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Patho Final Exam Concept Review Study Guide

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Patho Final Exam Concept Review Study Guide
Vegetative state verses brain death
Vegetative state
Loss of awareness and intellectual function but continued brainstem function
Result of diffuse brain damage
Person unresponsive to external stimuli
If consciousness recovered may have significant neuro impairment.
Locked-in syndrome
Individual is aware and capable of thinking but is paralyzed and cannot communicate due to
brain damage (may only be able to move their eyes to say yes or no)
Criteria for brain death (declared clinically and legally dead)
Cessation of brain function
Including function of the cortex and the brainstem
Flat or inactive electroencephalogram (EEG)
Absence of brainstem reflexes or responses
Absence of spontaneous respirations when ventilator assistance is withdrawn
Establishment of the certainty of irreversible brain damage by confirmation of cause of the dysfunction
Evaluation twice by different physicians
Indicators of increased ICP
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
Ischemia and eventual infarction of brain tissue
Increased ICP is common in many neurological problems.
Brain hemorrhage, trauma, cerebral edema, infection, tumors, abnormal circulation of CSF
Early signs—if cause is not removed
Decreasing level of consciousness or decreased responsiveness (lethargy) 1st sign often
Severe headache
From stretching of dura and walls of large blood vessels
Vomiting
Often projectile, not associated with food intake
Result of pressure stimulating the emetic center in the medulla
Papilledema (visualize w ophthalmoscope)
Caused by increased ICP and swelling of the optic disc
Vital signs
Development of cerebral ischemia
Vasomotor centers respond in attempt to increase arterial blood supply to brain
(causes vasoconstriction) *known as Cushing reflex
Systemic vasoconstriction
Increase of systemic blood pressure—more blood to brain to relieve ischemia
Baroreceptor response
In carotid arteries
Increased blood pressure by slowing heart rate
Chemoreceptor response
Respond to low carbon dioxide levels
Reduction of respiratory rate
Improved cerebral circulation
Relieves ischemia
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Patho Final Exam Concept Review Study Guide

Vegetative state verses brain death

  • Vegetative stateLoss of awareness and intellectual function but continued brainstem function ▪ Result of diffuse brain damage ▪ Person unresponsive to external stimuli ▪ If consciousness recovered may have significant neuro impairment.
  • Locked-in syndrome ➢ Individual is aware and capable of thinking but is paralyzed and cannot communicate due to brain damage (may only be able to move their eyes to say yes or no)
  • Criteria for brain death (declared clinically and legally dead) ➢ Cessation of brain function ▪ Including function of the cortex and the brainstem ▪ Flat or inactive electroencephalogram (EEG) ➢ Absence of brainstem reflexes or responses ➢ Absence of spontaneous respirations when ventilator assistance is withdrawn ➢ Establishment of the certainty of irreversible brain damage by confirmation of cause of the dysfunction ➢ Evaluation twice by different physicians Indicators of increased ICP
  • 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 ➢ Ischemia and eventual infarction of brain tissue
  • Increased ICP is common in many neurological problems. ➢ Brain hemorrhage, trauma, cerebral edema, infection, tumors, abnormal circulation of CSF
  • Early signs —if cause is not removed ➢ Decreasing level of consciousness or decreased responsiveness (lethargy) 1 st^ sign often ➢ Severe headache ▪ From stretching of dura and walls of large blood vessels ➢ Vomiting ▪ Often projectile, not associated with food intake ▪ Result of pressure stimulating the emetic center in the medulla ➢ Papilledema (visualize w ophthalmoscope) ▪ Caused by increased ICP and swelling of the optic disc
  • Vital signs ➢ Development of cerebral ischemia ▪ Vasomotor centers respond in attempt to increase arterial blood supply to brain (causes vasoconstriction) *known as Cushing reflex ➢ Systemic vasoconstriction ▪ Increase of systemic blood pressure —more blood to brain to relieve ischemia ➢ Baroreceptor response ▪ In carotid arteries ▪ Increased blood pressure by slowing heart rate ➢ Chemoreceptor response ▪ Respond to low carbon dioxide levels ▪ Reduction of respiratory rate ➢ Improved cerebral circulation ▪ Relieves ischemia

