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Patho Final Study Guide
Pathophysiology (NSG 211)
Marian University
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Pathophysiology: NSG 211 Exam 5 Review
Consider: Etiology, Process, Signs and Symptoms, Complications of topics below...
Pyelonephritis
Glomerulonephritis: signs symptoms
Urolithiasis: causes, signs / symptoms, complications
Renal failure: causes, signs / symptoms, complications
Comas, Vegetative state: definitions
Posturing: prognosis
Aphasia: types, areas affected
Types of speech and writing dysfunctions from neurological injury
ICP: early signs and symptoms of increased ICP
Cushing Reflex
Meningitis
Meningitis: Inflammation of the brain meninges or spinal cord Pathophysiology: o Micro-organisms reach the brain via the blood by... *Nearby tissue (mucosa) *Direct Trauma / Surgery Microbes bind to nasopharyngeal wall and cross mucosal barrier attaching to choroid plexus
o After entering CSF, infection spreads rapidly in CNS Inflammatory response leads to Increased ICP, as pia mater become edematous Exudate covers the brain and fills the sulci (grooves) Exudate is present in CSF (spinal tap), blood vessels of brain dilate and rupture
Etiology: o Can be Viral or Bacterial Children: predominantly less than 1 year old Neisseria meningitis (meningococcus) Streptococcus pneumonia Signs & Symptoms: o HA or Irritability o Back Pain o Photophobia o Nuchal Rigidity (move chin to chest it hurts/ or when laying on back and lift chin up, the knees will pop up) Kernig’s / Brudzinski’s signs
Bacterial: MOST Deadly Spinal Tap: CSF
Turbid/cloudy (WBC)
Low Glucose
(Lie them down on back, bring chin to chest, knees will come up to relieve pressure on spine – Nuchal rigidity) Bending knees decreases ICP o Fever / Chills o Leukocytosis o Signs of Increased ICP (Vomiting, Irritability, Lethargy, Seizures)
Bacterial: Most Deadly Spinal Tap: CSF Turbid / Cloudy (WBC) Low Glucose (bt. Eat glucose
***Most antibiotics will not pass through the blood brain barrier, so hard to treat bacterial infection.
Autonomic dysreflexia: Causes, process
Autonomic Dysreflexia Sudden massive reflex sympathetic discharge o Associated with spinal injuries at T-6 and above Pathophysiology: o Stimulus initiates positive feedback stimulation of ANS Hypertension, Bradycardia, and risk for death How? o Most often stimulus: distended bladder or colon Stimulus below injury ascends to send message to brain; however, it is blocked by spinal lesion at site of injury Injury “Fireworks” stimulate SNS below lesion SNS => Vasoconstriction => Hypertension=> Diaphoresis
HTN stimulates baroreceptors to activate PNS: 1. PNS signals to SNS to shut off, But Cannot reach site due to lesion below 2. PNS (Vagus) signals SA node to slow HR Causes bradycardia o Since ascending SNS stimulus not blocked, and original stimulus not relieved, SNS stimulation increases More Vasoconstriction induces more severe HTN
o MRI: May show plaque lesions in CNS o CSF: elevated protein, gamma globulin, and elevated lymphocytes Treatment: Target Immune Response & Spasticity o Glucocorticoids – to target the immune response o Immuno-modulators: Suppressor T-cells o Interferon o (Many of the treatments will reduce the immune response) o Muscle relaxants
o Physical Therapy to maximize motor function Balance and strength o Speech / language pathology if needed
MS progresses in many different ways. o Usually begins in the legs o Can attack cervical spine Avoidance of: o Stress, Fatigue, Injury, infection
Parkinson Disease Definition: o a progressive, degenerative disorder affecting motor function Loss of function and coordination through the extrapyramidal tracts Tracts that make everything super smooth With dopamine, make movements coordinated and smooth Prevalence: o 60,000 new cases annually. o Most cases are Idiopathic Pathophysiology: o Degeneration of the basal ganglia due to misfolded a-synuclein proteins of the substantia nigra Resultant decreased production of dopamine adversely affects muscle control o Signals from the cerebral motor cortex are processed through the basal ganglia, with dopamine from the substantia nigra establishing negative feedback and smoothing motor movements. Loss of dopamine from the substantia nigra results in: o 1) Loss of Inhibition, 2) Increased Cholinergic (muscle contraction) Etiology: o Primary: Most cases: Idiopathic Usually after age 60 o Secondary: post-Encephalitis Trauma (TBI) Vascular Disease Signs & Symptoms: o 1.) Loss of Dopamine: Loss of smooth muscle control Resting Tremor, shuffle-gait, Balance Disturbance High fall risk o 2.) Cholinergic Upregulation: Muscle Rigidity Torticollus, Stooped posture, Dysarthria Torticollus is stiff neck Other: o Mood / sleep disorders, Depression, Difficulty Concentrating
