carry Hb but membranes are fragileShort life span
Megaloblastic Anemia Shape is oval instead of biconcave
Megaloblastic Anemia Membrane on cell very filmsyCells appear macrocytic with large nuclei
Folic Acid deficiency Etiology:Diet (Rare): Due to ^ amounts of folate in diets-Leafy green vegetables-Fortified cereals and grains
Folic Acid deficiency Etiology:Potential causes Pregnancy- ^ demand during fetus growth
Folic Acid deficiency Etiology:Potential causes Malnutrition/ ETOH abuse
Folic Acid deficiency Etiology:Potential causes Malabsorption syndromes (celiac)
Folic Deficiency Patho Anemia results from apoptosis of erythroblasts
Folic Deficiency: Clinical Manifestations Severe cheliosis
Folic Deficiency : Clinical Manifestations Stomatitis- Mucosal suface is changing.
Folic Deficiency: Clinical Manifestations Painful mouth ulcers
Folic Deficiency: Clinical Manifestations Dysphagia
Folic and B12 Deficiency: B12 is essential for DNA synthesis
Folic and B12 Deficiency: Found in all foods of animal origin
Etiolgy of B12 deficiency Dietary (rare)May be in found in strict vegetarians
Etiolgy of B12 deficiency Defective intestinal absorption
Etiolgy of B12 deficiency Gastrectomy/ inflammation/ malabsorption syndromes
Etiolgy of B12 deficiency Pernicious Anemia
Etiolgy of B12 deficiency Chronic atrophic gastritis
Absorption of B12 B12 must be bound to intrinsic factor for absorption
Absorption of B12 Intrinsic factor comes from the gastric parietal cells
Absorption of B12 Once bound together the complex travels to the ileum for absorption
Pernicious Anemia More prevalent in females
Pernicious Anemia Most cases occur from an autoimmune gastritisGastritis affects IF
Pernicious Anemia Clinical manifestations develop slowlyWhat can occur if this type of anemia is not treated? untreated anemia is fatal because of heart failure, has to work so much harder to oxygenate tissues.
Pernicious AnemiaClinical Manifestations PallorLethargy/ fatigueNausea/ vomitingStomatitis
Pernicious AnemiaClinical Manifestations DypsneaNeurologic symptoms:Parasthesias- weakness/ numbness/ tingling/ dementia
Aplastic Anemia- (normocytic-normochromic) Damage to bone marrow erythropoiesis
Aplastic Anemia- Bone marrow unable to produce RBC/ WBC/ platelets (hypocellular)Characterized by pantocytopeniaBone marrow is mostly fat
Aplastic Anemia- Etiology Primary (idiopathic) 75% of all casesSecondary- chemical agents (15% of cases)
Aplastic Anemia- Etiology 20 to chemotherapy, radiation, etcFamilial trait (10%)Onset of symptoms is insidious
Aplastic Anemia- Clinical Manifestations PetichiaeEccymosisHemorrhagePallor
Aplastic Anemia- Clinical Manifestations WeaknessInfectionsSOBArrhythmias
Anemia of Chronic Disease Anemia resulting from v erythropoiesis 20 to chronic disease or inflammationEg) AIDS, rheumatoid arthritis, lupus, chronic renal failure
Anemia of Chronic Disease Anemia is usually mild to moderate in severity
Anemia of Chronic Disease Anemia develops after 1-2 months of disease activity
Anemia of Chronic disease -(ACD)causes that will result in ACD (2 of 4) Decreased erytroyte lifespanSupressed production of erythrocytes
Anemia of Chronic disease -(ACD)causes that will result in ACD (2 of 4) Ineffective bone marrow response to erythopoiethinAltered iron metabolism
Sickle Cell Disease(normocytic-normochromic anemia)Etiology Inherited autosomal recessive disorder that must be passed on from both parentsHbA is replaced with HbS due to a point mutationShortens the RBC lifespan to 16 days
Sickle Cell Disease(normocytic-normochromic anemia)Patho When exposed to conditions of low oxygen the hemoglobin’s shape is distorted into a sickled shape this is known as HbS
Sickle Cell Disease(normocytic-normochromic anemia)Patho The HbS molecules bind together to form a long chain (polymerization)-> results in the structural change to the RBC (sickle shape)
Sickle Cell Disease(normocytic-normochromic anemia)Patho Sickling can cause hemolysis
Sickle Cell Disease(normocytic-normochromic anemia)Distinguishing RBC RBC: 120 days life spanHb has normal oxygen carrying capacity12 – 14 g of Hb per mlRBC destroyed at normal rate
Sickle Cell Disease(normocytic-normochromic anemia)Distinguishing Sickle Cell Sickle Cell:16 day life spanHb has decreased oxygen capacity6 – 9 g of Hb per mlRBC destroyed at accelerate rate
Sickle Cell Disease(normocytic-normochromic anemia)Clinical Manifestations AnemiaPallorPainJaundiceSwelling of extremitiesDyspneaInfectionsFatigue
Sickle Cell Disease(normocytic-normochromic anemia)(thrombotic crisis) What has occurred to the cells and where does this occur? Cell starts to sickle to micrcirculation to an obstruction in circulation
Sickle Cell Disease(normocytic-normochromic anemia)Causes:(thrombotic crisis) Causes: InfectionExposure to coldDehydrationLocalized hypoxemia
Sickle Cell Disease(normocytic-normochromic anemia)Symptoms:(thrombotic crisis) Symptoms: Painful swelling of hands and feet, may also affect joints
Polycythemia (Erythrocytosis) Chronic myeloproliferative disorderPrimary- Polycythemia Vera Actual increase in the number of blood cellsRBC (primarily)/ WBC/ platelets Due to increased production by the bone marrow
Secondary polycythemia Any condition that causes decreased oxygenHigh altitude (hyperplasia)Heart diseasePulmonary diseaseStimulates the bone marrow to produce RBC
Polycythemia Clinical Manifestations Enlarged spleen:abd painHypercoagulability:thrombosis & occlusionPlethoraHTN: risk for anginaHepatomegaly:portal HTN
Quantitative vs Qualitative Disorders Both terms refer to leukocytes (WBC) & encompasses all cells in this groupingGranulocytes (Neutrophils, basophils, eosinophils)Monocytes (macrophages)Lymphocytes (T & B cells)
Quantitative vs Qualitative DisordersQuantitative: the amount of cells are either ^ (end in ‘osis’) or v(end in ‘penia’)
Quantitative vs Qualitative DisordersQualitative: function of the cells are impaired
LymphocytosisInfectious mononucleosis Acute viral infection of B lymphocytes
LymphocytosisInfectious mononucleosisHow is it transmitted? Saliva
LymphocytosisInfectious mononucleosisIncubation: 4-8 weeks
LymphocytosisInfectious mononucleosisWhat is the Etiology? EBV (herpes Viruses)
Mononucleosis Sore throatFeverAmlaiseArtralgiasLymphadenopathyThick exudate in pharnyxFatigue
Leukopenia Low WBC count
Leukopenia Caused by ^ destructionChemotherapyRadiationAplastic anemiaCertain cancersAutoimmune disease
Leukopenia Results in a decreased ability to fight infections
Leukopenia Neutrophils mostly affected-> neutropenia
Leukopenia If severe loss–> granulocytopenia or agranulocytosisThis can cause life threatening infections.
Leukocytosis increased WBC
Leukocytosis Can be a normal protective response:StressorsInfectionPregnancy
Leukocytosis Can be due to a pathologic condition:Malignancies or hematologic disorders
Leukemia Affects leukocyte cellsMalignant neoplasm of myeloid or lympoid cells.It can affect both myeloid and lymphoid tissue
Leukemia Features:^ proliferation in the bone marrowv differentiation & v sensitivity to apoptosisRelease of immature cells into circulationResults in pantocytopenia ( affects all the cell types)
Leukemia Can be acute or chronicEtiology: unknown but a genetic abnormality is present in some cases (Philadelphia chromosome)
Acute Leukemia Undifferentiated/ immature cellsResults in overcrowding in the bone marrowOnset: abruptShort survival time
Chronic Leukemia Cells are more differentiated but have impaired functionOnset: slow progressionLonger life expectancy
Acute myeloid leukemia (AML) Progresses quicklyAffects myeloid cellsUndifferentiated, immature WBC with crowdingMore common in adultsCan affect children
Acute lymphocytic leukemia (ALL) Progresses quicklyAffects lymphoid cellsUndifferentiated, immature WBC, affects RBCMost common type in children
Chronic myeloid leukemia (CML) Slow progressingAffects myeloid cellsCells are mature- lack functionalityAffects adult
Chronic lymphoid leukemia (CLL) Slow progressingAffects lymphoid cellsAffects adults
Leukemia- Clinical manifestations Fatigue (anemia)Bleeding (thrombocytopenia)Fever (due to infection)Anorexia & wt lossLymphadenopathy- swollen lymph nodesBone pain due to increased pressure from WBC production increase
Lymphoma Malignant tumor of the lymphoid tissuesPresents with lymphadenopathyClassified as Hodgkin’s or non- Hodgkin’s Lymphoma
Hodgkin’s LymphomaHow is this characterized? Malignant lymphoma that progresses from one lymph node to another.
