Unit 1 Fluid Status and Lab Values PDF

**[Unit 1 fluid status and lab values]** Fluid regulation: - Hypothalamus: feeling of thirst, vasoconstriction, vasodilation - Endocrine: adrenocorticotropic hormone (ALDO), antidiuretic hormone (pituitary gland, holds onto fluid to prevent dehydration) - Renal: renin angiotensin aldos...

**[Unit 1 fluid status and lab values]** Fluid regulation: - Hypothalamus: feeling of thirst, vasoconstriction, vasodilation - Endocrine: adrenocorticotropic hormone (ALDO), antidiuretic hormone (pituitary gland, holds onto fluid to prevent dehydration) - Renal: renin angiotensin aldosterone (vasocontraction/dilation, Na retention/excretion, maintain BP) Starlings' hypothesis states that the fluid movement due to filtration across the wall of a capillary is dependent on the balance between the hydrostatic pressure gradient and the oncotic pressure gradient across the capillary Fluid spacing: - 1^st^ spacing body fluids are normally distributed in the ICF and ECF compartments - 2^nd^ spacing accumulation of interstitial fluid, edema - 3^rd^ spacing accumulation of fluid between serosal membranes, ascites, effusions, peritoneal fluid Albumin: (protein made in liver) (takes fluid from second space into cell) - Plasma protein, increase vascular volume by increase colloidal/oncotic pressure Hypertonic: pulls water from the cell (shrinks) Isotonic: no effect on the cell (maintenance) Hypotonic: water moves into cell (fills up) IV fluids: - Maintenance (NPO for test, nausea) - Replacement (trauma, disease, emesis, diarrhea, lyte imbalance) - Colloids: large molecules (proteins) don't pass through semi permeable membrane, remain in intravascular compartment, oncotic pressure pulls fluid in - Crystalloid: small molecules that pass through semi permeable membrane, electrolyte (Na, K) and non-electrotype (dextrose) Assess: - Ins and outs, vital signs, increase thirst, fatigue, headache, dizziness, decreased urine output, nausea, muscle cramps (these could indicate dehydration) **Dehydration:** - Causes: too much in or too little out, cells cannot function, body response by pulling needed fluid from the periphery Assess: vital signs (temp, pulse, resp, BP, O2, pain), inspect (dry mouth, dry skin, dark urine, sunken eyes, skin breakdown), palpation (weak thready pulse, delayed turgor, ABD pain), percussion (abdomen), auscultation (decreased bowel sounds) Do: blood work, urine test Lab values: hematocrit would be high if pt was dehydrated, also watch hematocrit Orders: - Vital signs (base line), IV bolus (circulation, treatment ASAP), lab work, foley catheter (ins and outs), urinalysis (infection), fluid balance sheet ( ins and outs), IV hour;y rate (so not putting pt in to fluid overload), pt must have 30mL output per hour **Fluid overload** - Too much in and not enough out (puts them at risk for skin breakdown and delayed healing) Assess: - headache, increased urine output, SOB, palpations, weight gain, edema - Vital signs (temp, pulse, RR, BP, O2, pain), inspection (JVD, cough, edema, skin breakdown), palpation (edema, rapid bounding pulse, pedal pulses), auscultation (resp crackles) Prioritize: furosemide 20mg IV x1, vital signs, hematology/chemistry, insert catheter, CXR, non-K sparing diuretic CNS: LOC, relief of headache, temperature CVS/PVS: BP, PR, peripheral pulses plus 2 Resp: resps and WOB GI: no abdominal pain, bowel sounds, stool. GU: urine output, urine colour, urine specific gravity Integ: colour, skin hydrated, skin turgor, MSKTL: no muscle cramps **Lab values:** Urinalysis: source is either midstream or catheter. Type: random, 24-hour collection (no bacteria to form). Urine C & S, culture: what's growing, sensitivity: antibiotics 24-hour urine: (6-6) - Urine urea and creatinine, low urea high in blood kidneys aren't working (serum is high) (dehydrated, acute renal injury) \*Functions of the blood: \* - Transportation: oxygen, nutrients, hormones, metabolic waste (CO2, ammonia, urea) - Regulation: fluid balance, electrolyte balance, body temperature - Protection: fight infection, prevent recurrent infection, coagulation - Blood: plasma, RBC, WBC, platelets A table with text and numbers Description automatically generated Neutrophils: these are high in bacterial infections Lymphocytes: high in viral infections Monocytes: phagocytosis, germs, viruses, bacteria, fungi, protozoa Eosinophils: high in parasitic infection Basophils: fights parasites, fungi, cancer cells Coagulation: - We want blood to clot when there is a lot of blood (hemophelia) and we do not want blood to clot when DVT/PE - APTT and INR are the main tests to assess blood clotting - Platelets: stick together to make clots, aspirin makes them slippery to prevent clots. Indications for platelets is thrombocytopenia and bleeding prophylaxis, bleeding with platelet dysfunction, massive transfusion protocol. Clotting cascade: vascular response, platelet plug, fibrin clot, clot dissolution MCV: mean corpuscular volume, measure of average size of a single RBC, used to classify types of anemia **Anemia:** - Normocytic (normal size): acute blood loss, chronic blood loss, renal disease, anemia of chronic disease, body cannot make enough iron