- Information
- AI Chat
NSG 211 Exam 5 Review
Pathophysiology (NSG 211)
Marian University
Recommended for you
Related Studylists
asu pathoPreview text
NSG 211 Exam 5 Review
Consider: Etiology, Process, Signs and Symptoms, Complications of topics below...
1. Pyelonephritis 2. Glomerulonephritis: signs symptoms 3. Urolithiasis: causes, signs / symptoms, complications 4. Renal failure: causes, signs / symptoms, complications: Types: Pre-Renal, Intra-Renal, Post-Renal (with examples) 5. Comas, Vegetative state: definitions 6. Posturing: types, prognosis 7. Aphasia: types, areas affected 8. Types of speech and writing dysfunctions from neurological injury 9. ICP: early signs and symptoms of increased ICP 10. Cushing Reflex: Cushing’s Triad 11. Meningitis 12. Autonomic dysreflexia: Causes, process, dangerous complications 13. Neuro Degenerative disorders: etiology, pathophysiology and typical manifestations of: Multiple Sclerosis, Parkinson’s Disease, ALS, Myesthenia Gravis, Huntington’s Disease. 14. TIA/CVA: types, etiology, differences, signs and symptoms, sequelae of each 15. Seizure disorders: “Partial” vs “generalized” definitions, causes, diagnostic tests, complications, aura 16. Fracture: healing process after injury and major fracture types 17. Osteoporosis: Risk factors, etiology, pathophysiology, manifestations and complications 18. Osteoarthritis: Risk factors, etiology, pathophysiology, manifestations and complications 19. Rheumatoid arthritis: etiology, pathophysiology, manifestations and complications 20. Gout: etiology, pathophysiology, dietary considerations
Pyelonephritis - pg 735- Definition - ineffective organism ascends urinary tract to ureters of the kidneys (upper urinary tract) Common causes ● urinary obstruction and reflux of urine from the bladder are most common, most occur in women. Table 32 has all common causes of pyelonephritis-pg. 7 37 Patho: ● involves ureters, renal pelvis, and medullary tissue. One or both kidneys may be involved. Purulent drainage fills renal pelvis and calyces and medulla becomes inflamed, tubule tissue sloughs off forming casts of tubule walls (casts are like molds of the wall tissue in the urine). Acute-microorganisms usually assoc with acute are E. coli, proteus, or pseudomonas. These microorganisms split urea into ammonia, making an alkaline urine that increases the risk of stone formation. The infection is spread by ascending uropathic microorganisms along the ureters, and can also occur by way of bloodstream. Acute rarely causes renal failure. Chronic- prevents elimination of bacteria and thus starts the process of progressive inflammation. Destruction of tubules and scarring w/impaired urine-concentrating ability. Lesions are termed chronic interstitial nephritis Signs and Sx: ● signs of cystitis (dysuria, urgency, foul smelling urine), flank pain (costrovertebral angle tenderness-lower back-cva tenderness), fever, malaise, nausea, and leukocytosis. Early sx of
chronic include htn frequency, dysuria, and flank pain. This can lead to kidney failure esp if pt has obstructive uropathy or dm. Urinalysis ● cloudy, foul-smelling urine, bacteria, pyuria (leukocytes) with casts (molds) , hematuria and proteinuria likely Complications:
- urinary retention, hydronephrosis(postrenal kidney failure), and renal artery stenosis ◦ Lower UTI - Cystitis (bladder), urethritis (STI), Prostatitis
Glomerulonephritis: signs symptoms-pg 737- Definition - inflammation of nephron and glomerulus caused by glomerular injury Patho: ● 1-2 weeks after streptococcal infection, primarily in children 3-7 y. Type III hypersensitivity reaction-antigen/antibody complexes are formed and lodged in the glomerular apparatus of the kidney-then inflammatory mediators such as complement, cytokines, IL, T-lymphocytes-then results in increased capillary permeability, then protein and rbc enter filtrate (urine), cell proliferation and congestion result in decreased gfr, increased fluid/waste retention Signs and Sx ● fluid retention (htn), facial and periorbital, then generalized edema, oliguria, malaise, fever, fatigue, headache (htn), anorexia/nausea Urinalysis ● oliguria w/smoky or coffee colored urine (gross hematuria, and proteinuria often 3-5 grams daily) Diagnostic tests ● elevated creatinine and BUN (decreased gfr and decreased renal filtration), metabolic acidosis (dec kidney function), elevated aso/ask titers Complications ● renal failure (intrarenal AKI), nephrotic syndrome-over 3 grams of proteinuria/day