Hodgkin’s LymphomaWhich cells are present? Presence of Reed- Sternberg cells. B cells (two Nucueli).
Hodgkin’s LymphomaPrognosis: RS cells are necessary for diagnosis.Approx. 75% are cured
Hodgkin's LymphomaClinical manifestations Fever, night sweatsWeight lossFatigueEnlarged cervical lymph nodesMediastinal massSplenomegaly
Non-Hodgkin’s Lymphoma AKA: B-cell neoplasm, T-cell neoplasms & NK-cell neoplasms
Non-Hodgkin’s Lymphoma Lacks Reed-Sternberg cells
Non-Hodgkin’s Lymphoma Proliferation of B or T or NK cells that become immortal
Non-Hodgkin’s Lymphoma Caused by chromosomal translocations
Non-Hodgkin’s Lymphoma Affects middle age >50 years
Non-Hodgkin’s LymphomaClinical ManifestationsEarly stages (low grade): Localized or generalized lymphadenopathyPainless swelling of lymphnodes
Non-Hodgkin’s LymphomaClinical ManifestationsHigh grade: SplenomegalyWeight lossNight sweats
Multiple Myeloma Malignant neoplasm of plasma cells
Multiple Myeloma Tumor cell masses occur in the bone marrow? destruction of the bone
Multiple Myeloma As malignant cells grow, it replaces normal plasma cells? v antibody production
Multiple Myeloma Over 65 age group affectedMost common cause of death is infection
Platelet Disorders ThrombocytopeniaThrombocythemia
Thrombocytopenia Decreased platelets in circulation
ThrombocytopeniaWhat are the causes? Decreased production. Increased production.
Thrombocytopenia Congenital or acquiredAquired attainted secondary to something else.
Acquired ThrombocytopeniaSecondary to: More common than congenitalViral infections (HIV, EBV, etc)Medications (heparin, chemotherapy, etc)Nutritional deficiencies (vB12 or folic acid)Bone marrow hypoplasia (aplastic anemia)
Increased consumption (quantitative)Heparin- induced (HIT): Immune mediated, adverse reactionHeparin combines with a platelet factor forming a complexComplex combines with IgGLeads to platelet activation
Increased consumption (quantitative)Heparin- induced (HIT): Almost an allergic reaction but notWill happen to patients who have been exposed to heparinSpleen filtering platelets throbocyteopiniaVeinous circulation
HIT Clinical Manifestations Risk for venous or arterial thrombosisDVT/ PEMI/ CVAThrombocytopenia (by approx. 50%)Lost 50% of platelets see more clotting then bleeding
Thrombocythemia AKA: thrombocytosisIncreased platelet countClassified as primary (reactive) or secondaryLeads to an increased risk of clottingCannot have heparin or warfarinDue to immune systemSpleenectomy is secondary
Reactive Thrombocythemiathe etiology? Inflammatory conditions (RA) or cancers
Reactive Thrombocythemia Production of cytokines–> ^ production of thrombopoietin? ^ megakaryocyte proliferation
Reactive ThrombocythemiaWhy is it classified as a chronic myeloproliferative disorder? Classified as chronic myeloproliferative disorder as there is also an increase in RBC
Reactive ThrombocythemiaWhat is the result of ^ RBC? Increase in contribution to blockage of blood flow in microvascular condition
Reactive ThrombocythemiaClinical Manifestations Risk for large vessels arterial / venous thrombosisMicrovascular thrombosisErythromelalgiaAcrocyanosis- Limbs go completely blue, congestion in vessels.
Vitamin K Synthesized in the large intestine and obtained through diet
Vitamin K Essential for production of clotting factors VII/ IX/ X and prothrombin–> essential for coagulation
Vitamin K v Amounts can be due to long-term antibiotic therapy
Vitamin K Without Vitamin K don’t produce prothrombin
Disseminated Intravascular coagulation (DIC) Syndrome resulting from a variety of clinical conditions (ie. Septic shock)
Disseminated Intravascular coagulation (DIC) Leads to widespread coagulationIncrease in Fibrin
Disseminated Intravascular coagulation (DIC) May lead to organ failure
Disseminated Intravascular coagulation (DIC)clinical manifestations IschemiaInfarction NecrosisThrombosisJaundiceHemorhoage
Hemophilia X- linked autosomal disorder
Hemophilia Coagulation deficiency:Type A: classic hemophilia (factor VIII)Type B (factor IX)
Hemophilia Both produce abnormal bleeding
HemophiliaClinical Manifestations Bruising, swellingReddness at jointsJoint pain & limited mobilitySpontanteous bleeding after minor trauma
Older adults are more affected by temperature extremes due to: Decreased shiveringSlowed BMRDecreased sweatingSlowed blood circulationChanges to the skinDecreased heat producing activities
Mechanisms of heat lossAutonomic nervous system: Evaporation- sweatingVasodilation- loss of heat at the surface
In relation to environmental temperature RadiationConductionConvection
Mechanisms of heat conservation Vasoconstriction by sympathetic nervous system
Mechanisms of heat conservation Dressing in layers, moving around & fetal position- how do these help with heat conservation? Dressing in layers traps heats, moving around produces heat, fetal position helps conserve body heat by keep in core heat.
Fever Temporary response to either endogenous or exogenous pyrogens
Fever Hypothalamus & brainstem cause:^ Heat production & conservationPeripheral vasoconstrictionEpinephrine release
Benefits of Fever Higher body temps aid in killing microorganisms by:Affecting growth and replication of organismDecreasing serum mineral levels need for bacterial replicationDepriving bacteria of a food source
Benefits of Fever Side effects of anorexia & somnolence v demand for muscle glucose^ cell breakdown & auto-destruction? prevents replication of infected cells^ activity of lymphocytes & neutrophils
Febrile seizures Affects children mostly especially boys <5 years oldCan occur with temps >39 Degrees C
Febrile seizures Brief and self-limiting, lasting < 5 min in approx. 40% of childrenProlonged febrile seizures are associated with the development of temporal lobe epilepsy
Hyperthermia ^ Body temp without hypothalamus triggerCan lead to nerve damage, convulsions & deathIncludes heat cramps, heat exhaustion & heat strokeHeat cramps –> loss of sodium caused by dehydration
Hypothermia Core body temp <350CCauses:Prolonged cold exposure? vasoconstriction, ^ blood viscosity, ischemic damage
HypothermiaCauses: Manifestations:Shivering^ Risk of coagulationWhat can happen if severe hypothermia occurs (26-280)? coagulopathy, ventricular fibrillation and asystole occurs and lost all cardiac output.
What can happen if severe hypothermia occurs? Between 26-28 Degrees Celcius? coagulopathy, ventricular fibrillation and asystole occurs and lost all cardiac output.
Pathways of Nociception Pain sensation travels afferent fibres v Thalamus (coordinate sensory information) v Somatosensory cortex vAwareness & reaction
Acute Pain Protective mechanismSudden onsetAlerts the individual that damage is occurringTransient pain that will resolve if stimulus removedPresents as increased HR, HTN, diaphorhesis & anxiety
Somatic pain Occurs in connective tissues (muscle bone skin).