Early: o Fatigue o Muscle Weakness and Aching o Decreasing flexibility o Less spontaneous changes in facial expression (flat affect) o Hand Tremors at rest
o Anti-glutamate riluzole (Rilutek) shows some promise at slowing progression
Myasthenia Gravis Definition: o an Autoimmune disorder that impairs the function of Acetylcholine (ACh) at the neuromuscular junction (NMJ), resulting in muscle weakness Pathophysiology: o IgG Antibodies to ACh-receptors block and destroy ACh receptor site o Prevents further muscle stimulation, leading to muscle weakness and rapid fatigue o Progression: typically initiates in facial area and progresses to the trunk
Etiology: o Autoimmune (Anti-ACh Ig-G) o Initiation is idiopathic o Women affected more than men o Onset usually 20-30 for Women (Later in men – over 50)
Diagnostic Tests: o EMG: Electromyelograph o Serum Antibodies (IgG) o Tensilon Test: When given, prolonged ACh activity seen at NMJ (Relief of symptoms) How? Blocks cholinesterase, thus prolonging ACh activity. Positive Tensilon Test supports MG diagnosis Signs & Symptoms: o Muscle weakness of the face and eyes develop quickly o Diplopia / Ptosis may impair vision o Nasal monotone speech pattern o Facial expression lost with sad-looking face (flat affect) o Chewing / swallowing become difficulty (Aspiration Risk!!) o Head drooping o Upper Respiratory Infections common from ineffective cough & airway clearance / dysphagia *Aspiration Pneumonia Risk! Myasthenia “Crisis” can be brought on by Triggers such as: o Infection o Stress o Trauma o Alcohol intake
Treatment: o Anticholinesterase agents (pyridostigmine or neostigmine) Anti and ace block each other out So increases acetylcholine o Glucocorticoids o Plasmapheresis o Thymectomy
Huntington Disease Definition: o An inherited degenerative disorder that manifests itself in midlife (30-50 years old) Named after Dr. George Huntington, who first described the “heriditary chorea” Chorea – sort of a strange dance Pathophysiology: o Autosomal Dominant gene expresses itself in midlife N-terminal mutant “Huntington” produces abnormally-folded proteins that accumulate as inclusions Progressive atrophy of the brain with neuronal degeneration
particularly in the caudate nucleus of the basal ganglia and the frontal cortex Ventricles dilate and Depletion of GABA (gamma-aminobutyric acid) occurs GABA helps control moods, muscles Etiology: o Autosomal Dominant disorder carried on Chromosome 4
Diagnostic Tests: o DNA: cysteine-adenosine-guanine (CAG) encoding for the mutant “Huntington” (htt)
Signs & Symptoms: o Mood swings & Personality changes o Restlessness o Choreiform- Latin:“khoreia”=“dance”: Non-repeating, excessive, spontaneous movements/gestures (“Chorea”) Ex: fidgeting hand movements, unstable dance-like movements, “milkmaid’s grip”, “harlequin’s tongue”, drops o Rigidity and Akinesia with Dystonia (rigid contractions causing twisting postures) Akinesia is the loss or impairment of the power of voluntary movement o Dementia: Intellectual impairment leading to dementia and often total loss of function
Treatment: o Symptomatic treatment of physical and psychiatric manifestations. o No treatment of primary cause
TIA / CVA: types, etiology, signs and symptoms, sequelae Vascular Disorders: TIA, CVA, Aneursym TIA: Transient Ischemic Attack o Temporary localized ischemia to the brain Full Recovery within 24 hours o Pathophysiology: A partial occlusion of an artery that occurs from: Atherosclerosis (CAD, DM, Smoking, HTN) Small emboli Vascular spasm o Signs & Symptoms Directly related to location of ischemia in the brain Patient conscious throughout Intermittent impaired function, such as: Muscle weakness in extremities Visual disturbances (Dec FOV, diplopia) Numbness/parasthesia in face Transient aphasia / confusion Lasts from a few minutes to 24 hours “FAS”: Face / Arm / Speech (quick analysis) smile, raise eyebrows and frown. Muscles symmetric Close eyes and raise arms. One are will drift if problem. Speech – clear? Slurred? **All symptoms resolve within 24 hours **No permanent impairment ** Often warning sign of impending CVA