Urolithiasis: causes, signs / symptoms, complications-pg 729- Definition - renal calculi/kidney stones Patho ● stones/calculi form anywhere in urinary tract, can be smooth/jagged. Deposits continue to build up increasing the mass, manifestations are only shown when stone causes an obstruction. This leads to pain and can cause hydronephresis Etiology ● common problem and tends to recur w/pts. ● 75% are d/t calcium salts (80% are calcium oxalate), hyperparathyroidism (hypercalcuria), metabolic disorders, alkaline urine (ph>7) increases oxalate formation ● Uric acid crystals can cause stones-gout, high purine diet, and cancer ● Infection can precipitate stone formation ● Urinary stasis -dehydration, immobility Signs and Sx ● result from irritation, infection and obstruction, flank pain (distention of renal capsule), renal colic (crampy flank pain, cva tenderness), nausea, vomiting, sns-cool moist skin and tachycardia Complications ● Dehydration, hydronephrosis, and post renal acute kidney injury
Coma definition: Vegetative state definition:
Posturing: Types Prognosis Decorticate - Cerebral cortex damage. Flex to the core, adducted arms. Higher portion of the brain, higher functioning part of brain. May be able to re-learn. Get higher points on Glasgow. It’s bad, but not as bad. Decerebate - brainstem and cerebellum that are demonstrating damage. Can’t reteach yourself how to re- breathe b/c you never learned it (it was automatic) and that’s why it’s worse. all 4 extremities in rigid extension. Hyper-pronation of forearms and plantar flexion of the feet.
Aphasia: Aphasia is impairment of comprehension or production of language w/impaired communication. The terms aphasia and dysphasia are often used interchangeably (the book uses aphasia p). Types Areas affected:
Expressive aphasia , also known as Broca , motor, or nonfluent aphasia, involves the loss of the ability to produce spoken or written language, w/slow or difficult speech. Verbal comprehension is usually present.
Receptive aphasia , also known as Wernicke , sensory, or fluent aphasia, involves the inability to understand written or spoken language. Speech is fluent, flowing at a normal rate, but words and phrases have no meaning.
Global aphasia is the most severe aphasia and involves both expressive and receptive aphasia (Broca’s & Wernicke’s). The individual is nonfluent/mute, can’t read/write, and has impaired comprehension, naming, reading/writing. It is usually associate w/a cerebrovascular accident involving the middle cerebral artery.
Types of speech and writing dysfunctions from neurological injury:
ICP: early signs and symptoms of increased ICP Etiology ● Brain hemorrhage ● Trauma ● Cerebral edema ● Infection ● Tumors Pathophysiology ● Brain tissue, CSF, and blood are encased in a non-expandable space (the skull); therefore, ICP INCREASES with ANY INCREASE in fluid or additional brain mass ● INCREASED ICP → less cerebral arterial blood supply and compression of brain tissue** ● Increased ICP at site of problem → spreads throughout the brain and CNS via CSF and blood → leads to widespread loss of function ● Increased ICP results in DECREASE in neuron function and eventual brain tissue death** Manifestations
● EARLY: Change in level of consciousness ● Headache ● Vomiting* – due to pressure on medulla ● Vital signs show Cushing’s Triad ● Vision changes* ○ Papilledema, double vision—due to increased pressure on optic nerve* ○ Pupils are fixed & dilated – uncal herniation: brain pressure causes tissue to try and escape through the hole where the spinal cord is connected to the brain putting pressure on the brainstem/cerebral cortex*
Increased ICP: Explained
Pathophysiology ● Early increased ICP → body attempts to compensate by shifting more fluid to the spinal cavity and increasing venous return to the brain → fluid shift causes hypoxia → hypoxia triggers peripheral VASOCONSTRICTION & cerebral VASODILATION Manifestation ● FIRST SIGN of increased ICP – change in level of consciousness ● Lethargy, decreased responsiveness, confusion, etc. ● As ICP increases – Cushing’s Reflex & Cushing’s Triad are invoked ● Systemic vasoconstriction is the body’s attempt to increase cerebral blood supply (helps to shift blood from extremities to the brain) ● Hypertension – TEMPORARILY increases cerebral blood supply (“squeezing the toothpaste tube”) ● Bradycardia – Baroreceptors in the carotid arteries respond to increased ICP parasympathetic stimulation of the SA node reduces heart rate ● Bradypnea – Chemoreceptors respond to low cerebral CO 2 levels (fast flow) → reduce respiratory rate temporarily improves cerebral ischemia, but returns continuing compression & rising ICP → cycle continues with increased peripheral vasoconstriction → leads to Cushing’s Triad** ● If ICP is not relieved, herniation will occur ○ Pupillary dilation (fixed) ○ Ptosis (eyelid drooping)—due to CN III compression*