Visceral pain Pain in internal organs and lining of body cavities.Associated with nausea, vomiting, restlessness
Referred pain Occurs in an area distant from the point of originVisceral sensory fibers enter the spinal cord along with sensory fibers from another point in the body? fibers converge? carry signals to the cerebral cortex
Chronic Pain Pain lasting > 3 months and may be persistentOnset can be sudden or develop insidiouslyDoes not respond well to usual therapy
Chronic Pain Persistent pain leads to physiological adaptation & behavioral and psychological changesExample includes neurogenic/ neuropathic painNeuralgia (pain in the distribution of a nerve)Phantom limb pain
Phantom limb pain Neuropathic pain from nerve trauma or diseaseAbnormal pain processingOccurs in pt’s who had pain prior to amputation
Phantom limb painCause: (theories) Hyperactivity of peripheral nervesScar tissue Neuroma formation
Fibromyalgia Chronic musculoskeletal syndromePresents with joint and muscle pain, fatigue & tender pointsDiagnosed through subjective dataNo definitive findings on lab tests
Cataracts: Opaqueness of the ocular lensThickening of lensIncidence ^ with age
Cataracts Changes in the lens proteins Causes v visual acuity, blurred vision, and v color perceptionChanges in eye’s metabolismDifficulty with colored vision
Glaucoma Vision loss due to damage of the optic nerve (death of optic nerve)What is occurring in the eye? Results in increased pressure with the eye (IOP) intra ocular pressureAqueous fluid becomes trap
Glaucoma Affects peripheral visionAngle: where cornea and iris meetClassified as:Closed angledOpen angled
Open Angle glaucoma Most common formOccurs due to blockage of the trabecular network? ^ IOPProgresses slowlyMost people are diagnosed once they have lost visionBecause eye compensates for peripheral vision
Closed Angle glaucoma Area between the cornea and iris has closedLeads to forward displacement of iris towards corneaFluid is unable to drain-> ^ IOPAbrupt onset, painfulRequires immediate medical attentionDecrease pressure in eye or person will become blind.
Symptoms of closed angle Sudden painHalos around lightsCorneal swellingRed eyeSudden decrease in visionFixed, dilated pupilHeadacheNausea & vomiting
Macular Degeneration Degeneration of the retinal maculaUsually age related (ARMD)Affects central visionClassified as dry (atrophic) or wet (exudative)Drusen deposits in the maculaDry- most commonWet- less common.
Dry AMD Most common typeAtrophy of retinal epithelial layerDrusen thins and dries out macula
Dry AMD Loss of photoreceptors? loss of central visionCan progress to wet AMD
Wet AMD Abnormal blood vessel growthVessels are leaky and weak-> scarring
Wet AMD Fluid lifts and damages the maculaCauses rapid loss of vision if untreated and can lead to retinal detachment
Retinal Detachment Fluid accumulation in the space between retina & epithelial pigmentMost common form: rhegmatogenous retinal detachment
Retinal Detachment Vitreous gel becomes more liquifiedSeparation deprives retina of oxygen & nutrients
Eyes & Aging Cornea is thicker & less curved? astigmatismv Anterior chamber size-> ^ IOP & glaucoma
Eyes & Aging Lens ^ in opacity & thickness-> changes in light, color vision, dark adaptation and cataractsLens loses elasticity? loss of accommodation
Eyes & Aging Retina v rods? more light needed to see an objectVitreous liquefaction-> possible retinal detachment
Ear infections Otitis externa:Occurs in the ear canalCommon cause is bacteriaOccurs after prolonged exposure to moisture
Ear infectionsOtitis externa:What symptoms will occur? Inflammation, swelling, drainage, obstruction & pain
Otitis media Infection of the middle earCommon in children
Otitis media Caused by bacteriaCan be acute or chronic
Otitis mediaWhich symptoms present? Tympanic membrane pressure, and fluid
What happens when cochlear hair cells degenerate and there is lose of the auditory neuron in the organ of Corti? Cochlear hair cells degenerate-> presbycusisLoss of auditory neuron in organ of corti -> presbycusis
What happen with degeneration of cochlear membrane? Degeneration in cochlear membrane -> conductive hearing loss
Reticular Activating System- ___ regulates attention & information processing
Reticular Activating System ____maintains consciousness (arousal)
Reticular Activating System Location starts at the top of the spinal cord
Reticular Activating System Alterations in arousal due to: infections/ tumors/ hypoxia/ drugs/ toxins/ etc
Reticular Activating System ____ filters and prioritizes sensory information to let mind focus
Altered Neurological FunctionFive categories for evaluation include: LOCPattern of breathingPupil changesOculomotor responseMotor response
LOC Person, place, and time
Determines nervous system functionLOC Determines nervous system functionAt highest cognitive capacities–> aware of person, place, timeConsciousness consist of awareness & arousal
Confusion: loss of ability to think rapidly
Disorientation: loss of place, time
Obtundation: difficulty staying awake
Stupor: takes more stimulation to wake up.
Coma: lack or complete lack of stimuli
What do respiratory patterns evaluate? What do respiratory patterns evaluate?
Cheyne-stokes respirations abnormal rhythm of breathing (periodic breathing) with altering periods of hyperventilation and apnea (cresendo-decrescendo pattern)
Oculomotor Response Eye movements & reflexes change with brain dysfunctionAbnormal movements or absent movements indicate what part of the brain is involved
Doll’s eyes phenomenon Turn head to the right eyes go to the left in parallel. Turn head to left, eyes go to the right in parallel.
Motor Response Evaluates level of brain dysfunctionDetermines which side of brain is damaged
Motor ResponseMovement is either: PurposefulInappropriate (posturing)Not present (unresponsive)
Decorticate posturing (core): bilateral flexion of elbox , wrist and externion with internal rotation of extermities
Decerebrate posturing extensor posturingAll 4 extermities in rigid extensionsIncreased tone of extensor muscles
Altered Neurological Function- ICP Pressure exerted within the cranial cavity
Altered Neurological Function- ICP Potential causes:TumorEdemaExcess CSFHemorrhage
Altered Neurological Function- ICP ^ ICP? v blood flow & can distort blood vessels & displace brain tissuesCan eventually lead to herniation of brain tissue
ICP progression Stages of ICP refer to the symptoms of increased pressure
ICP progressionWhat is occurring between Stage 1 & 2? Compensation is occurring
ICP progressionWhat is occurring in Stage 3? Shows decompensation with changes to mental status
ICP progressionStage 4 Herniation occurs and Blood supply affected
Brain Death: Irreversible brain damageBrain cannot maintain body’s internal homeostasisAbsence of cerebral hemisphere functionAbsence of brainstem’s vital centers
Cerebral Death: Irreversible comaDeath of cerebral hemispheresBrainstem and cerebellum still functionBrain damage is permanentPerson does not follow commands, speak or have voluntary movement
Vegetative state Arousal returns but is sluggishUnawareness of self or environmentLoss of cognitive functionBlood pressure & breathing are maintainedBrainstem reflexes intact
Locked-in SyndromeWhat has happened to voluntary muscles? Completely paralysis of voluntary musclesIs the individual conscious? What about their thoughts and level of arousal?
Locked-in Syndrome Thought and level of arousal intact
Locked-in SyndromeAre they able to communicate through speech? Perceptions and emotions intactUnable to communicate through speech, but can communicate through their eye movementsStroke or brain damage. Some form of cerebral death but awake & conscious
Locked-in SyndromeWhat has occurred with eye movement? Eye movement intact
Locked-in Syndrome Stroke or brain damage. Some form of cerebral death but awake & conscious
Seizure Episode of abnormal electrical activity in the brain due to excessive stimulation
Convulsion Spasmodic contractions of any or all muscles in the body
Seizure Etiology Diseases of the nervous systemCerebral lesionsCerebral traumaGenetics(cont'd)
Seizure Etiology InfectionVascular disease (stroke)Emotional or physical stressFeverEnvironmental stimuliEtc…….
Epilepsy Chronic, recurrent pattern of seizuresNo underlying causeClassified as primary or secondary
Status Epilepticus Medical emergencyMultiple seizures with continuous electrical activity without recoveryCan result in brain damage & deathStatus epilepticus seizures that last longer than 5 mins.