Etiology: May be Primary (idiopathic) or Secondary (acquired) o Onset occurs before age 20 in 75% of cases o Congenital malformations, Drug / alcohol abuse, Infection, Tumors, CVA’s, Post-TBI’s o Two drugs that cannot be stopped abruptly because of seizure activity. Alcohol Benzodiazapines o Most seizure activity is idiopathic. Rule out all problems If someone has recurring seizures, then they have epilepsy. Diagnostic Tests: o EEG: Electroencephalogram o Direct Observation o MRI may detect structural abnormalities (Secondary may be caused by a tumor / mass)
Seizure Disorders Partial Seizures: o Single focus often in cerebral cortex (sensory-motor cortex): often Unilateral o May or May Not cause loss of consciousness .. progress to generalized seizure Generalized Seizures: o Involves multiple foci in BOTH cerebral hemispheres and brainstem o Always associated with a Loss of Consciousness o Oxygen consumed at 60-70% higher rate during ictal (sz) stage Prolonged seizure can rapidly result in anoxic brain injury – a major concern
Complications of Generalized Seizure Disorder: o Tonic-Clonic (grand mal) can cause permanent damage (bodily injury or anoxia) o Status Epilepticus: seizure that is not stopping Respiratory Impairment, Excessive skeletal muscle activity Leads to hypoxia, hypoglycemia, acidosis, hypotension, and potential brain damage
Seizure Disorders—Partial Seizures Partial Seizures: “Simple” or “focal seizures” o Arise from the epileptogenic focus related to the area of damage in the cortex o Occur in children and adults o May have an aura Signs & Symptoms: Partial Seizures *Repeated jerking movements of extremity *Sensation of tingling *Auditory or visual experiences *May be No loss of consciousness *bizarre behaviors like repeatedly clapping hands *Visual or auditory hallucinations or feelings of de ja vu *Unresponsive to persons around them (but no LOC)- “space out” *Retrograde Amnesia and drowsiness after seizure (often) Seizure Treatments: for partial seizures o Treat primary cause, if known o Avoid triggers: Hypoxia, Bright lights, Loud Noises, Hypoglycemia
Medications: similar to meds for general seizures o Anticonvulsants: *phenytoin *valproic acid *gabapentin Anticonvulsants. Raise the seizure threshold
o Benzodiazepines: *lorazepam *diazepam
Often used for emergent case of seizure disorders.
Status Epilepticus: Medical Emergency. o Requires Oxygenation, Fluids, Barbiturates (Phenobarbitol) Barbiturates often cause drowsiness
Seizure Disorders - Generalized Etiology: o Idiopathic 4 Genes Identified as having a role in seizure development Familial Incidence is more evident in seizure onset of young children Precipitating Factors: o Loud Noises o Bright lights o *Biochemical stimuli (smells, etc) *Stress *strobe lights *Hypoglycemia *Medication *Hyperventilation (alkalosis)
Signs & Symptoms: Generalized Seizures o Petit mal (“absence seizures”) Last 5-10 seconds Occur several times / day Brief loss of consciousness Sometimes transient facial movements (Eyelid twitching) patient often appears as ”Staring”, then resume activity o Grand mal (Tonic-clonic seizures) Spontaneous occurrence or after simple seizure Prodromal signs: (nausea, irritability, muscle twitching) Aura: (peculiar visual or auditory sensation) Loss of consciousness Strong Tonic muscle contractions, including cry/noise Clonic stage of muscle contraction, followed by subsiding contractions Postictal stage – after seizure
Fracture injury process and fracture types
Fracture is a break in the continuity of bone
- Pathophysiology: o When bone breaks, bleeding from the blood vessels and periosteum (bone portion) occurs. o Bleeding and inflammation occur in the soft tissue surrounding the fracture o Hematoma formation often occurs o Necrosis may result if the inflammation or hematoma comprise blood supply