Cushing Reflex: Cushing’s Triad Etiology ● Increased ICP Pathophysiology ● Consequence of increased ICP that is not relieved ● Cerebral ischemia stimulates Cushing’s reflex from the vasomotor centers of the brain Manifestations (Cushing’s Triad)** ● INCREASED blood pressure ● WIDENING pulse pressure ● SBP increases, DBP decreases ● DECREASED heart rate (bradycardia)
Treatment & Prevention ● BACTERIAL – treated with antibiotics; started ASAP or death can occur** ● VIRAL – meningococcal vaccine, pneumococcal vaccine, & Hib vaccine ○ Hib at 2 months ○ Pneumococcal (PCV13) at 2 months ○ Meningococcal usually given at 11-12 years of age unless immunocompromised (then given at 2 or 9 months)
Autonomic dysreflexia: Causes, process, dangerous complications Etiology ● Sudden massive reflex sympathetic discharge ● Associated with spinal injuries at T6 & ABOVE Pathophysiology ● Stimulus initiates positive feedback stimulation of ANS → causes bradycardia, hypertension, & risk for death How? ● Most often stimulus → distended bladder or colon* ● Stimulus BELOW spinal injury ascends to send message to the brain; however, it is BLOCKED by spinal lesion at site of injury ○ Injury “fireworks” stimulate SNS below lesion ● SNS VASOCONSTRICTION → HYPERTENSION → DIAPHORESIS ● Hypertension stimulates baroreceptors to activate PNS 1. PNS signals to SNS to shut off → cannot reach site due to lesion below 2. PNS (vagus nerve) signals SA node to slow heart rate → causes bradycardia ● Ascending SNS stimulus is not blocked & original stimulus is not relieved → SNS stimulation INCREASES → MORE vasoconstriction → induces MORE severe hypertension Complications ● SNS stimulation → hypertension → PNS vagus nerve stimulation → SA node bradycardia → malignant hypertension → CVA, MI, Aneurysm, Respiratory failure Treatment ● STIMULUS MUST BE RELIEVED** ● Periodic (intermittent) catheterization (q8h) ● Bladder scans ● Bowel hygiene
-
NeuroDegenerative disorders: etiology, pathophysiology and typical manifestations of: -
Multiple Sclerosis
Definition: A progressive demyelination and sclerosis of the neurons in the CNS ● Neurons of the brain, spinal cord, & cranial nerves are affected ● Characterized by remissions & exacerbations with progressive debilitation ● Several types with each type having different progression & severity Etiology ● Age: 20-40 years old ● More common in WOMEN ● More frequent in those of EUROPEAN descent ● Idiopathic** ○ Believed to be autoimmune (Type II & Type III hypersensitivity reactions) ○ Genetics, immunologic, environmental, or viral infections are possible triggers* Pathophysiology ● Loss of myelin interferes with impulse conduction in CNS (brain and spinal cord) ● ALL types of fibers may be affected (motor, sensory, & autonomic) ● Initially: lesions occur as inflammatory response with loss of myelin in white matter of CNS ● Later: larger areas of inflammation & demyelination cause plaques (sclerosis) ● Plaques are frequently visible in the ventricles, brainstem, and optic nerve**
- Increased cholinergic (muscle) Manifestations
- Loss of dopamine: ● Loss of smooth muscle control → tremor, shuffle-gait, balance disturbance
- Cholinergic upregulation: ● Muscle rigidity → torticollis, stooped posture, dysarthria
- Other: ● Mood, sleep disorders, depression, difficulty concentrating EARLY: ● Fatigue ● Muscle weakness & aching ● Decreasing flexibility ● Less spontaneous changes in facial expression (flat affect) ● Hand tremors at rest ● Tremors decrease with voluntary movement or sleep ● “Pill rolling” motion of the hands LATE: ● Mask-like faces ● Shuffling steps , stooped posture, bent elbows (due to decreased muscle flexibility) ● Head, leg, & hand tremors ● Dementia
Treatment
Medications: ● Dopamine replacement (Levodopa/Carbidopa) ● Muscle relaxants (Anticholinergic drugs)
● Investigative therapies ● Multidisciplinary care ● Physical therapy
ALS
Definition: Amyotrophic= “muscle wasting” + Lateral Sclerosis= “hardening” or “scaring” of the lateral corticospinal tracts (motor UMN) Etiology: ● Idiopathic —mitochondrial dysfunction, oxidative stress, cytoplasmic inclusions result in inflammation ● Prevalence higher in MEN ● Age: 40-60 years most common, peak age of 60-70 years ● Linked to chromosomal abnormalities ● Familial: only accounts for 10% of cases