Seizure Terminology Aura: visual, sound, smells
Seizure TerminologyProdroma: occurs hours or days before seizure starts
Seizure TerminologyTonic phase increased muscle tone
Seizure TerminologyClonic phase contraction and relaxation
Seizure TerminologyPostictal state seizure stops, they appear confused, tired and may have a headache
Seizure TypesGeneralized Occurs in both hemispheres
Seizure TypesGeneralized May results in loss of consciousness
Seizure TypesGeneralized Involves an aura
Seizure TypesGeneralizedTonic- clonic (loss of consciousness)Also known as: Grand maul seizure
Seizure TypesGeneralizedAbsence (lapses of consciousness)Also known as: petite maul
Seizure TypesGeneralizedTypes: Myoclonic (conscious)
Seizure TypesPartial (focal) Seizures Occur in a focal area of the brainImpairment of consciousness
Seizure TypesPartial (focal) SeizuresDivided into: Simple partialComplex partial (involves an aura)
SeizureClinical Manifestations Depends on type of seizure
Acute Confusional StateDefine Delirium Acute trasient disorder of awareness
Acute Confusional StateCauses drug intoxication, ETOH/ drug withdrawal, fever, trauma, electrolyte imbalances, head injury…etc
Acute Confusional StateAffects Attention, sleep-wake cycle, behaviors
Acute Confusional StateClinical manifestations Confusion, delusions, hallicinations, loss of concentration, restlessness, irritability, insomnia, poor appetite
Dementia Progressive deterioration of brain function
Dementia Impairment of intellect, memory, language & behavior
Dementia Classified according to etiologic factors:Infection (encephalitis/ neurosyphilis/ AIDS/ Crueutzfeldt-Jacob)Drug intoxication (ETOH)TumorsNeurodegenerative disorders (Alzheimers/ Huntington’s/ vascular)
DementiaClinical Manifestations Depends on area of brain affected
DementiaClinical Manifestations May include:Memory lossImpaired judgmentHallucinationsSleep disordersDepressionApathyFallsanxiety
Alzheimer’s Disease Leading cause of dementia
Alzheimer’s Disease Etiology: unknown
Alzheimer’s Disease Brain has neuritic plaques & neurofibrillary tanglesConcentrated in cerebral cortex & hippocampus
Alzheimer’s Disease Loss of acetylcholine
Alzheimer’s Disease Results in loss of neurons & brain atrophy
Alzheimer’s Disease Progression from mild short-term memory loss to total loss of cognitionDisorientation/ confusionInability to problem solveBehavioural changes
Alzheimer’s Disease Apraxia- Complete inability to perform purposeful or skilled motor acts in the absense of paralysis, sensory loss, abnormal posture, and tone, abnormal involuntary movements, incoordination, or inattentiveness.
Huntington’s Disease Autosomal Dominant Disorders
Huntington’s Disease AKA: chorea
Huntington’s Disease Inheritance of one dominant gene can cause the diseaseOffspring have a 50% chance of expression
Huntington’s Disease Degeneration of basal ganglia & cortical region of brain
Huntington’s Disease Clinical manifestations Behavioral changesCognitive impairmentChorea
Huntington’s Disease Clinical manifestations Symptoms appear in adulthood (25- 45)
Parkinson’s Disease Chronic neurodegenerative disorder
Parkinson’s Disease Dopamine deficit- 80% dopamine gone when symptoms appear
Parkinson’s Disease Degeneration of basal ganglia–> affects extrapyramidal system
Parkinson’s Disease Stooped postureFlat affect, mask-like face
Define hypotonia: Decreased muscle tone
Hypotonia Due to v excitability of neurons–> v muscle activity
HypotoniaWhat are muscle cells replaced with? Muscle cells are replaced with connective tissue and fat
Hypotonia Muscle mass atrophies
Hypertonia Increased muscle tone
HypertoniaWhich neurons are damaged? Caused by upper neuron damage
Hypertonia Involuntary muscle contraction or spasticity
Hypertonia Individual tires easily
Hypertonia Muscles are enlarged and firm
Hypertonia Can be seen in patients with Parkinsons and cerebral palsy
Paresis weakness
Paralysis loss of muscle function
Hemiparesis unilateral weakness
Hemiplegia unilateral paralysis
Upper motor syndromes include spasticity, hypertonia & hyperreflexia
Lower motor syndromes impaired voluntary & involuntary movement & flaccid paralysis
Upper Motor Neuron SyndromeEtiology lesions to brain or spinal cord above the ant. HornMS, tumors, inflammation etc
Upper Motor Neuron SyndromeEtiology Associated with pyramidal syndrome
Upper Motor Neuron SyndromeResults in: HypertonicitySpasticityHyperreflexic(+) Babinski reflex: stroke bottom of foot- toes curl/ stretch up reflex
Pyramidal tract syndrome disorder of the pyramidal tracts of the spinal cord (corticospinal tracts)
Pyramidal tract syndromeResults in: motor dysfunction with muscle overactivity, clonus & spasms
Spinal shock: Complete cessation of spinal cord function following a spinal cord injury or a lesion
Spinal shock: Motor paralysis & loss of sensation occursReflexes below the level of injury are absentFlaccid paralysis, loss of bowel and bladder control
Spinal shock: If injury occurs above the pons-> hands and arms are affected
Lower Motor Syndrome LMN carry nerve impulses from UMN to skeletal muscle
Lower Motor Syndrome LMN syndrome involves paralysis or weakness to the muscles affected
Lower Motor Syndrome Results in:HypotonicityHyporeflexiaDenervation(–) Babinskini reflex
Amyotrophic Lateral Sclerosis Lou Gehrig Disease
Amyotrophic muscle wasting
Amyotrophic Lateral Sclerosis Upper & Lower Motor Disease
ALS Progressive degenerative disorder of upper & lower motor neurons
ALS-What is the cause of death? progressive muscle weakness that leads to respiratory failure
ALS- Fatal disease with no remissions and no cure
ALS Death of neurons, axon degeneration and demyelination
ALS-Clinical Manifestations Affects coordinationAffects speechAffects swallowingHyptonia
ALS-Clinical Manifestations Muscle paresis leading to eventual paralysisLoss of diaphragm control? respiratory paralysisDoes not affect thought and cognition
Alterations in complex motor performance Refers to disorders of posture or gait
Alterations in complex motor performanceDisorders of posture include: DystoniaChoreaAthetosis- abnormal contraction of hands and feet.
Alterations in complex motor performanceDisorders of posture include: Decorticate posturing
Alterations in complex motor performanceDisorders of posture include: Decerebrate posturing
Alterations in complex motor performanceDisorders of posture include: Basal ganglion posture
Traumatic Brain Injury Alteration in brain function caused by an external force
Traumatic Brain Injury Causes: MVA’s/ falls/ sports injuries/ assaults
Traumatic Brain Injury Classified as closed or open blunt force trauma
Traumatic Brain Injury Damage occurs through primary, secondary & tertiary injury
Traumatic Brain Injury Primary Injury Caused by the impactCan be focal (direct) or diffuse
Traumatic Brain Injury Secondary injury Indirect & due to the primary injury
Traumatic Brain Injury Tertiary injury Develops days or months laterDue to systemic complications
Traumatic Brain Injury Molecular Neuronal injuryBrain TraumaCell edemaMitochondrial dysfunctionActivation of inflammationLoss of BBBIschemiaAxonal injuryNeurological deficits
Closed head injury More common typeHead strikes a hard surface or an object
Closed head injury Dura mater remains intact, brain tissue is not exposedCan be a focal injury or a diffuse injury
Focal Brain injury Injury occurs at a specific siteOccurs in both open and closed head injury
Focal Brain injury Compression of the skull and rebound effectsIncludes coup or contrecoup injuries, contusions, hematomas
Contusion Blood leaking from an injured blood vessel
Contusion Most common in the frontal lobe
Contusion Effects occur 18-36 hours post injury
What is the result of brain edema around damaged neural tissue? Damage or death of brain cells may occur
Brain Contusion Clinical Manifestations Changes to attention, memory, emotion, behaviour
Brain Contusion Clinical Manifestations Immediate loss of consciousness
Brain Contusion Clinical Manifestations Loss of reflexes
Brain Contusion Clinical Manifestations Transient apnea
Brain Contusion Clinical Manifestations Brief period of bradycardia & hypotension
Subdural HematomaWhat is the most common cause of an subdural hematoma? MVA
Subdural HematomaClassified as: Acute: develop rapidly
Subdural HematomaClassified as:Subacute develop over 48 h to 2 weeks
Subdural HematomaClassified as:Chronic: found in alcoholism
Diffuse Injury Widespread areas of the brain are damaged
Diffuse Injury Damage to axonal fibres & white matter
Diffuse Injury Occurs in whiplash & rotational injuries
Diffuse Injury Axonal damage–> v speed of information processing & v attention span
Spinal Cord Trauma Spinal injuries can be due to hyperextension, fractures, dislocations, or rotational forces
Spinal Cord TraumaClassified as:primary injury: Initial mechanical trauma & immediate tissue destruction
Spinal Cord TraumaSecondary injury: Begins minutes after injury with inflammation, ischemia, edema etc.