due to chronic demand and inflammation. females (episodic) - Microcytic (small): iron deficiency - Macrocytic (to big): megaloblastic, vitamin B12/folate deficiency, alcoholism, hypothyroidism, error in bone marrow production, COPD, erythropoietin administration, more O2 Problem of destruction: (cells aren't the right shape) - Intrinsic: Abnormal shape (sickle cell), G6PD enzyme (common in men), membrane lysis (vasculitis) - Extrinsic: trauma, antibodies/autoimmune, infections/toxins Sickle cell anemia: chromosome abnormality, RBC are different shape, which means they do not flow properly, the off-shape ones stick together in joints, and this is very painful, not enough oxygen getting past the clot. Pain is main symptom Symptoms of Anemia - Fatigue, fainting, yellowing eyes, SOB, chest pain, angina, spleen enlargement, weakness - SOB is common because increased RR, low hemoglobin means less oxygen transported Do: - Hematology (RBC, WBC, HBg), diet, iron supplements, not very common to get meds for this but sometimes B12 Anemia can seem like normal lie, is common as people age because body slows down, people with renal failure are at risk of anemia because kidneys help make erythropoietin. **Electrolytes:** element when dissolved in water, dissociates inti ions and conducts an electric current *Sodium (Na, 135-145):* function is to maintain water balance, Na follows water, if pt blood pressure is high go on low sodium diet, helps with transmission of nerves impulses, and acid base balance. Regulated by the renal system and ADH, too much salt can cause hypertension and not enough urine. - Hypernatremia: lots of Na. fatigue, agitation, coma, seizures, weigh gain, hypertension, edema, weakness - Hyponatremia: lose Na. GI loss (vomiting/diarrhea), renal loss, resp complications, burns, high output wounds, headache, irritability, confusion, coma. Losing volume causing pt to lose salt *Potassium (K, 3.5-5):* muscle contractions, conduct nerve impulses, promote cellular growth and maintain normal cardiac rhythm, regulated by the renal system (void). It pt has high potassium insulin dextrose is the cure. - Hyperkalemia: increased intake, impaired renal function, metabolic acidosis. Assessments: weak skeletal muscle and leg cramping, ECG, fast/irregular pulse. - Hypokalemia: lose too much fluid, loss of Na intake. Assessments muscle weakness, fatigue, legs cramping, nausea and vomiting\*\*, slow weak pulse Hyperkalemia treatment: - This is a medical emergency because it can cause deadly cardiac arrythmias. - Need to move K from the serum into the cell from the ECF to ICF. Cardiac monitoring, Humulin R IV not subq because it does not act fast enough, dextrose because insulin drops BP and keeps glucose up, IV furosemide to pee out the K, PO/PR kayexalate to absorb the K, Ventolin neb will shift the Kt and so will IV calcium gluconate Hypokalemia treatment: - IV treatment is high alert. IV replacement is 10 mmol/L gradually, NEVER push K because if is given to fast can cause the heart to race and body won't be able to respond. PO replacement (oral K) People with diabetes who require large doses of insulin are at risk of hypokalemia because insulin draws K into the cell which means serum K will be low. You always measure K out of cell. *Chloride (CL, 96-106):* helps maintain acid base balance, regulates by following Na and K *Urea (3.6-7.1):* BUN/ blood urea nitrogen. Measures the amount of urea nitrogen in the blood, indicates how well kidneys are filtering and excreting waste, byproduct of protein metabolism, formed in liver, helps identify fluid status, low in alcoholic cirrhosis as liver cannot convert ammonia to urea, regulated by the renal system *Creatinine (53-106 males, 44-97 females):* waste product of muscle metabolism, regulated by the kidneys, muscle contraction and is used to diagnose kidney failure. Excreted in urine. - High creatinine in pyelonephritis (kidney infection), diabetic neuropathy, rhabdomyolysis (trauma, RBC damaged go through and plug up kidneys, cant flush out anything), severe dehydration, renal failure - Low creatinine in decreased muscle mass, inadequate protein intake *Calcium (Ca, total 2.25-2.75, ionized 1.05-1.3):* development of healthy teeth and bones, transmission of nerve impulses, cardiac contraction, blood clotting, large muscle contraction, vitamin D makes it active form (so body can use it). For high and low Ca the symptoms are the same, if phosphate is low then calcium is high. If someone's phosphate is high give them Ca. body will only use what they need and pee out the rest, Serum calcium is low body will take it from bones which means bones loose density and are more likely to get fractures. As calcium increases phosphorus decreases, ionized calcium is the active form and vitamin D and calcitriol make it the active form. Excess Ca is not stored. - Hypercalcemia: to much. Hyperparathyroidism cancers invade bone and calcium leeches out. Assessments: impaired memory, confusion, fatigue, muscle weakness, constipation, abnormal heart rhythm, renal calculi - Hypocalcaemia: to little. Parathyroid went on a holiday, acute pancreatitis, blood transfusions, diet/absorption, vitamin D deficiency. Assessments: ECG changes (dangerous), hyperreflexia, tetany(dangerous), muscle cramps, fatigue, numbness in fingers, toes and lips - Tetany: test this to test for hypocalcaemia, Chvostek's: tap on cheek bone, trousseau's (flex hand forward), and when taking BP see if there is cramping when it inflates Hypocalcaemia treatment - Diet, raw milk, yogurt, kale, cheese, sardines, watercress, almonds, bok choy, okra, broccoli *Magnesium (Mg, 0.74-1.07):* carbohydrate metabolism, protein synthesis, help control serum glucose and blood pressure, muscle contraction and relaxation, Mg is regulated by GI tract and kidneys - Hypermagnesemia: too much. Renal failure, prenatal treatment of preeclampsia, assessments: nerve and muscle function, hypotension, urinary retention, fatigue, facial flushing, can progress to muscle paralysis, coma, resp muscle failure and cardiac arrest - Hypomagnesemia: to little. GI loss (vomiting, diarrhea, NG loss), renal loss, chronic alcoholism, prolonged malnutrition, serum glucose over 10 mmol. Assessments: can mimic hypocalcaemia, cardiac, neuromuscular, confusion and seizures - Magnesium IV replacement is high alert med, PO isn't high alert. If administered to fast can cause hypotension, cardiac arrest and respiratory arrest. Magnesium has been shown to aid recovery from depression, improve premenstrual syndrome, reduce hyperactivity in kids with ADHD, adjunct treatment for patients with schizophrenia *Phosphate (PO4, 0.97-1.45):* helps control function of the muscle, RBCs and nervous system, deposited with calcium, needs healthy renal system and as phosphate rises calcium decreases - Hyperphosphatemia: too much. Renal failure, chemotherapy, large doses of vitamin D, do same assessments as hypocalcaemia because calcium and phosphate are opposite in values - Hypophosphatemia: too little. Malnourishment, malabsorption syndrome, TPN, alcohol withdrawal, post DKA. Assessments: altered CNS, muscle weakness, increased WOB\< cardiac dysrhythmias and rhabdomyolysis *Glucose (fasting 4.6, non-fasting 3.6-10):* glucose provides energy for the cells, regulated by the liver, kidneys and pancreas. - Hyperglycemia: too much. Caused by too much food, too little insulin, illness and stress (release cortisol), steroid use. Assessments, thirst (polydipsia), frequent urination (polyuria), loss of appetite or polyphagia, fatigue, confusion, drowsiness, flushed dry skin, fruit like breath odour, rapid deep breathing, nausea, vomiting, abdominal cramping, increased temp. Hot and dry sugar high - Hypoglycemia: too little. Too little food, too much insulin or oral diabetic medication, extra exercise. Assessments: shaky/light-headed, nausea, nervous, irritable, confused, unable to concentrate, hungry, tachycardia, diaphoretic, headaches, weak, numbness, tingling in tongue or lips, child, cold sweats, very low levels they will be confused, disoriented, loss of consciousness, seizures and comas. Cool and clammy need some candy Arterial blood gases: measures CO2, O2, H+, HCO3, ability of body to balance moving O2 into and CO2 out of the blood. Measures how much O2 using and how much CO2 giving up **[Unit 2 Cardiovascular ]** Blood pressure: - SBS: systolic pressure is the peak arterial pressure that occurs during ventricular contraction, full ventricle and full atrium - DBP: diastolic pressure is the minimal aortic pressure just before ventricle ejects blood during relaxation. Resting/filling pressure don't want it to rest to zero. - Low blood pressure means no filling/pushing which me no O2 which causes no sending/pumping anything - Cardiac output: ability to perfuse, pushing forward. Heart rate times stroke volume. You can assess this by dizziness, cap refill, skin colour, peripheral pulses, making good urine. - SVR: systemic vascular resistance, force opposing blood moving within a vessel, stress, plaque and saturated fat can increase resistance, anxiety, shock, sleep and viscosity can decrease resistance **Hypertension:** continues to increase \>20%. Sustained/constantly elevated SBP of \>140 or a combined 140/90 mmHg, lower for patients with diabetes 130/80, because 130 for diabetic because thick viscous blood. There is a lot of forced on the contraction, has to work really hard and use more oxygen making the person tired, and during diastole I the body cannot relax enough it can't fill up properly causing edema, SOB. White coat HTN is a stress response. Primary: too much salt intake, water follows sodium, hang on to much volume, can cause water retention, stress can cause HTN because of the fight or flight response, insulin resistance increases blood sugar (which increases BP), obesity: a lot of volume to perfuse, body working a lot harder Stages of HTN: - Stage 1: 140-159/90-99 - Stage 2: SBP\>= 160, DBP \>= 100 - Isolated HTN: SBP \>140, DBP\ - Generally, more destructive than ischemic strokes - Between 35-53% die within the first month and most of these deaths are within the first two days - 1/5 people suffering from this will be functionally independent six months after the stroke Intracerebral Bleed (10%) - Ruptured vessels - Bleed into brain tissue - Cause: HTN, AV malformations, thrombolystic/ coagulation therapy - Signs and symptoms: sudden onset, severe headache, neuro deficits, nausea, vomiting, increased ICP, hypertensive, decreased LOC in half of pateints - HTN is the most important risk factor. 