Pathophysiology ● Affects UPPER & LOWER motor neurons of the cerebral cortex, brainstem, & spine ● No inflammation ● Loss of UPPER motor neurons → HYPERreflexia ● Loss of LOWER motor neurons → FLACCID PARALYSIS ● Decreased muscle tone & decreased reflexes are the end result** ● Loss of neurons is diffuse & asymmetrical ● NO REMISSION → eventual respiratory failure leads to death** Manifestations INITIALLY: ● Upper extremity weakness & muscle atrophy with loss of motor control ADVANCED: ● Falls ● Muscle cramps or twitching ● Dysarthria ● Difficulty swallowing ● Respiratory failure → CAUSE OF DEATH*** ● Respiratory failure usually occurs within _3-5 years of diagnosis_*
Treatmen t
● NO TREATMENT AVAILABLE TO STOP PROGRESSION ● Anti-glutamate riluzole (Rilutek) shows some promise at slowing progression
Myasthenia Gravis
Definition: An autoimmune disorder that impairs the function of Acetylcholine (Ach) at the neuromuscular junction (NMJ), resulting in muscle weakness Etiology ● Autoimmune – anti-ACh IgG ● Initiation is idiopathic ● WOMEN are affected more than men ● Age: onset usually around age 40 in WOMEN & later in MEN over age 50 Pathophysiology ● IgG antibodies to ACh receptors → block & destroy ACh receptor site → prevents further muscle stimulation → leads to muscle weakness & rapid fatigue ● Progression → typically initiates in facial area and progresses to the trunk Manifestations ● Muscle weakness of the face and eyes develops quickly ● Diplopia/ptosis may impair vision ● Nasal monotone speech pattern ● Facial expression lost with sad-looking face ( flat affect ) ● Chewing/swallowing difficulty (ASPIRATION RISK)* ● Head drooping
● DNA: cysteine-adenosine-guanine (CAG) encoding for the mutant “huntingtin” (htt) Treatment ● NO TREATMENT FOR PRIMARY CAUSE ● Symptomatic treatment of physical and psychiatric manifestations
TIA / CVA: types, etiology, differences, signs and symptoms, sequelae of each - KELSEY
TIA: Transient ischemic attack ● Temporary localized ischemia to the brain, full recovery in 24 hours Patho: ● a partial occlusion of an artery that occurs from Atherosclerosis (CAD, DM, smoking, HTN), small emboli, or vascular spasm S/S: ● directly related to location of ischemia: pt is conscious, intermittent impaired function, muscle weakness in extremities, visual disturbance, numbness, paresthesia in face, transient aphasia,or confusion ● Will last a few min to 24 hours ● FAS: Face, Arms, Speech ● All symptoms resolve within 24 hours, no permanent impairment but often a warning sign of impending CVA CVA: Cerebral Vascular Accident ● Leading cause of disability and #3 cause of death in women Patho: ● brain attack, infarction/necrosis of brain tissue from ischemia, central area of necrosis with surrounding ischemia Etiology: ● Throbotic: total occlusion of thrombus or embolus, Hemorrhagic: rupture of cerebral blood vessel Risk Factors: ● same as TIA (HTN, DM, CAD, smoking) and history of TIA S/S: ● directly related to location and size of infarction, collateral circulation determines function deficit, first is flascid paralysis, THEN spastic weeks later. ● Functional deficit increases in the first 48 hours -> inflammation extended necrotic area. ● Occlusions or Hemorrhage in large areas -> coma or LOC, death Hemorrhagic Strokes: ● blinding headache with marked deficits, vomiting, coma, Cushing’s triad
Seizure disorders : “Partial” vs “generalized” definitions, causes, diagnostic tests, complications, aura Seizures: ● Spontaneous, transient disruption in the brain caused by excessive electrical cortical activity ● Pt’s with seizures have a lower threshold (hyper-excited) to stimulations and when over stimulated can cause a seizure ● Stimulation results in motor and sensory activity that spreads throughout the brain ● Seizures are characterized by their localization and clinical feature ● Can by primary (idiopathic) or secondary (acquired)
● Onset before age 20 occurs in 75%, can also be caused by congenital malformations, drug/alcohol abuse, infection, Tumors, CVAs, Post TBI’s Partial Seizures ● Simple or focused seizure often in the cerebral cortex ● Occur in one area related to the damage in the cortex, often unilateral ● May progress to generalized seizure ● Occurs in children and adults ● Pt might have a aura: sometimes it may be feelings of nausea, a particular smell Signs and symptoms: ● repeated jerking movements of the extremities, tingling sensation, auditory or visual experience, may be NO LOSS of consciousness, weird behaviors like repeatedly clapping hands, deja vu, unresponsive while conscious, space out, retrograde amnesia of what occurred right before the seizure, and drowsiness after the seizure. Treatments: ● treat primary cause id known, avoid triggers like hypoxia, bright lights, loud noises, hypoglycemia. Medications: ● seizure medications ending in “-pam” are used in emergent cases. Anticonvulsant medications will raise the seizure threshold to decrease the chance of having a seizure.