Spinal Cord TraumaSeverity of InjuryInjury at or above C6 results in? Quadripleqia (tetraplegia)
Severity of InjuryInjury between T1-T12 results in? Paraplegia
Spinal Cord TraumaClinical Manifestations Activity of cord cells at or below injury ceases
Spinal Cord TraumaClinical Manifestations Person presents with spinal shockLoss of reflex functionFlaccid paralysisLoss of bladder/ rectal controlTransient drop in BpPoor thermal regulation
Autonomic hyperreflexia (dysreflexia)What is occurring in the body? Due to stimulation of SNS –> life-threatening which can lead to a CVA
Autonomic hyperreflexia (dysreflexia)What is the associated cause? Caused by a distended bladder or rectum
Autonomic hyperreflexia (dysreflexia)Symptoms: Sudden HTNBradycardiaPounding headacheBlurred vision
CVA’s Cerebrovascular Accidents
Cerebrovascular Accidents Hardening of plaque along artery walls
CVA'S Stroke
CVA'S Occlusion of cerebral artery–> Impairment of cerebral circulation
CVA's- StrokeResult of:Hemorrhagic cerebral hemorrhage
CVA's- StrokeResult of: Ischemic TIA/ thrombotic/ embolic/ lacunar
CVA's- StrokeRisk Factors HTN is the greatest risk factor
CVA's- StrokeRisk Factors AtherosclerosisDiabetesSmokingHigh cholesterol levelsHigh sodium intakeAtrial fibrillationPolycythemiasEtc….
Transient Ischemic Attack (TIA) Transient episode of neurological dysfunction
Transient Ischemic Attack (TIA) Result of focal cerebral ischemia
Transient Ischemic Attack (TIA) Sudden focal loss of neurologic function
Transient Ischemic Attack (TIA)Symptoms: weakness, confusion, loss of balance, visual disturbances, sudden headache
Transient Ischemic Attack (TIA) Warning sign of an impending stroke
Thrombotic Stroke Arterial occlusions in arteries supplying brain vIncreased coagulation leading to a thrombus vInadequate cerebral perfusion vPermanent neurologic deficits
Atherosclerosis thickening of arterial walls
Thrombotic StrokeEtiology Accumulation of scar tissue & cholesterol deposits
Thrombotic StrokeEtiology Obstructs arterial blood flow–> hypoxia / ischemia/ inflammation
Thrombotic StrokeEtiologyPrimary cause? Atherosclerosis–> thickening of arterial walls
Embolic StrokeWhere has this formed? Formed outside the brain.
Embolic Stroke Fragments of thrombus break and travel through circulation
Embolic Stroke Involves obstruction in small vessels or bifurcation? ischemia
Embolic StrokeRisk factors: A-fib, recent MI, or thrombus formed in left side of heart or in common carotid artery
Define lacunar strokes: Small stroke that occulde small arteries (aka microinfarcts)
Lacunar Stroke Predominately affect the basal ganglia-Results in motor & sensory deficits
Lacunar Stroke Arteries become tortuous
Lacunar Stroke High risk patients include Diabetics, and patients with high blood pressure
Clinical Manifestations of Occlusive CVA’s Cellular edema–> compression of capillaries
Clinical Manifestations of Occlusive CVA’sOpposite to infarct Right CVA = Lt sided weakness & affected sensation
Clinical Manifestations of Occlusive CVA’sOpposite to infarct Left CVA = Rt sided weakness & affected sensation
Clinical Manifestations of Occlusive CVA’s Hemiparesis- weakness to one side of the body – facial droop – hand grip weak or absent Blurred vision or diplopiaAphasiaAtaxia
Hemorrhagic StrokeRupture of cerebral artery that results in? intracranial bleeding, and hemorrhagic stroke
Hemorrhagic Stroke Compression of adjacent brain tissue & brain ventricles
Hemorrhagic Stroke Related to severe hypertension, CAD, ruptured aneurysm, AV malformation
Hemorrhagic Stroke Affects large portions of the brain
Hemorrhagic StrokeClinical Manifestations Varies depending on location & size of bleed
Hemorrhagic StrokeClinical Manifestations Altered LOCExcruciating headacheHemiparesis, dysphagiaVisual loss on one side
Intracranial Aneurysm Weak buldging areas of arterial wall
Intracranial AneurysmEtiology includes: ArteriosclerosisTraumaInflammation
Intracranial Aneurysm Can be unilateral or bilateral
Arteriovenous Malformation Rare congenital lesions
Arteriovenous Malformation Can cause hemorrhagic strokes
Arteriovenous Malformation Blood vessel structures in the brain are either thin or abnormally large
Arteriovenous MalformationClinical manifestations: HeadachePossible seizure disorderIntracerebral bleeding
Subarachnoid Hemorrhage Blood escapes from injured vasculature into the subarachnoid sp
Subarachnoid Hemorrhage Blood irritates meninges and other neural tissue
Subarachnoid Hemorrhage Inflammatory response occurs–> impaired CSF reabsorption –> ^ ICP
Subarachnoid HemorrhageClinical manifestations HeadacheTransient changes in LOCNausea and vomittingVisual and speech disturbancesStiff neckPhotophobia (Light sensitivity)
Headaches Typically a common, benign condition
Headaches May or may not have known triggers
Headaches Recurrent headaches require further follow-up to rule out serious conditions (meningitis, tumor, CV disease)
Benign headaches classified as: MigraineClusterTension
Migraine Moderate to severe headaches
MigraineHow long do these last for and who do they more commonly affect? -Lasts from 4 hours to 3 days-Affects women more then men.
Migraine May or may not include an aura
MigraineClinical PhasesPhase 1 Premonitory phaseCan occur hours before onsetMay experience neck pain, depression, food cravings
MigrainePhase 2 Migraine AuraNot all people experience auraAura can last one hour or longerPresent as visual or sensory
MigraineClinical Phases 3 Headache phaseSymptoms last from 4- 72 hours
MigraineClinical Phases 4 Recovery phaseCan occur from several hours to days
MigraineClinical Manifestations NauseaVomitingPhotophobia (light sensitivity)Phonophobia (sound sensitivity)Pulsating painUnilateral head pain (pain on one side of head)Pain that worsens with activityScalp tenderness
Cluster HeadachesWho does this primarily affect? Men between 20 to 50 years of age.
Cluster HeadachesCause? Cause unknown
Cluster HeadachesWhy are they referred to as clusters? These headaches occur in clusters for a period of days followed by a long period of spontaneous remission.
Cluster Headaches are? Are episodic & chronic
Cluster HeadachesPain level and duration? Extreme pain intensity & short durations
Cluster HeadachesTriggers? Triggers are similar to the ones that cause migraines
Cluster Headaches Headaches begin without warning
Cluster HeadachesClinical Manifestations Severe unilateral tearing & burningPain around one eye or temporal pain Pain lasting 30 min to 2 hoursReddening of eyeDrooping eyelidPain in midface & teethPtosis
Tension Type Headaches Most prevalent type of headache
Tension Type Headaches Mild to moderate headache
Tension Type Headaches Sensation of pressure around the head
Tension Type Headaches May last several hours to several days
Tension Type Headaches Not aggravated by physical activity
Tension Type Headaches Can be due to stress, anxiety, poor posture
MeningitisDefinition: Inflammation of the brain or spinal cord
MeningitisEtiology: Infectious meningitis may be caused by bacteria, viruses, fungi, parasites, or toxins
Aseptic meningitis no specific pathogen identified & disease is treated symptomatically
Meninges function: Protect the brain & spinal cord from injuryProvide a blood supply to skull & brain tissueAllow for the flow of CSF
Bacterial meningitis Systemic blood stream infection obtained via respiratory droplets
Bacterial meningitis Bacteria multiply in the subarachnoid space
Bacterial meningitis Bacteria & toxins irritate & induce inflammation in meninges
What symptoms present with irritation of the meninges?1st: Inflammation and irritation- throbbing headache beccomes severe, photophobia becomes severe, nuchal rigidity, positive Kernig and Brudzinski signs.
What symptoms present with irritation of the meninges?2nd: local tissue dysfunction- cranial nerve palsies
What symptoms present with irritation of the meninges?3rd: Irritation and damage to cranial nerves- (cranial nerves II, III, IV, VI, V,VII, VIII)
MeningitisClinical Manifestations Throbbing headache, neck stiffness and rigidity, and decreasing responsiveness. purpuric rash involving skin and mucous membrane, nausea vomiting, increased ICP
MeningitisClinical Manifestations v Oxygen to brainv AlertnessConfusion
MeningitisClinical Manifestations Impaired focal brain functionHemiparesis, Hemiplegia, ataxiaSeizures
Lyme DiseaseHow is lyme disease spread? Tick-borne spirochete bacterial infection which involves the peripheral and central nervous system
Lyme DiseaseWhat body systems does the bacteria affect? The peripheral and central nervous system
Lyme DiseaseTick larvae are able to evade host immune system how? Evade immune survellance by inhibiting complement killing, producing surface proteins that block phagocytic recognition (antigen variation), hiding in the extracellular matrix.
Lyme DiseaseIncubation period 3- 32 days
Lyme DiseaseStage 1 Acute, localized, what is a characteristic sign?Burning sensationGeneral malaise, flu-like symptomsPossible stiff neck & headache
Lyme DiseaseStage 2 is classified as? Systemic infection
Lyme DiseaseStage 2 Cardiac & neurological symptoms developPalpitationsDysrhythmiasSOBHeadacheMeningeal inflammation
Lyme DiseaseStage 3 Classified as? Chronic stage
Lyme DiseaseStage 3 Chronic stage can occur? up to 2 years after initial bite
Multiple SclerosisChronic inflammatory disease resulting in? degeneration of CNS myelin, scarring or formation of plaque, and loss of axons
Multiple SclerosisEtiology? Caused by autoimmune response to self-antigens in genetically susceptible individuals
Multiple SclerosisStats: Leading cause of neurological disability in early adulthood (between 20-40 years of age)
Multiple Sclerosis Life expectancy is not altered by MS
Multiple Sclerosis Genetic & environmental factors are implicated in disease onset (virus infection)
Multiple Sclerosis Disease affects white and gray matter
Multiple Sclerosis Abnormal autoimmune response? Activation of CD4 & CD8 cells
Multiple Sclerosis T cells attack myelin sheath
Multiple Sclerosis Activation of B cells, complement & inflammatory cells–> diffuse injury throughout CNS–> death of neurons
Multiple SclerosisAreas affected: optic nerve, spinal cord, cerebellum
Multiple SclerosisClinical Manifestations Impaired central visionImpaired color visionInflammation & swelling of optic discNystagmus
Multiple SclerosisClinical Manifestations Stiffness, slowness, weakness, hypotonia in musclesAtaxiaBowel & bladder symptoms
Multiple SclerosisDiagnosis: Based on signs & symptomsNeurological examMRI? scarring or plaques in CNSLumbar puncture of CSF? presence of antibodieEvoked potential test
Multiple SclerosisTreatment: Goal? prevention of permanent neurological damageUse of corticosteroids, immunomodulators
Guillain Barre SyndromeDefine: an acquired, acute inflammatory demylinating or axonal disorder caused by a humoral or cell-mediated immunological response, or both, directed at peripheral nerves.
Guillain Barre SyndromeWhat system does it affect? Results in muscle denervation & atrophy
Guillain Barre SyndromeWhat is this autoimmune, syndrome triggered by? by a preceding bacterial or viral infection. Molecular mimicry (cross-activation of self-epitopes & pathogen derived peptides by autoreactive T & B cells) is associated with autoimmune injury.
Guillain Barre Syndrome Recovery can occur over weeks to years
Guillain Barre SyndromeClinical Manifestations Numbness, pain, parasthesiasWeakness of limbsSome will experience paralysis of limbs & respiratory musclesFacial weakness affectingSwallowingChewingcoughing
Cerebral Palsy Disorder of movement, muscle tone or posture
Cerebral Palsy Damage to upper motor neurons
Cerebral Palsy Damage may occur prenatal, perinatal or postnatal period
Cerebral Palsy Affects motor function, sensory function and cognition
Cerebral Palsy Non-progressive disease
Cerebral Palsy Clinical Manifestations Vary based on the degree of impairmentVision or hearing impairmentSeizuresDysphagiaSpasticigtyAtaxiaHypotonia
Rett Syndrome Rare postnatal sex-linked dominant disease that affects girls
Rett Syndrome Progressive disorder leading to loss of mental capacity & motor skills.
Rett SyndromeDisease features small hands, small feet and microcephaly that develops postnatally
Rett SyndromeWhat is a feature in this disorder Develops in 1st year of life, -> loss of mental capacity and motor skills, then loss of purposeful hand movements, stereotypical hand wringing and flapping
Rett SyndromeOnset develops between 6-18 months of age
Rett SyndromeClinical Manifestations Hand wringing or flappingPlacing hands in mouthLose use of handsLoss of speechInability to feed selfUncoordinated breathing
Cardiovascular disease is the leading cause of death worldwide
By changing to ______ _______, it can delay the onset of heart disease or stroke by as much as 14 years. to healthy behaviours
Diseases of the Arteries- Form of arteriosclerosis
Arteriosclerosis Inflammatory disease from ^ cholesterol levels
Arteriosclerosis Thickening & hardening of vessels
Arteriosclerosis Due to the accumulation of lipid-laden macrophages
Arteriosclerosis Results in ischemia
Arteriosclerosis Leading the cause of CAD & CVD
Arteriosclerosis Injury to endotelial cells in the artery wallvInflammation & release of cytokinesvMacrophages adhere to injured endotheliumvRelease enzymes & toxic oxygen radicals-> oxidized LDLvFurther damages vessel wall
Lipid-laden macrophages Once LDL has become oxidized the macrophages surround the fatty material
When macrophages becomes filled with lipids they are known as? The macrophages become filled with lipids forming a foam cell
Describe a fatty streak Once foam cells accumulate increase in numbers -> fatty streak
Lipid-laden macrophages-Clinical manifestations Inadequate tissue perfusion due to obstruction
Lipid-laden macrophages-Can lead to: CAD- coronary artery diseaseHTNThrombosis formationMI
What is the most common cause of occluded coronary arteries? Occluded coronary arteries most commonly caused by arteriosclerosis
Coronary Artery DiseaseOther risk factors include: cigarette smoking, obesity, HTN, sedentary lifestyle, dyslipidemia (abnormal fat metabolism)
CAD-What is the result when there is vblood supply of myocardial cells? Leads to decreased blood supply that leads to ischemia
What is the result of a complete occlusion of the artery? Complete occlusion of artery -> infarction
Hypertension acronym: HTN
Elevated blood pressure (>140/90)
Hypertension Leads to functional and structural changes in heart
Hypertension ^ cardiac output or ^ peripheral resistance
Hypertensionclassified as: PrimarySecondaryMalignant
Blood Pressure:Normal (<120)/(<80)
Prehypertension Systolic: 120-139Diastolic: 80-89
HypertensionStage 1: Systolic: 140-159Diastolic: 90-99
HypertensionStage 2: Systolic: Greater than or equal to 160Diastolic: Greater than or equal to 100Diastolic: 100-
Essential/Primary Hypertension – No known cause
Essential/Primary Hypertension – Multifactorial disease
Essential/Primary Hypertension – Increase peripheral resistance & blood volume
Essential/Primary Hypertension – Risk factors: Family history (hx), age, gender, raceDietary sodium, smokingObesity, ETOH consumption
Secondary Hypertension Secondary to underlying disease process or other
Secondary Hypertension Direct cause identified
Secondary HypertensionCauses Renal, endocrine or vascular disorders
Secondary HypertensionCauses: Pregnancy
Secondary HypertensionCauses: Stress
Secondary HypertensionCauses: Medications
Malignant Hypertension Rapidly progressive
Malignant Hypertension Diastolic >140 mmHg
Malignant HypertensionCan result in: Encephalopathy
Malignant HypertensionCan result in: Cerebral edema
Malignant HypertensionCan result in: Organ damage
Malignant HypertensionCan result in: Renal damage
Hypertension-Can result in for the:Central nervous System Stroke
Hypertension-Can result in for the:Cardiovascular system Hypertrophy & Heart failure
Hypertension-Can result in for the:Cardiovascular system Myocardial ischemia
Hypertension-Can result in for the:Cardiovascular system Peripheral hypoxemia
Hypertension-Can result in for the:Cardiovascular system Aneurysm
Hypertension-Can result in for the:Cardiovascular system Retinal vascular sclerosis