- Healing process is affected by fracture type, foreign body, age disease (DM, anemia) indirect healing: o Hematoma formation o Granulation tissue: Hematoma serves as supply of fibrin network/granulation Capillary regeneration: new capillaries extend into granular tissue Phagocytosis: phagocytes and fibroblasts migrate to site of injury o ProCallus: (before- pre-bone) Chondroblasts begin to form cartilage in a “procallus” Procallus= fibrocartilaginous callus/bond fuses two sections of bone
Pathophysiology: o Recall: bone remodeling is constant reabsorption (-clasts) and reformation (-blasts) balance o During bone remodeling, reabsorption (osteoclasts) exceeds bone formation (osteoblasts). Leads to thinning and “hollowing out” of bone, more susceptible to fracture
Osteoporosis Signs & Symptoms: *Asymptomatic early in disease (Rationale for early DEXA Scanning) Note: Most bone growth by Age 20, Thinning begins at age 30! *Often initial symptom is Pathological or Compression Fractures *Back Pain or disc compression *Kyphosis – curvature of spine forward *Scoliosis (lateral variation of spine curvature) *Spontaneous Fractures (Hip Fracture, then patient falls) *Delayed bone healing after fracture Treatment: *Dietary supplements of Calcium and Vitamin D *Biophosphonates (stimulate osteoblast activity) *Calcitonin (usually nasal spray): Inhibits parathyroid hormone activity *Regular weight-bearing exercise stimulates osteoblast activity *Raloxifene (Evista): Estrogen stimulator in bone Inhibits action in breast / uterus as treatment for these cancers
Osteoarthritis: OA Definition: o Degenerative “wear and tear” disorder of load-bearing / overused joints Etiology: *Estimated 1 in 3 adults in the US have some degree of OA *Primary: Idiopathic *Secondary: Injury to joint or overuse / misuse Pathophysiology: o *Articular cartilage of weight-bearing joints incurs structural fissures. o *Damage occurs from excessive stress, injury, or metabolic breakdown o *Surface of the cartilage becomes rough, worn, less smooth on movement o *Tissue damage causes the release of enzymes from chondrocytes, which accelerates the disintegration of the cartilage matrix o *Eventually, subchondral bone may be damaged, allowing cyst and spur formation of osteocytes on the bone ends. o *This “new bone” is rough, and spur-like, decreasing joint function o *Pieces of osteocytes and cartilage break loose into synovial cavity, causing irritation and can precipitate a secondary inflammation *Eventual result is closing of joint space with new bone growth Decreased ROM of joint. Pain.
*No systemic signs or symptoms exist in Osteoarthritis (Stays Local) NOT systemic
Signs & Symptoms: of Osteoarthritis *Pain & Stiffness especially after overuse and extended rest *Decreased joint mobility / ROM
*Crepitus *Xray--- decreased joint space (spurs) Treatment: *Minimize stress to the joint *Ambulatory aids and Orthotic devices *Glucocorticoid Injection & NSAIDS (help secondary inflammatory process) *Joint Replacement
Rheumatoid arthitis Definition: o An autoimmune disorder causing chronic, systemic inflammatory disease o Can effect other parts of the body because it is systemic
Prevalence / Etiology: *Affects about 1% of the population *Fingers, Feet, wrists, knees *Women affected > Men *Increased incidence with Age *Genetics a factor Familial predisposition Pathophysiology: o *Insidious onset, characterized by remissions and exacerbations o *Symmetrical involvement of small joints (especially hands / feet) o *Abnormal immune response to citrunillization of arginine (Ab response to arginine) Involves T-cells, B-cell Immunoglobulins Thought to be Types III and IV Hypersensitivity o Causes synovial membrane inflammation, characterized by: Vasodilation Increased permeability Formation of thickened synovial fluid, called “pannus” Exudate in joint causes Red swollen, painful joints (synovitis) o *During subsequent exacerbations, cartilage erosion, fibrosis, and pannus formation continues to worsen joint function
Characterized by damage to all 3: Joint (synovial), Cartilage, and Bone!
Rheumatoid Arthritis Signs & Symptoms: Joint: *Joint stiffness *Red, Swollen joints *Atrophy of muscle *Bone misalignment *Muscle spasms Ulnar deviation Fingers drift toward the ulna rather than the thumb *Contractures / Deformities Boutonniere Deformity – thumb drifting toward the radius *Joint eventually fixed
Systemic: *Marked fatigue *Depression / Malaise
Patho Final Study Guide
Course: Pathophysiology (NSG 211)
University: Marian University