5 to 6% risk with rTPA. But if SICH (Spontaneous Intracerebral Hemorrhage) occurs the risk of death is ≥ 50%. Arteriole- venule. Increased pressure in the venule because of capillary bypass. Often occurs during activity. Sudden onset with progression of symptoms as bleed progresses. Signs and symptoms will depend on the area of the brain affected- Pons vs Cerebellum, subthalami, the extent of the bleed Subarachnoid bleed - Bleed into subarachnoid space - Cause: ruptured aneurysm - Signs and symptoms: worst headache of my life, decreased LOC, nuchal rigidity Aneurysm repair - Surgical (clip or banding) - Endovascular (angioplasty/stent), coil - 35% of people who have a hemorrhagic stroke due to a ruptured aneurysm die during the first episode. Fifteen percent die from subsequent bleeding. Approximately 20% of clients will have multiple aneurysms. Treatment of an aneurysm involves clipping, wrapping, or coiling the aneurysm to prevent rebleeding. A frequent surgical procedure used to prevent rebleeding is clipping of the aneurysm (Fig. 59-6). Endovascular techniques may also be used. In the procedure known as *coiling,* a metal coil can be inserted into the lumen of the aneurysm via interventional neuroradiology (Fig. 59-7). Guglielmi detachable coils (GDCs) provide immediate protection against hemorrhage by reducing the blood pulsations within the aneurysm. Eventually, a thrombus forms within the aneurysm, and the aneurysm becomes sealed off from the parent vessel by the formation of an endothelialized layer of connective tissue. GDCs provide an alternative therapy to traditional surgical clipping of aneurysms. Cerebral vasospasm: narrowing of the large blood vessels at the base of the brain, at risk 7-10 days post SAH, lysis of SA clot = release of metabolites, interaction of metabolites within the vessel = endothelial damage = vasospasm - At risk of post SAH bleed due to vasospasm (7-10 days post SAH) = rebleed or infact Cerebral vasospasm is most likely due to an interaction between the metabolites of blood and the vascular smooth muscle. During the lysis of subarachnoid blood clots, metabolites are released. These metabolites can cause endothelial damage and vasoconstriction. In addition, release of endothelin (a potent vasoconstrictor) may play a major role in the induction of cerebral vasospasm after subarachnoid hemorrhage - ENDOTHELIIN- 21 AA which are usually released in a balancing act of blood pressure -- Increase release with SAH Clinical manifestation of a stroke - Motor function - Communication - Affect - Intellectual function - Spatial perceptual alterations - Elimination - Do not differ based on type of stroke. More so where the stroke happened- what tissue is affected = what clinical manifestations. Motor Function: mobility, resp function, swallow and speech, gag reflect, self-care. Skilled voluntary movement, integration of movement, muscle tone and reflexes. Contralateral- pyramidal pathway crosses at the level of the medulla. Facial features ipsilateral. Communication: Left hemisphere dominant for speech. Comprehension, ability to speak maybe both (aphasia) motor control of speech. Affect: control emotions, exaggerate, unpredictable, depression, body image. Intellectual function: memory and judgement- too quickly , over analyze, language , interfere with ability to learn. Spatial-Perceptual Alterations: R sided most likely. May or may not be aware of it. Elim- most of the time- temporary -- most common issue Constipation due to dehydration, lack of bowel tone. Contralateral vs ipsilateral (NEGLECT) A homonymous hemianopsia is the loss of half of the field of view on the same side in both eyes.  It occurs frequently in stroke and traumatic brain injuries due to the connections and wiring of the visual system with the brain. The visual images that we see to the right side travel from both eyes to the left side of the brain, while the visual images we see to the left side in each eye travels to the right side of the brain. Therefore, damage to the right side of the posterior portion of the brain can cause a loss of the left field of view in both eyes. Likewise, damage to the left posterior brain can cause a loss of the right field of vision. (Hom-on-ee-mous Hem-ee-opsia) Nursing management: acute(12-72 hours) vs rehab - ABC, BP, fluid and electrolytes, temperature, seizures Example: cast study on slide A- altered LOC, Airway, Aspiration risk- intubation? Artificial airway? Prevent tongue from falling to back of the throat. How long? Consider trach? B: Resp distress- o2?