Generalized Seizures Etiology: ● idiopathic (early onset), 4 genes identified as having a role in seizure development, familial incidence is more evident in seizure onset of young children Precipitating factors: ● loud noises, bright lights, biochemical stimuli (smells, ect) stress, hypoglycemia, medications, alkalosis (hyperventilation) S/S: ● Petit mal (absence seizure): last 5-10 seconds, occur several times a day, brief but LOSS of consciousness (subtle), transient facial mvmts, eyelids twitching, pts is starring or spaced out. ● Grand mal (Tonic-Clonic seizures): spontaneous onset or follows a simple seizure prodromal signs (nausea, irritability, muscle twitching), can sometimes feel it coming, AURA (peculiar visual or auditory experiences), will have LOSS OF consciousness, strong tonic muscle contractions, crying-like noise, Clonic stage of muscle contraction followed by subsiding contractions, brain is burning through a lot of oxygen, postictal stage (post seizures knocked out/ asleep)
Fracture : Definition: A break in the continuity of bone Pathophysiology: ● When bone breaks, bleeding from the blood vessels and periosteum occurs. Bleeding and Inflammation occur in the soft tissue surrounding the fracture. Hematoma formation often occurs. Necrosis may result if the inflammation or hematoma compromise blood supply Healing Process: Affected by fracture type, foreign body, Age, Disease (DM, Anemia) Indirect healing : Hematoma Formation Granulation Tissue: Hematoma serves as supply of fibrin network / granulation Capillary regeneration: new capillaries extend into granular tissue
● *Muscle Spasms inducing pain ● *Tissue Ischemia (hematoma/inflammation) ● *Compartment syndrome: “6 P’s” ● Pain / Pallor / Pulseless / Paresthesia / Paresis / Pressure ● *Fat Embolus (long bone fractures) ● *Nerve Damage (compression / Ischemia) ● *Failure to heal / healing deformities ● *Osteoarthritis or stunted growth
Osteoporosis : Risk factors, etiology, pathophysiology, manifestations and complications -
Definition: A common metabolic bone disorder characterized by decrease in bone density and mass, combined with loss of bone matrix and mineralization (Ca++) ● Bone Density T-Score: 1.5-2 below norm = Osteopenia o >2 below norm = Osteoporosis Etiology: ● Women affected more than often than Men (Small, light bone structure) ● Factor in 1 Million Fractures annually ● Bone Density Testing (DEXA, etc) recommended from age 50+ ● Lack of Calcium intake (especially as child) ● Smoking ● Aging : Decreased osteoblasts with age-- Bone “buildup” peaks at age 30, slows as age 20. Decreased Mobility or sedentary lifestyle (Exercise stimulates osteoblasts) ● Hormonal : Hyperparathyroidism, Cushing Syndrome, Glucocorticoid use ● Estrogen Deficiency: Low exercise / Post-menopausal. Change in RANKL/OPG/RANK System ● RANKL overexpression = Extended osteoclasts life à bone breakdown ● Minerals : Low Calcium or Vitamin D; Excessive Phosphate consumption Pathophysiology: ● Recall: bone remodeling is constant reabsorption (-clasts) and reformation (-blasts) balance ● During bone remodeling, reabsorption (osteoclasts) exceeds bone formation (osteoblasts). Leads to thinning and “hollowing out” of bone, more susceptible to fracture 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 ● *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 ● *Bisphosphonates (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 breast / uterus E)
Osteoarthritis:
Risk factors:
etiology:
pathophysiology:
manifestations and complications:
Rheumatoid arthritis:
etiology:
pathophysiology:
manifestations and complications:
Gout:
etiology:
pathophysiology:
dietary considerations:
NSG 211 Exam 5 Review
Course: Pathophysiology (NSG 211)
University: Marian University
- Discover more from:
