Final part 5 Flashcards
S/S of peritonitis
Increased HR, BP, temp, stiff plap belly,
Labs for pancreatitis acute
Panc enzymes, hypoca+,
Liver, triglycerides, glucose, bilirubin,
Chronic pancreatitis and about the two types
Irreversible structural damage to the pancreas. This includes fibrotic tissue, strictures, and calcification, Scaring, dilation, stones pass.
Obstructive- Gallstones that cause inflam of sphincter or odi-cancer of amp, duodenum, pancreas, or cystic fibrosis,
Non-obstructive- Inflam and sclerosis in head of pancreases and duct, alcohol abuse
manifestations of chronic pancreatitis
Swelling, mass, chronic ab pain, or no pain, mal absorption, weight loss, constipation, DM!, increase in cholesterol, heavy burning not relieves by food or antacids, mild jaundice, dark urine-from bile, Steatorrhea
Gallbladder disease two types and risks
Cholelith-Stones
Cholecys- Inflam of gallbladder usually from cholelith
Balance of chole, bile salts, ca+, and Na+=precipitation
Infections or alterations in metab or chole or stasis
immobility, pregnancy, inflam or obstruction, lesions-all cause obstruction
Manifestatons of choelith
Pain is severe-none, more pain when stone is moving or obstructing, may be in shoulder or scap, tachy, diaphoresis, tender RUQ pain,- 3-6 hours after meal or when laying down
Manifestations of chole sis
fat intol, dyspepsia, heart burn, flatulence, inflam with leuko and fever, ab regidity
Total gal stone obstruction symptoms
Jaundice, dark urine, clay stools, pruritus, intol of fat, bleeding tendencies, steatorrhea
Complications of gal bladder disease
Cholesis, gangrenous, subphrenic abcess, pancreatitis, cholangitis, billiary ducts, fistulas, bil cirrhosis, perionitis, choledocholithiasis.
Tx for cholecycsitis
Pain control, NSAIDS, anticholenergics, antibiotics, choleystestomy, Fluids and electrolytes, NG tube in severe N/V,
Surgical tx for choleitis
Laperascopic cholecystectomy- Removal through holes, minimal post pain, normal activity in 1 week, few complications, clear lq, same day discharge
or open- removal through right subcostal incision
t-tube-Inserted into the common bile duct,
ESWL
esophageal cancer patho history and risks
Usually advanced disease by the time of diagnosis, it narrows the esophagus, Risks-Increase with age, BE, smoking, alcohol, Obestiy, abestos, cement dust, achalasia-delayed emtying, gerd, barrets
Manifestatons of Esoph cancer
Progressive dysphagia-meat, soft food, lq Pain is latep substernal epigastric, back that increases with swallowing-even spit, Weight loss Sore throat, choacking hoarseness\regur with blood tinged Hemmorrhage-if trach May cause obstruction common metastasis to lungs and liver
Diagnosis for esoph cancer
Endoscope biops
ultrasound
CT/MRI
Bronchoscopy
Tx for Esoph cancer
Surg-esophagectomy-removal
esophagastromy -resection to stomach
esophagoenterostomy-resection to colon- lap or open
Photodynamic lasor therapy- no sun 3-6 weeks
Chemo and radiation
Post of esoph cancer
Watch respiratory, pain control, Chest tube, TPN, Swallow study, HOB 30 and for 2hr after meal
Surg risk for esoph cancer
DysR, anastomatic leaks, fistulas, edema, respiratory distres, dysruption of medial sternal lymph nodes
Care for E cancer
Airway, respiratory, swallow B4 oral fluids, high fowlers, tube feeding tol, pain
Lower GI obstruction types
Mechanical- Detectable, commonly found in sm intestine, surgical adhesion-small intest and colorectal cancer-Large intest
non mechanical- Paralytic illeus, pseudo- acting like theres an obstruction- critically ill, trauma, burns. vascular- no blood to intestines- a fib, art obstruction, clots, heart valve issues, heart attack, congestive fail
Types of lower gi obstruction
Adhesions, intessuseption, hernwas, tumors, volvus,
Steps of lower obs
1.obstruction- build up fluid, gas, intestial contents-prox
Collapse- distal
2. Increase in bowel distension- reabsorption of fluids
3. increase pressure- cap perm, fluids into 3rd space
4. loss of blood volume
5, ischemic bowel no blood supply
Sm in lower GI
Rapid onset
Early- Colckly, intermit ab pain, NV in large ammounts, projectile vom with bile, if long standing smells like poop
Lg in obstruction s/s
Gradual onset, vom it rare, ab pain present but low grade, ab distention increased new onset of constipation and no flatulus
diagnosis of bowel obstruction
Labs
x ray-ct scan
Sigmoidoscopy/colonoscopy
Increase in WBC, H and H, BUN and creatinine
Tx for lower GI obstruction
When do you need surgery
conservative, NPO, rest, NG tube, IV fluids-NS or lac ringers, Pain control
if strangulated or tx not effective, May need colonosctomy or illiostomy
What are the biggest concerns with Lrg bowel obstructions
Ischemia, peritinitous, sepsis
CFS contents
Stroke: 1 (make sure you know the screening indicators for tPA use
d to produce localized fibrinolysis by binding to the fibrin in the thrombi
● Given IV to prevent cell death with ischemic stroke
● Tissue plasminogen activator (tPA)- Reestablish blood flow, given within 3 to 4.5 hours of onset of clinical signs of ischemic stroke –pts screened carefully
● Patient screening includes: noncontrast CT scan or MRI to rule out hemorrhagic stroke, blood tests for coagulation disorders, GI bleeding, storke, head trauma within the past 3 months, major surgery within 14 days, internal bleeding within 22 days
● Monitor patients VS and neuro status, control BP SBP <185
Spinal Shock: 30-60 min after injury
Spinal Shock: 30-60 min after injury
● Loss of sensation, decreased reflexes, absent thermoreg, or flaccid paralysis below injury level
● Days to weeks after injury
Neurogen shock
Neurogenic Shock (injury above T-6)
● Loss of SNS innervation/tone (cervical or high thoracic injury)
● Peripheral vasodilation = venous pooling, low CO
● Give fluids, vasopressors
● Respiratory: hypoventilation, C4= loss of resp fctn
● Cardiovascular: bradycardia
● hypotension- (Neurogenic shock)
● Urinary: neurogenic bladder-atonic bladder initially
● Gastrointestinal: hypomotility
● Temperature: unable to regulate-lack of SNS/nerve disruption to hypothalamus
● Integumentary: pressure ulcers/skin breakdown
Autonomic Hyperreflexia (Injury T6 or higher)
● Uncompensated cardiovascular response from SNS
● Triggered by stimuli at or below T6-
● Blood vessels constrict
● S/S= HTN, HA, bradycardia, diaphoresis-above level of injury
● piloerection- below level of injury
● PNS responds to B/P- reduces HR but can’t dilate peripheral vessels below level of injury
● Causes: most common-bladder distention, bowel impaction, tight clothes, pressure ulcers, pain
Treatment of Autonomic Hyperreflexia
● Sit patient upright or elevate HOB 45 degrees
● Identify the cause of stimuli
o Insert catheter/look for kink
o Resolve bowel impaction
o Remove restrictive clothing
● Notify healthcare provider
● Monitor B/P & give B/P meds (vasodilators) if s/s continue
● If left untreated= possible stroke, MI, status epilepticus
c4, c6, t6, L1
c4-Tetra and paralysis of respiratory, C6-tetra with pa in hands and arms, T6 para below chest, L1-Para below waist