- Respiratory muscle strength can decrease after a stroke: Brain stem injury?? C: brady, tachy, irreg? ECG? Cardiac Monitor? HTN? Seizure? Meds? What do you want to know? Onset? HA, visual disturbance, FAST, Comorb? HTN, HF, AF Bloodwork, IV access, Treat BP- be careful, Anticipate CT Post stroke- Pt at risk of DVT, esp in affected side. Contralateral hemiparesis (worse in the arm and face than in the leg), dysarthria, hemianesthesia, contralateral homonymous hemianopia, aphasia (if the dominant hemisphere is affected) or Aphasia- production (cerebral) or understanding of speech (Temporal)- anomic -- word retrival failures. Neuro- manage stroke deficits as a collaborative team Cardio- DVT proph, manage any co-morbidities, fluid balance MSK- maintain optimal function- prevent joint contractures- Passive ROM exercises, Prevent dependent edema, hemiplegic shoulder (2-3 weeks -- couple months) INTEG- Skin breakdown- Braden scale assess risk GI- Swallow assessment- (Decreased LOC, decreased gag reflex and impaired swallow are assessed) NPO until this has been done. Incontinence constipation GU- Incontinence **[Week 8 GI]** **Gastro esophageal reflux disease**- GERD - Syndrome - Most prevalent acid related disorder - No single cause - Risk factors: incompetent lower esophageal sphincter, impaired esophageal motility, decreased gastric emptying Assess: pyrosis (heartburn, especially while laying flat), severe inflammation: discomfort after each meal, lasts for up to 2 hours, coughing, hoarseness, or wheezing at night, regurgitation, dysphagia, odynophagia (painful swallowing). Eructation (belching), flatulence or bloating after eating - GI assessment - Barium swallow - Upper GI endoscopy (biopsy) Do: HOBE \30 degrees (sleep, 30 min post meals), medications (antacids, proton pump inhibitors(pantoloc), histamine 2 receptors (Pepcid), prokinetics (metoclopramide, can have side effects)). Surgery (fundoplication) Teach: lifestyle, diet, low fat to increase emptying, low caffeine, know irritants, low dairy, small frequent meals decrease distention, low acid goods, smoking, stress, weight loss, medications Complications: gastric acid sits on esophageal mucosa, repeat exposure = fibrosis and scarring = esophageal stricture. Hiatus hernia (usually no symptoms), esophagitis, barrettes esophagus, respiratory symptoms Barrett's esophagus - In GERD, stomach contents wash back into the esophagus, damaging esophagus tissue - As the esophagus tries to heal itself, the cells can change to the type of cells found in Barrett's esophagus - Increase risk of cancer **Peptic ulcer disease:** - Erosion of the GI mucosa resulting from the digestive action of HCI and pepsin - GI tract comes in contact with gastric secretions (lower esophagus, stomach, duodenum, post-surgical sites) Types: acute, chronic (based on mucosal involvement), gastric and duodenal Gastric ulcer: normal- low secretions of gastric acid, H. Pylori presents in 60-80% (may be enhanced by smoking), more common on lesser curvature, more common in women and older adults, drug induced and pain after eating Duodenal ulcer: associated with high HCL secretions, 80% of all peptic ulcers, H.pylori present in 80-85 percent, men and post-menopausal women, drug induced, COPD, cirrhosis, pancreatitis, hyperparathyroidism, smoking/drug/alcohol use Pathophysiology of peptic ulcers - Acidic environment, auto-digestion, HCI released, tissue injury results, histamine released, increased acid and pepsin release, increases permeability, prostaglandin suppression - Caused by H. Pylori, (ASA, NSAIDS, steroids and stress) Assess: - May have no symptoms - Pain assessment (burning, cramp like, midepigastric, empty stomach or post, backpain) - Bleeding - Medication relief - GI assessment (mouth and ABD) - Lab values (hematology, lytes, antibody (IgG), liver enzymes, stool OB) - H.pylori Do: - Urine, blood, breath, tissue biopsy (endoscopy), treat with Abx (amoxicillin) - Meds (pain control anti-ulcer enteric coated antibiotics) - Surgery (vagotomy) Teach: - Rest - Bland diet - Stress management - Recognize symptoms of exacerbation/perforation - Medication compliance: H2 blockers, PPI, antibiotics, antacids, cyto-protective Complications: - Acute exacerbation (bleeding, pain, nausea, vomiting) - Retreatment, blood products, endoscopy - Perforation (peritonitis), NG tube, LCSn, gastric decompression, IV fluids, blood products - Gastric outlet obstruction (NG tube, LCSn, gastric decompression, IV fluids, electrolyte replacement) Post-Op Complications - Dumping syndrome (vagal effects, weakness/dizziness post meals, frequent stools, lack of nutritional absorption) - Post prandial hypoglycemia (bolus carbs, hyperglycemia, insulin release, hypoglycemia) - Bile reflux (alkaline reflux) **Ulcerative Colitis and Crohn's** - Inflammatory bowel disease - Autoimmune (ulcerative colitis, Crohn's disease) - Idiopathic inflammation - Ulceration - 10,000 new cases / year - Varied symptoms - Unpredictable remissions - Acute exacerbations (inflammation) Caused by: - Environmental (industrialized world), genetics (white, Jewish, Scandinavian, 1^st^ degree family, twins) - Male - Autoimmunity - Age (teens and early adulthood), second spike (age 50-70 years) Colitis: limited to the surface lining of the colon Crohn's: inflammation extends into the bowel muscle wall, can affect any part of the digestive tract Ulcerative colitis: - Inflammation and ulceration of the rectum and the colon, starts in the rectum and moves in a continual fashion toward the cecum. Mucosa and submucosa Patho: - Inflammation, abscess formation, abscess erodes into submucosa, ulcers form - Cause: bleeding, diarrhea, lose