Hypertension-Can result in for the:Renal System Renal failure
Aneurysm- Localized dilation or outpouching of a vessel wall and can occur in any blood vessel
Aneurysms Occur due to arteriosclerosis or HTN
Aneurysms Most commonly occur in the thoracic or aortic abdominal area
Aneurysms Classified as true or false aneurysms
True AneurysmInvolves all layers of the arterial wall
True AneurysmResults in weakening of the vessel wall
True Aneurysm Can be fusiform or saccular
False Aneurysm AKA pseudoaneurysm
False Aneurysm Collection of blood leaking from an artery or vein that is contained by surrounding tissue (extravascular hematoma)
Aortic Dissection Tear occurs to the inner layer of the aorta
Aortic Dissection Blood will enter the arterial wall
Aortic Dissection Results in separation of inner and middle layers
Myocardial Ischemiaacronym: MI
Myocardial Ischemia Occurs with an imbalance between coronary supply & myocardial demand
Myocardial Ischemia causes include: Tachycardia
Myocardial Ischemia causes include: Exercise
Myocardial Ischemia causes include: HTN, hypertrophy
Myocardial Ischemia causes include: Atherosclerotic plaques (most common cause)
Myocardial Ischemia Clinical manifestations Presents as Angina
Myocardial Ischemia Types include: Stable angina (angina pectoris)
Myocardial Ischemia Types include: Prinzmetal angina
Myocardial Ischemia Types include: Silent ischemia
Myocardial Ischemia Types include: Unstable angina
Stable Angina Known as angina pectoris
Stable AnginaWhat is this caused by? Caused by gradual narrowing and hardening of arterial walls
Stable AnginaClinical manifestations Transient substernal pain from the build up of lactic acid caused by lack of oxygen
Stable AnginaClinical manifestations Pain is recurrent and predictable
Stable AnginaClinical manifestations Pain is relieved by rest and nitrates
Prinzmetal Angina Also known as vasospastic angina
Prinzmetal Angina Unpredictable transient ischemia occurring at rest
Prinzmetal Angina Occurs with or without atherosclerosis
Silent Ischemia Atypical presentation
Silent Ischemia Symptoms of angina do not present & may have non-specific symptoms
Silent Ischemia Stress can be a contributing factor
Silent Ischemia More common in women
Silent Ischemia Diagnoses occurs with stress testing
Unstable Angina Dangerous type of angina
Unstable Angina Reversible myocardial ischemia
Unstable Angina Signals the atherosclerotic plaque has ruptured-> sign of an impending infarction
Unstable Angina Transient thrombotic vessel occlusion & vasoconstriction
Unstable Angina Does not follow a predictable pattern & can occur without exertion
Myocardial Infarction Total Obstruction of one/more coronary arteries
Myocardial Infarction Prolonged Ischemia -> irreversible damage to myocardial tissues
Myocardial Infarction Subdivided into STEMI or non-STEMI
STEMIST elevated MI ST elevated MIRefers to a transmural infarct (full thickness) with complete blockage of a coronary artery
NSTEMINon- ST elevation MI Partial thickness infarct (subendocardial)
NSTEMINon- ST elevation MI Non-occlusive
NSTEMINon- ST elevation MI ST depression on ECG
NSTEMINon- ST elevation MI Can lead to serious heart damage if not treated
MI Clinical manifestations Persistent chest painPallorDiaphoresisN&VRapid pulse
Myocardial InfarctionClinical manifestations Not relieved with nitroglycerinNot relieved with rest
Time after MI: 6-12hrs Tissue Changes: no changeStage of healing: not started
Time after MI: 18-24 hrs Tissue Changes: Pale to gray, slight pallorStage of healing: Inflammatory response
Time after MI: 2-4 days Tissue Changes: Visible necrosisStage of healing: Proteolytic enzymes, lipolysis, glycogenolysis
Time after MI: 4-10 days Tissue Changes: Area soft, fatty center, hemorrhage in infarct areaStage of healing: Collagen matrix is laid
Time after MI: 10-14 days Tissue Changes: Weak, scar tissueStage of healing: Area mushy and vulnerable to stress
Time after MI: 6 weeks Tissue Changes: Scarring completeStage of healing: In elastic scar tissue replaces necrotic myocaridum
Dysrhythmias Most common complication
Dysrhythmias Due to functional impairment of myocardium
Dysrhythmias Brough on by ischemia, hypoxia, ANS imbalances, electrolyte disturbances
Dysrhythmias Severity depends on size & site of infarct
Organic Brain syndrome Acute or chronic
Organic Brain syndrome Caused by impaired blood flow to brain from MI
Organic Brain syndrome Caused by impaired blood flow to brain from MI
Organic Brain syndrome Symptoms of confusion, impaired memory, agitation
Organic Brain syndrome Physiology not psychological problem
Acute pericarditis Acute inflammation of the pericardium
Acute pericarditis Common to occur after MI
Acute pericarditis Anterior chest pain worsens with respiratory effort
Acute pericarditis Can lead to a pericardial effusion, constriction & cardiac tamponade
Pericardial Effusion Accumulation of fluid in pericardial cavity
Pericardial Effusion Occurs from pericarditis
Pericardial Effusion Can lead to cardiac compression (tamponade)
Pericardial Effusion Tamponade interferes with RA filling-> v ventricle filling-> right side Heart Failure
Heart FailureImpaired pumping capacity of the heart-> impaired cardiac output (CO)
Heart FailureResults in a build-up of blood and fluids within the organs and tissues –>v perfusion of tissues
Heart Failure Compensatory mechanisms are activated as CO decrease but are short acting
Heart FailureLeft heart failure congestive heart failure- either systolic or diastolic
Heart Failure:Types: Right heart failure
Heart Failure:Types: High-output heart failure
Left heart failure Any condition that impairs left ventricle pumping (MI)
Left heart failure Increases the workload of the left ventricle (HTN, myocardial ischemia, valvular disorders)
Congestive Heart Failure (left heart failure)Systolic failure: Loss of contractile ability
Congestive Heart Failure (left heart failure)Systolic failure:Ventricle contracts poorly & empties incompletely not enough blood pumped into circulation
Left heart failure:Diastolic failure Stiffness of the ventricles & loss of relaxation
Left heart failure:Diastolic failure Impairs ability to fill with blood between contractions
Left heart failure:Diastolic failure Results in v cardiac output
SNS stimulation (catecholamines) –>^ HR & ^ PVR & ^ force of contraction
RAAS:Aldosterone: vasoconstriction & ^ fluid volume–> ^ BP
RAAS:Angiotensin II: increases preload and afterload
Dilation & Hypertrophy–> heart chambers enlarge to maintain CO, heart ^ muscle mass
Vasopressin (ADH)–> vasoconstriction & renal fluid retention
Right sided heart failure Inability of right ventricle to move deoxygenated blood forward in pulmonary circulation
Right sided heart failure Results in backward movement of blood into systemic circulation
Right sided heart failureEtiology Typically results from left side heart failure
Right sided heart failureEtiology Pure right ventricular failure occurs with any process that restricts blood flow to the lungsCor pulmonale (from pulmonary HTN)
High-Output Heart FailureInability of the heart to supply body with blood despite: Adequate blood volume
High-Output Heart FailureInability of the heart to supply body with blood despite: Normal cardiac contractility
High-Output Heart FailureEtiology: Anemia- lack ofHeart failure O2
High-Output Heart FailureEtiology: Septicemia- bacterial infection
High-Output Heart FailureEtiology: Hyperthyroidism- increase meataboliam, increased heart rate
High-Output Heart FailureEtiology: Beriberi- Vit B1 deficiency (malnurtrition, alcoholics)
Valvular Dysfunction Damage to heart valves occur in the innermost lining of the heart wall (endocardium)
Valvular Dysfunction Damage is either congenital or acquired
Valvular DysfunctionStenosis: constriction & narrowing–> affects blood flow
Valvular DysfunctionRegurgitation: faulty leaflets–> leaking of blood between chambers
Aortic stenosis is the most common abnormality
Aortic stenosisEtiology Congenital
Aortic stenosisEtiology Aging
Aortic stenosisEtiology Rheumatic heart disease- inflammation of the joints and tissues
Classic Manifestations: Angina
Classic Manifestations: Syncope
Classic Manifestations: Heart failure
Aortic stenosisOther manifestations: Decreased Bp
Aortic stenosisOther manifestations: Slow HR
Aortic stenosisOther manifestations: Faint pulse
Aortic stenosisOther manifestations: Narrowed pulse pressure- systolic – diastolic blood pressure. The closer the numbers are the narrower the pulse pressure.