▪ Short time ▪ Increasing ICP causes ischemia to recur; cycle will repeat

  • ICP continues to rise, blood pressures rises ➢ Increased pulse pressure is significant in people with ICP. (difference bt systolic and diastolic); caused by slow heart rate and intermittent rapid cycling of the Cushing’s reflex Brain tumors
  • Space-occupying lesions that cause increased ICP
  • Benign and malignant tumors can be life-threatening. ➢ Unless accessible and removable
  • Gliomas form the largest category of primary malignant tumors ➢ Classified according to cell derivation and location of the tumor
  • Primary malignant tumors rarely metastasize outside the CNS.
  • Secondary brain tumors ➢ Metastasize from breast or lung tumors ➢ Cause effects similar to those of primary brain tumors
  • Signs and symptoms ➢ Site of tumor determines focal signs ➢ Seizures often first sign ➢ Headaches (increased ICP), vomiting, lethargy, irritability, personality and behavioral changes, possible unilateral facial paralysis or visual problems ➢ Do not cause systemic signs of malignancy ▪ Will cause death before they cause general effects
  • Treatment —may cause damage to normal CNS tissue ➢ Surgery if tumor is accessible ➢ Chemotherapy and radiation (many are radioresistant)
  • Interference with blood supply ➢ Local damage and manifestations depend on cerebral artery involved
  • Hemorrhage ➢ Increased ICP will cause local ischemia and generalized symptoms.
  • Global cerebral ischemia ➢ Impaired perfusion of entire brain ▪ Loss of function and generalized cerebral edema ▪ Brain death if not reversed quickly TIA’s: Transient Ischemic Attack
  • May occur singly or in a series
  • Result from temporary localized reduction of blood flow in the brain ➢ Partial occlusion of an artery ➢ Atherosclerosis ➢ Small embolus ➢ Vascular spasm
  • Signs and symptoms ➢ Difficult to diagnose after the attack ➢ Directly related to location of ischemia ➢ Intermittent short episodes of impaired function ▪ e.g., muscle weakness in arm or leg ➢ Visual disturbances ➢ Numbness and paresthesia in face ➢ Transient aphasia or confusion may develop
  • Inflammation of the membranes (meninges) surrounding the brain & spinal cord
  • Can be caused by: ➢ Viral (most common in US) usually mild and clears on it’s own if person has normal immune response ➢ Bacterial (serious and can be fatal) 2 vaccines available that cover four strands ➢ Other rare causes: fungal parasitic, amebic, non-infectious (cancer, lupus, etc)
  • Different age groups are susceptible to infection by different causative organisms.
  • Children and young adultsNeisseria meningitidis or meningococci ➢ Frequently carried in the nasopharynx of asymptomatic carriers ➢ Spread by respiratory droplets ➢ Occurs more frequently in late winter and early spring
  • NeonatesEscherichia coli most common causative organism ➢ Usually in conjunction with a neural tube defect, premature rupture of the amniotic membranes, difficult delivery
  • Young children ➢ Most often caused by Haemophilus influenzae ▪ More often in the autumn or winter
  • Older adultsStreptococcus pneumoniae— major cause
  • Signs and symptoms ➢ Sudden onset is common. ➢ Severe headache ➢ Back pain ➢ Photophobia ➢ Nuchal rigidity ➢ Kernig sign (next slide) ➢ Brudzinski sign (next slide) ➢ Vomiting, irritability, lethargy, fever, chills with leukocytosis ➢ Progression to stupor or seizures
  • Diagnostic tests ➢ Examination of CSF (obtained by lumbar puncture)
  • Treatment ➢ Aggressive antimicrobial therapy ➢ Specific treatment measures for ICP and seizures ➢ Glucocorticoids ▪ Reduction of cerebral inflammation and edema Parkinson’s Disease