surface area for absorption (loss of fluid and lytes) - Pseudo-polyps form (shorten colon) Assess: - \# and characteristics of diarrhea, presence of blood, pain (cramping), fever, fatigue, anorexia, weight loss, S/S of dehydration and electrolyte imbalance - 60 second assessment (circulation/pain) - Vital signs (fever/tachycardia) - ABD assessment - MSKTL: peripheral arthritis, ankylosing spondylitis, sacroiliitis, osteoporosis, finger clubbing - Integ: erythema, pyoderma gangrenosum - Mouth: aphthous ulcers (stomatitis) - Ophthalmological: conjunctivitis, uveitis, episcleritis - Hepatobiliary: gallstones, primary sclerosing cholangitis, portal vein thrombosis - GU: kidney stones Lab values: low RBC, low hemoglobin, low hematocrit, low Na, low K, low CL, low magnesium, high CRP, high ESR, low albumin Inflammatory markers: CRP: c reactive protein, made by liver, increases with inflammatory diseases. Normal is less then 10 mm/L ESR: erythrocyte sedimentation rate, rate the RBC's settle in 1-hour, non-specific increases with inflammation. (female normal: \ - Partial or complete - Mechanical or non-mechanical - Metabolic process creates gas, distention, increased ABD pressure, impaired blood supply, fluid in peritoneal cavity, loss of circulating volume Intestinal obstruction Patho: - Increased fluid, gas and intestinal content - Increased distention distal bowel may collapse - Decreased absorption of fluids stimulates intestinal secretions - Increased pressure of lumen - Increased capillary permeability to perineum = edema, hypovolemia, necrosis Mechanical: adhesions, tumor, volvulus, diverticulitis Non mechanical: paralytic ileus, peritonitis, inflammatory, spinal \# A: adhesions B: inguinal hernia C: intussusception D: polyps E: mesenteric occlusion F: neoplasm G: volvulus Clinical Manifestation: Small intestine- onset (rapid), vomiting (frequent and copious), pain (colicky, camplike, intermittent), bowel movement (feces for short time), abdominal distention (dependent upon location of obstruction, minimal to greatly increased) Large intestine- onset (gradual), vomiting (late manifestation), pain (low grade, cramping abdominal pain), bowel movement (absolute constipation), abdominal distention (greatly increased) DO: fluids, NPO, how to decompress the abdomen, non-ostomy, ostomy  **[Week 9 MSKL]** **Total Knee Replacement (TKA)**\ - who needs this: Rheumatoid arthritis (chronic systemic, autoimmune disorder), Osteoarthritis (chronic, articular, degenerative) Assess: - Post op (ABS\< O2, IV, foley) - Dressings - Palpate pulses, system assessment, pain assessment and dermatomes Do: - For pain: ice, positioning - Epidural, PCA, IV, PO - PCA pump (SR vs IR, addiction vs pain control) Prevent DVT/PE - Assess: risk, INR/PTT/platelets, lung sounds, surgical site, vital signs - Do: early ambulation, prophylactic anticoagulant (rivaroxaban), pneumatic stockings, PCD's - Teach: mobility, fluid, signs and symptoms Prevent Infection - Assess: dressing, wound, surrounding tissue, infected wound (osteomyelitis) - Do: best practice prevention of surgical site infection (SSI), sterile technique, on time antibiotics - Teach: keep it dry and clean, signs and symptoms, when to report and increase of pain Increase mobility - Assess: pain, knowledge, limitations, tolerance, safety - Do: collaborate with PT, reinforce use walker - Teach: reinforce PT teaching, discharge planning to pt and family Prevent pressure ulcers - Assess: head to toe, risk assessment (Braden scale) - Do: position changes, nutrition, pain management, pressure relief devices, mobility and fluids - Teach: mobility, position changing and pain management **Arthritis:** - Joint inflammation Osteoarthritis: most common type in Canada, destruction of the synovial joint, progression is slow, no inflammation present, cartilage destruction, not a normal finding with aging, repetitive stress on weight bearing joints Etiology and Patho: direct damage to cartilage or joint instability, been linked to estrogen reduction, genetic factors and obesity Non modifiable risks: age, female Modifiable: obesity, sedentary exercise level, previous ligament damage, occupation, walking, standing, kneeling, repetitive strain Symptoms: decreased ROM, crepitus, change in joint shape, asymmetrical Initial pain: decrease with rest, increase with joint use, described as a deep ache Progressive pain: pain at rest or with activity, sleep loss, loss of function, referred pain Clinical manifestations: Systemic- fatigue, fever, and organ involvement not characteristics of OA Joints- range from mild discomfort to significant disability, localized pain and stiffness, crepitation Deformity- specific to joint involved, can appear as early as 40 years old Most common joints: cervical vertebrae, hip, proximal interphalangeal, knee, metasorphalengeal, lower lumbar vertebrae, carpometacarpal, distal interphalangeal Assess: - Pain - Mobility limitations - Stiffness - Timing - Weakness - Deformity - Issues with ADL - ADL aids - Past medical History - Previous injury - Previous MSKTL surgery - Medications - Work and leisure activities Inspect: - Muscle and joint size - Swelling - Redness - Asymmetry - Masses - Deformity - Limb length - Contracture - Spinal curvature - Expect symmetry and continuity Palpate: - Skin temperature - Muscle - Joint capsule Note - Heat - Tenderness - Swelling - Masses - Fluid - Support joints being examined -- need to be relaxed - Compare L and R - Age related ROM: passive, active, normal, limited, contractures, pain, crepitation, stabilize joint being assessed, support related joint Muscle strength: test each muscle group, push/pull, resistance, assess bilaterally, age related and disease related may see different atrophy Do: - X-ray, bone scan, CT, MRI, radiography, synovial fluid assessment (yellow, no indication of inflammation), lab values (ESR usually normal, ESR increases acutely) - Inflammatory markers: C-reactive protein, made by liver, increases with inflammatory disease. Erythrocyte sedimentation rate, rate the RBC's settle in 1-hour, non-specific increase with inflammation - Rest, joint protection, assistive devices, heat/cold, exercise, nutrition - Drug therapy: acetaminophen, narcotic analgesia, ASA, HRT, NSAODS (ibuprofen, Celebrex), voltaren, intra-articular injections (corticosteroids), antibiotics - Surgery- reconstructive arthroscopic Teach: - Pain control, physical mobility, ADL, reduce hazards, reduce repetitive strain, weight loss, assistive devices, meds, TLR, nutrition, goals, Rheumatoid arthritis - Chronic, systemic autoimmune disease, inflammation of connective tissue, affects synovial joints, exacerbation/remission, usually develops between ages 25-50, more common in women - Not infective, genetically susceptible person has immune response to an antigen causing inflammatory response - Non modifiable risks: genetics, environment Signs and symptoms - Affects joints symmetrically (on both sides equally), most frequent attacks are in wrists, hands, shoulders, knees, and ankles - Rheumatoid nodules: appear under skin, firm, non-tender, granuloma type masses, usually on joints of fingers and elbows, persistent, infection, complications Assess: joint involvement, serology, acute phase reactants (CRP, ESR, RF), duration of symptoms - Pain - Mobility limitations - Stiffness - Timing - Weakness - Deformity - Pain - Issues with ADL aids Inspect: expect symmetry and continuity - Muscle and joint size - Swelling - Redness - Asymmetry - Masses - Deformity - Limb length - Contracture - Spinal curvature Palpate: - Skin temperature - Muscle - Joint capsule - Heat - Tenderness - Swelling - Masses - Fluid *Ulnar drift deformity swan neck deformity* ulnar drift.jpg *Boutonniere deformity hallux valgus deformity*  Do: - Positive rheumatoid factor, C-reactive protein, ESR, synovial fluid analysis, x-ray, Rheumatoid factors are proteins produced by your immune system that can attack healthy tissue in your body. High levels of rheumatoid factor in the blood are most often associated with autoimmune diseases, such as rheumatoid arthritis - ESR: Useful when evaluating some types of arthritis, Help confirm a diagnosis of certain conditions, including Giant cell arteritis, Polymyalgia rheumatic, Rheumatoid arthritis. A sed rate test can also help determine the severity of your inflammatory response and monitor the effect of treatment. - CRP: The level of C-reactive protein (CRP), which can be measured in your blood, increases when there\'s inflammation in the body. - Meds: NSAIDS, disease modifying antirheumatics (DMARDS), corticosteroids, biological agents - Surgical interventions: arthroplasty- Complete replacement or reconstruction of joint, most common causes for procedure = RA, OA, Minimally invasive surgery, Implants are cemented in place, May require revisions after several years **Osteoporosis** - Chronic progressive metabolic bone disorder, low bone mass (osteopenia), structural deterioration of bone tissue bone fragility, primary versus secondary causes, most common in hips, spine and wrists, more common in women - Nutrition - Heredity - Decreased: calcium - Deficient: estrogen - Limited: exercise - Alcoholism - Malnutrition - Smoking - Caffeine intake - Gender - Hormones Risk meds: - Steroids, chemotherapy, anti-seizure meds, some antacids, thyroid hormones Risk comorbidities: - Inflammatory diseases (bowel and joints), renal disease, hyperthyroidism, alcoholism, liver cirrhosis, diabetes Signs and symptoms: - no initial symptoms, kyphosis, pain due to collapsed vertebrae, loss in height, stress fractures  Do: bone mineral density (BMD), dual energy X-ray absorptiometry, serum calcium, phosphorus, ALP elevation Teach: fall prevention, weight bearing exercise, nutrition, vitamin D, medications, HRT, calcitonin, Fosamax **[Week 10 Perioperative ]** Pre-operative nursing management: confirm identity, establish pre-op baseline, patient assessment, bloodwork, diagnostics, checklist, pre-op bath, IV, teaching, psychosocial Preoperative anxiety: fear of unknown, death, anesthetic, disruption of life functions, financial concerns Intraoperative nursing: Types of anesthesia: general- IV, inhaled, local- topical, regional, and conscious sedation (Goal is paralysis, amnesia, stop nerve impulses and muscle relaxants) Post operative nursing: Phases of postanaesthetic care PACU: - phase 1- care during the