Mitral Valve Prolapse Syndrome Most prevalent in young women (20-40)
Mitral Valve Prolapse Syndrome Possible genetic etiology
what is occurring in the mitral valves Anterior and posterior cusps of mitral valve billow upwards during systolic
Mitral Valve Prolapse Syndrome Usually asymptomatic
Mitral Valve Prolapse Syndrome Myxomatous degeneration of leaflets
Mitral Valve Prolapse SyndromeResults in: thickened, floppy cusps
Mitral Valve Prolapse SyndromeResults in: Elongated chordae tendinae
Mitral Valve Prolapse SyndromeResults in: Regurgitant murmur
Mitral Valve Prolapse SyndromeResults in: Often asymptomatic & do not require medical management
Infective Endocarditis Infection and inflammation of the endocardium–> valve malfunction–> ^ risk of emboli
Infection and inflammation of the endocardium–> valve malfunction–> ^ risk of emboli
Infective Endocarditis Classified as infective or non-infective
Infective: Bacterial infection caused by staph or streptococcus that results in vegetations
Non-infective: Formation of a sterile thrombus from endocardial damage
Infective Endocarditis Clinical Manifestations FeverGeneral malaiseWeight loss
Infective Endocarditis Clinical Manifestations Cardiac murmursOsler’s nodes seem on hands or toes, painful immune complexes triggers inflammatory response.Janeway lesions
Varicose Veins & Venous Insufficiency Superficial dilated veins with blood pooling
Varicose Veins & Venous InsufficiencyCauses: Venous distention from gravityIncompetent valves
Varicose Veins & Venous InsufficiencyCauses: PregnancySitting crossed legged from long periodsConstrictive clothing
Varicose Veins & Venous Insufficiency Can progress to venous insufficiency
Chronic Venous Insufficiency Due to varicose veins and incompetent valves
Chronic Venous Insufficiency Inadequate venous return? circulatory stasis & tissue hypoxia
Chronic Venous Insufficiency Can lead to the formation of a venous ulcer
Deep Vein Thrombosis (DVT) Clot formation in the large veins of the lower extremities
Untreated DVT will ^ risk of thromboembolization
What does the Triad of Virchow consist of? Venous stasisEndothelial damageHypercoagulable state
Arterial Thrombus formation Any condition that activates the coagulation cascade can result in the formation of a thrombus
Arterial Thrombus formationIncludes : atherosclerosis damage and, aneurysms changes vessels shape, endocarditis, septic shock
Arterial Thrombus formationproblems Thrombus can occlude artery –> ischemia in tissues supplied by artery
Arterial Thrombus formationproblems Thrombus can dislodge–> thromboembolism
Embolisms Bolus of matter circulating in the blood stream
Embolisms Travels until it cannot pass through a vessel due to its size
Embolisms Can lead to ischemia or infarction in tissues distal to the obstruction
EmbolismsTypes: Thromboembolism
EmbolismsTypes: Air embolism
EmbolismsTypes: Fat embolism
Thromboembolism Vascular obstruction from a dislodged thrombus
Thromboembolism Can be associated with abnormal heart rhythms (A-fib or A-flutter)
Thromboembolism Heart chamber can’t empty completey
Air Embolism Room air that enters circulation through IV lines
Air Embolism Ischemia and necrosis can occur if air totally blocks vessel
Fat Embolism Trauma to long bones causing globules of fat to form in blood
Fat Embolism Globules are from fatty bone marrow
Fat Embolism Platelets adhere to fat globules
Shock occurs when CV system is unable to maintain perfusion to tissues, cells and organs
Shock This results in impairment of cell metabolism, tissue function, v O2 & nutrient delivery & v waste removal
Shock Shock affects oxygen delivery and use as well as glucose
Shock Can progress to organ failure & death
Shock Typically classified by type of underlying pathophysiologic process
Types of Shock Cardiogenic
Types of Shock Hypovolemic
Types of Shock Neurogenic
Types of Shock Anaphylactic
Types of Shock Septic
Cardiogenic Shock Inadequate or ineffective cardiac pumping resulting in v blood flow to tissues & organs
Cardiogenic Shock Heart contractility is ineffective–> v CO
Cardiogenic ShockEtiology: Any condition that v contractility or causes pump failure
Cardiogenic ShockEtiology: MIHFPericarditis
Cardiogenic ShockEtiology: AneurysmsDysrhythmiasEtc…
Hypovolemic Shock Loss of whole blood plasma or interstitial fluid in large amounts
Hypovolemic ShockCompensation includes: Catecholamines–>^ HR & SVRRAAS
Neurogenic ShockEtiology: Trauma to spinal cord results in sudden loss of autonomic & motor reflexes
Neurogenic ShockEtiology: Depressive drugs that affect supply of oxygen to brain
Neurogenic Shock Without SNS stimulation, vessels walls relax–> vasodilation and hypotension & bradycardia
Anaphylactic Shock Widespread hypersensitivity to an allergen
Anaphylactic Shock Result in vasodilation peripheral pooling and related hypovolemia
Anaphylactic Shock Severe shock with symptoms developing rapidly
Septic Shock Begins with systemic inflammatory response syndrome
Septic Shock Triggered by either a gram (+) or gram (-) positive bacteria
Septic Shock Results in an inflammatory response and the release of chemical mediators
Septic Shock 1. Source of infection.2. bacteria enters blood3. leaking blood vessels
Multiple Organ Dysfunction Syndrome MODS
Multiple Organ Dysfunction Syndrome Progressive dysfunction of 2 or more organ systems
Multiple Organ Dysfunction Syndrome Due to an uncontrolled inflammatory response severe illness or injury
Multiple Organ Dysfunction Syndrome Etiology: sepsis & shock are the most common causes
Multiple Organ Dysfunction Syndrome common triggers: Severe burnsMajor surgeryAcute pancreatitis
Multiple Organ Dysfunction Syndrome common triggers: Liver failureRenal failure
Primary MODS Initial organ injury that results in ischemia or v perfusion
Primary MODS v Perfusion can be localized or generalized
Primary MODS Results in a stress response and inflammatory response that primes macrophages & neutrophils
Secondary MODS Due to excessive inflammatory reaction
Secondary MODS Where does this occur? Primed macrophages release mediators that damage endothelium throughout body
Maldistribution of Blood Flow Uneven blood flow to organs, large vessels and capillary beds
Maldistribution of Blood FlowCaused by: ^ capillary permeability, generalized vasodilation, endothelial dysfunction and impaired microvascular circulation
Maldistribution of Blood FlowResults in: Impaired tissue perfusionand decreased O2 to cells
Maldistribution of Blood FlowResults in: Shunting of blood due to loss of autoregulation
Maldistribution of Blood FlowOrgans most severely affected are? lungs, splanchnic bed (circulation of GI tract), liver and kidney
Shunting of blood Loss of autoregulation from inflammatory mediatorsMediators override normal vascular controls
Interstitial edema Microvascular permeability–> v O2 to cells
Capillary obstruction Microvascular thrombi
Clinical Manifestations of 2nd degree MODS24-72 hours: Low grade feverTachycardiaTachypnea
Clinical Manifestations of 2nd degree MODS24-72 hours: ARDS –acute respiratory distress syndromeHepatic, intestinal, renal failure
Clinical Manifestations of 2nd degree MODSwhat can occur in 14-21 days: Liver failure –> abd distention/ jaundice
Clinical Manifestations of 2nd degree MODSwhat can occur in 14-21 days: Enchephalopathy -> confusion to deep coma

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