of hands

  • Progressive degenerative disorder
  • Dysfunction of the extrapyramidal motor system ➢ Progressive degeneration ➢ Imbalance between excitation and inhibition Excess stimulation affects movement and posture. ▪ Resting tremors ▪ Muscular rigidity ▪ Difficulty initiating movement ▪ Postural instability
  • Primary or idiopathic Parkinson’s disease ➢ Usually develops after age 60
  • Secondary parkinsonism caused by: ➢ Encephalitis ➢ Trauma (e.g., sports injury) ➢ Vascular disease ➢ Drug-induced (e.g., phenothiazine tranquilizers)
  • Early signs and symptoms ➢ Fatigue ➢ Muscle weakness, muscle aching, ➢ Decreased flexibility ➢ Less spontaneous changes in facial expression ➢ Tremors in the hands at rest, repetitive pill-rolling motions
  • Later signs and symptoms ➢ Tremors affect hands, feet, face, tongue, lips ➢ Increased muscle rigidity ➢ Difficulty initiating movements ➢ Slow movements ➢ Lack of associated involuntary movements ➢ Characteristic standing posture is stooped , leaning forward

➢ Propulsive gait

➢ Complex activities become slow and difficult.

  • Other functions affected ➢ Chewing and swallowing become difficult. ▪ Prolonging eating time ▪ Recurrent drooling
  • Face might resemble a mask ➢ Blinking of eyelids reduced ➢ Blank, staring face ➢ Impairs communication
  • Treatment ➢ Removal of cause, if known ➢ Dopamine replacement therapy ▪ Levodopa—dopamine precursor ➢ Anticholinergic drugs

Decorticate vs Decerebrate positioning

  • Decorticate posturing: ➢ indicates severe dysfunction of the cerebral cortex has occurred. ➢ Aka: the flexor response or mummy pose ➢ Thinking, speaking, and remembering may be impaired.
  • Decerebrate posturing: ➢ Extensor posturing ➢ Considered worse, in response to brain stem injury (- impact on ability to breath, regulate BP, etc.) ➢ Secondary: could indicate that the brain has herniated into the brain stem

Seizures

  • Seizures
  • Caused by spontaneous, excessive discharge of neurons in the brain ➢ Causes ▪ Inflammation ▪ Hypoxia ▪ Bleeding in the brain ➢ Often manifested by involuntary repetitive movements or abnormal sensations (aura)
  • Generalized ➢ Absence seizures (petit mal) ➢ Tonic-clonic (grand mal) ➢ Myoclonic (brief, shock-like jerks of a muscle or a group of muscles.
  • Partial ➢ Simple partial ➢ Complex partial (psychomotor)
  • Continuous seizures (status epilepticus) ➢ Increased metabolism of glucose and oxygen ➢ May be life-threatening (>5 min, sometimes may hear >30 min) Visceral pain vs somatic pain
  • Somatic pain: conducted by sensory nerves ➢ From skin (cutaneous), bone, or muscle
  • Visceral pain: travels by sympathetic fibers ➢ Originates in organs ➢ May be acute or chronic Types of Pain
  • Referred Pain
  • Source may be difficult to determine.
  • Pain may be perceived at site distant from source ➢ Characteristic of visceral damage in the abdominal organs
  • Heart attack or ischemia in the heart
  • Phantom Pain ➢ Usually in adults ➢ More common if chronic pain has occurred ➢ Can follow an amputation ▪ Pain, itching, tingling ➢ Usually does not respond to common pain therapies ➢ May resolve within weeks to months ➢ Phenomenon not fully understood
  • Aphasia ➢ Inability to comprehend or express language ➢ Receptive (Sensory) —damage to Wernicke’s area ➢ Expressive (Motor) —damage to Broca’s area ➢ Mixed, global—damage to both areas or to the fibers and tracts between them
  • Dysarthria ➢ Motor dysfunction affecting muscles used in speech Neuro: visual loss (hemianopia) Depends on site of damage in visual pathway
  • Optic chiasm damage ➢ Vision lost in both eyes if chiasm is totally destroyed ➢ Partial loss ▪ Depends on particular fibers damaged
  • Optic tract or occipital lobe damage ➢ Loss of the visual field on side opposite to that of the damage Cellular adaptations (ch 1) Cellular response to injury
  • Apoptosis