immediate post anaesthesia period, focused on patients' basic life sustaining needs, constant, vigilant monitoring - phase 2- surgery patient is ambulatory - extended observation- ongoing care for patients who will be admitted to the unit and those who require observation or interventions Post-op respiratory care: - resp rate, effort, SPO2, oxygen flow and type, resp assessment, breathing techniques, teaching incentive spirometer Post-op cardiovascular care: - BP, pulse, rate rhythm and amplitude, fluid and electrolyte imbalances, consider blood loss, fluids received and preoperative status, N&V, assessments, watch labs, measure ins and outs, syncope Post-op PV/ neuro - Assessments, consider type of surgery, VTE risk factors, may be placed on prophylactic anticoagulation, leg/ankle exercises, pneumatic stockings, early ambulation, monitor for VTE formation - Neuro: A&O x3, consider type of anesthesia, pain control Post- op pain assessment - PQRSTUV: assess at least q2h when stabilizing pain, refer to physicians orders, PCA pain management Post-op GI - Nausea and vomiting, anesthesia/opioids, delayed gastric emptying, slowed peristalsis, resumption of oral intake - Ileus: non mechanical, abdominal distention, pain and tenderness, may require NG - GI assessment, flatulence/stool. Position, ambulation, consider diet Post-op GU - Monitor ins and outs, stress from surgery can increase ALDO and ADH and that causes a decrease in urine output, oliguria could signal impaired renal perfusion, bladder scan/catheter needs Post-op Integ - SSI, purulent discharge, isolation of organism from wound fluid/tissue, pain, tenderness, local edema, warmth - Assess wound bed, wound edge and peri wound, the appearance, size, exudate, edema, pain and drains Post-op teaching - Wound care, nutrition and fluids, personal care, medication (pain), return to ADL, ambulation, follow up care **[Week 11 immunity]** The ability to prevent infection, and fight diseases, the body recognizes mutations and foreign cells and destroys them. The body recognizes self and does not destroy. Antigen, usually a protein, can be nucleic acids, polysaccharides, lipoproteins, stimulates the immune response Active immunity: natural- disease exposure, artificial- immunization Passive immunity: natural- innate, from mom to baby, artificial- receive antibodies when exposed to the antigen (immunoglobins) Lymphocytes: - B lymphocytes: bone marrow humoral immunity: produce antibodies (immunoglobulins) memory B cells. Response when a person is exposed to an antigen the second/subsequent times. Active immunity - T lymphocytes: thymus cell mediated immunity. T cytoxic (attack), T helper (CD4), T suppressor (CD8) (stop, battle is over), natural killer, dendritic cells, memory T cells, need cytokine. Cytokine - Proteins that control the immune system, growth, activity - Tell the immune system when to get to work, signals the inflammatory response to do its job A diagram of cells multiplying Description automatically generated - Bacteria, viruses, cancer cells, parasites, fungus Disorders: - primary/congenital/ born with. Rare Serious, A deficiency in an immune component, usually sex linked (XY), Immune system weakens as born missing parts of the immune system -- B Cell, Persistent infections, Auto-inflammatory diseases, Opportunistic infections, Tumor growth - secondary/acquired/get later in life: More common, usually less severe (disease/medications/toxin exposure/environment), Age, Burns/trauma, Starvation, Medications- chemotherapy/steroids, Cirrhosis, Renal failure, Radiation, Cancers, Diabetes, Disease, AIDs Life Cycle HIV\ https://coursewareobjects.elsevier.com/objects/elr/Canada/Lewis/medsurg4e/IC/jpg/Chapter017/017003.jpg Signs and symptoms - acute: see initial symptoms within a few weeks. Acute flu like infection - years of low virus levels: asymptomatic - chronic: early, intermediate, late A screenshot of a test results Description automatically generated HIV testing - pregnancy testing, Co infection- Hep B/C; TB, STI clinics, signs and symptoms consistent with HIV, requests, age 13-64, illness of unknown causes, rapid testing Pros and cons. HIV was not always part of pregnancy testing lab testing: - HIV antibody test, HIV viral load, CD4 counts, CD4 fraction, resistance testing (genotype, phenotype), HLA B5701 antigen testing, drug levels. (low CD4 is bad) - Diagnostic tests: CXR, based on symptoms Do: - ABCs, lab tests, treat symptoms - Baseline CXR, CBC and diff, LFT's, 'Lytes, glucose, LDL/HDL, total cholesterol, Serology for HSV, VZV, CMV, TOXO, Hepatitis A, B and C, Tuberculosis screening - Imunization, pneumovax, Tdap, Hep A and B - Assess readiness, stages of change, prochaska, DiClemente - Antiretroviral therapy (how are they different: stop virus replication, mulitple drugs needed, grouped by their job in stopping reproduction) HAART: goal of treatment is to stop HIV from entering the CD4 cell - Decrease viral load, maintain/raise CD4 counts, delay HIV related symptoms and opportuinitic infections, prevent transmission to other Teach medication and immune reconstitution: atypical inflammation, associated with immune system recovery, first 2 month of HAART, CD4 count \