➢ Refers to programmed cell death ▪ Normal occurrence in the body but can be changed by virus or disease process ▪ Ex: HIV leads to AIDS partially through T-Helper cell depletion by apoptosis. ▪ Ex: RBC

  • Ischemia (common cause of injury) ➢ Decreased supply of oxygena ted blood to a tissue or organ; results in reduced cellular metabolism.
  • Can be causedlocally : blocked artery – could lead to stroke (if blocked to brain) or heart attack (if blocked to the heart) ➢ systemically : low blood pressure, constriction of blood vessel, or clot ex: ischemic colitis (if mild treatable, if severe leads to gangrene, bowel perforation, or sepsis) ▪ *extent of cellular dysfunction depends on the magnitude and duration of ischemia - Anaerobic metabolism prevails, which < cell pH
  • Hypoxia ➢ Reduced oxygen in tissues

➢ Common s/s:

▪ Changes in color of your skin ▪ Confusion ▪ Fast heart rate ▪ Rapid breathing ▪ Sweating ▪ Wheezing ▪ Cough ➢ Causes : lung disease (asthma, COPD, emphysema, pneumonia etc), trauma, heart problems, anemia (low # of RBC), etc.

  • Physical damage ➢ Excessive heat or cold ➢ Radiation exposure
  • Mechanical damage ➢ Pressure or tearing of tissue
  • Chemical toxins ➢ Exogenous: from environment (oxidant sources could include cigarette smoke, stress, bad foods, drugs, etc) ➢ Endogenous: from inside the body (ex: DNA damage from chromosomal defects)
  • Necrosis ➢ the death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply. Staging of cancer
  • Essential to standardize comparative studies of treatments and outcomes
  • Used to estimate prognosis
  • Most common system used is the TMN system: ➢ Size of primary tumor (T) ➢ Involvement of regional lymph nodes (N) ➢ Spread (metastasis) of tumor (M)

Types of hypersensitivity reactions p 121-126; table 7- 5 Ty p e Example Mechanism Effects I Hay fever; anaphylaxis IgE bound to mast cells; release of histamine and chemical mediators Immediate inflammation and pruritus II ABO blood incompatibility IgG or IgM reacts with antigen on cell–complement activated Cell lysis and phagocytosis III Autoimmune disorders:

SLE,

glomerulonephritis Antigen–antibody complex deposits in tissue–complement activated Inflammatio n, vasculitis IV Contact dermatitis: transplant rejection Antigen binds to T- lymphocyte; sensitized lymphocyte releases lymphokines Delayed inflammation SLE, systemic lupus erythematosus.

  • IgG ➢ Most common in blood (80-85% of plasma antibodies, appears in all bodily fluids)
  • IgM ➢ First to increase in immune response; too large to easily cross membranes so it is present in the vascular system
  • IgA
  • IgE
  • IgD ➢ In secretions ▪ Tears ▪ Saliva and mucous membranes ▪ Colostrum ➢ Allergic response (ex: allergic rhinitis/hay fever- effects 20 million Americans) ➢ Causes release of histamine and other chemicals ➢ Results in inflammation

➢ Attached to B cells and is present in the plasma ➢ Activates B cells

  • Types of ImmunityHumoral immunity (B cells involved) : Antibodies are produced to protect the body.

Immobility: respiratory effects

  • Decreased metabolism so less demand for O
  • Respiration slow and shallow
  • Deep breathing and coughing more difficult if supine in bed
  • Drugs ➢ Sedatives and analgesics ▪ Depress neuromuscular activity and respiratory control center
  • Increased secretions in the lungs, stasis of secretions ➢ Pneumonia (hypostatic) ➢ Atelectasis
  • risk for aspiration due to position Common skin lesions p 144 Skin infections p 148- 150

  • May be caused by bacteria, viruses, fungi, other types of microbes, parasites
  • Caused by opportunistic microbes
  • Minor abrasions or cuts
  • Serious infections may develop.
  • Causative organism needs to be identified for appropriate treatment
  • Bacterial Infections ➢ Cellulitis (erysipelas) ▪ Infection of the dermis and subcutaneous tissue ▪ Usually secondary to an injury ▪ May be iatrogenic (caused ▪ medical intervention) ➢ Causative organism ▪ Usually Staphylococcus aureus ➢ Sometimes Streptococcus ➢ Frequently in lower trunks and legs ▪ Especially in individuals with restricted circulation in the extremities; also in immunocompromised individuals ▪ Area becomes red, swollen, and painful ▪ Red streaks may develop, running along lymph vessels proximal to infected area
  • Furuncles (boils) ➢ Usually caused by S. aureus ▪ Begins at hair follicles ▪ Face, neck, back ▪ Frequently drains large amounts of purulent exudate ➢ Autoinoculation ▪ Squeezing boils can result in spread of infection to other areas of the skin. ➢ Carbuncles ▪ Collection of furuncles that coalesce to form a large infected mass
  • Impetigo ➢ Common infection in infants and children ▪ May also occur in adults ▪ S. aureus—highly contagious in neonates ➢ Lesions commonly on face ➢ Transmission may occur through close physical contact or through fomites ➢ Pruritus common ▪ Leads to scratching and further spread of infection

➢ Treatment

▪ Topical antibiotics in early stages ▪ Systemic administration if lesions are extensive

  • Antibiotic-resistant strains of S. aureus are increasing in numbers. o Local outbreaks of infection may result.
  • Pediculosis ➢ Pediculus humanus corporis —body louse ➢ Pediculus humanus capitis —head louse ➢ Pediculus humanus pubis —pubic louse ➢ Female lice lay eggs on hair shafts. ➢ After hatching, louse bites human host, sucking blood for production of ova

Cardiac cycle and terms: p 227- 228

  • The cardiac cycle refers to the alternating sequence of diastole, the relaxation phase of cardiac activity, and systole, or cardiac contraction, which is coordinated by the conduction system for maximum efficiency Blood pressure and heart rate p 229- 231
  • Blood Pressure ➢ The top number is the pressure your heart exerts when blood is ejected from the left ventricle (systolic pressure), and the bottom number is the amount of pressure in your arteries between beats, when the ventricles are relaxed (diastolic pressure). ➢ The numeric difference between your systolic and diastolic blood pressure is called your pulse pressure. ➢ What is a normal blood pressure? ➢ (normal 120/70 at rest) ➢ What blood pressure or higher means a patient has hypertension? ➢ 140/90 or higher ➢ What blood pressure is considered a hypertensive emergency? (risk for stroke, go to ER) ➢ 180/110 or higher ➢ Blood pressure (BP) is altered by cardiac output, blood volume, and peripheral resistance to blood flow

Cardiac dysthymias: table 12- 2

  • Sinus Nose Abnormalities ➢ Bradycardia ▪ Regular but slow heart rate ➢ Tachycardia ▪ Regular rapid heart rate ➢ Sick sinus syndrome ▪ Marked by altering bradycardia and tachycardia - Often requires mechanical pacemaker
  • Atrial Conduction abnormalities: ➢ Premature atrial contractions or beats (PACs, PABs) ▪ Extra contraction or ectopic beats ➢ Atrial flutter ▪ Atrial heart rate of 160 to 350 beats/min - AV node delays conduction— ventricular rate slower ➢ Atrial fibrillation ▪ Rate over 350 beats/min - Causes pooling of blood in the atria - Thrombus formation is a risk. Congestive heart failure p 246- 250 Left Sided CHF Right Sided CHF Causes Infarction of left ventricle, aortic valve stenosis, hypertension, hyperthyroidism Infarction of right ventricle, pulmonary valve stenosis, pulmonary disease (cor pulmonale) Basic Effects Decreased cardiac output, pulmonary congestion Decreased cardiac output, systemic congestion, and edema of legs and abdomen Forward effects (decreased output) Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance Compensations Tachycardia and pallor, secondary polycythemia, daytime oliguria Tachycardia and pallor, secondary polycythemia, daytime oliguria Back Up Effects Orthopnea, cough producing white or pink-tinged phlegm, shortness of breath, paroxysmal nocturnal dyspnea, hemoptysis, rales Dependent edema in feet, hepatomegaly and splenomegaly, ascites, distended neck veins, headache, flushed face