Final Exam Study Guide (DK) PDF

Module 1: Inflammation and Autoimmune Inflammation (3) ● Inflammatory process ○ Vascular and cellular response to injury ○ Nonspecific immune response ○ Normal, expected response expect when its prolonged or exaggerated ○ Triggers: organisms, trauma, incisions, chemicals, heat/cold, tissue ischemia...

Module 1: Inflammation and Autoimmune Inflammation (3) ● Inflammatory process ○ Vascular and cellular response to injury ○ Nonspecific immune response ○ Normal, expected response expect when its prolonged or exaggerated ○ Triggers: organisms, trauma, incisions, chemicals, heat/cold, tissue ischemia ○ Goal: remove/dilute agents, localized injury/infection ■ Veins constrict to hold injury local ● Cardinal signs of inflammation ○ Redness ○ Heat ■ Mast cells → release histamine → dilation to increase local blood flow → deliver WBC to affected area ■ → redness and heat as arteries dilate bringing hemoglobin and heat to the surface ○ Swelling ■ Increased vascular permeability (gaps open in capillaries) → shifting of fluids ■ Movement of WBC through vascular gaps → phagocytosis ○ Pain/tenderness ■ Increased vascular permeability → swelling → stretching → pain ■ Pain is felt in parietal lobe of sensory cortex ○ Loss of function ■ Chronic inflammation →fibrosis and scarring → loss of function ● Cellular response to inflammation ○ Injured tissue → mast cells ruptures → release histamine → capillaries dilate → increase permeability → WBC (neutrophils) move to areas in need → chemotaxis → phagocytosis ○ Diapedesis: WBC moving from capillaries into tissue spaces ○ 1st Neutrophil chemotaxis: WBC (neutrophil) moves → phagocytosis ○ 2nd Monocytes: leaves blood vessel → matures to macrophage = antigen presenting cell which then presents antigen to T cells → T cells present antigen to B cells → B cells produce antibodies → plasma cells develop and produce antibodies ● Labs ○ Increased WBC ○ Increased ESR (erythrocytes sedimentation rate) ■ Distance RBC fall after separation from plasma ■ More at the bottom of the tube = more inflammation ■ Fibrinogen → clumping RBC → increase ESR ○ Increased CPR (c-reactive protein) ■ Generated in liver ■ Binds to foreign material ○ CRP and ESR are nonspecific inflammatory response ■ Inflammation subsided if there is a drop in ESR or CRP ● Fever ○ Immune system response to inflammation → pyrogens trick the hypothalamus to thinking it's cold → increase body temperature ○ Interleukins affect on the hypothalamus ○ Hyperthermia r/t increase movement of WBC and increase neutrophil activity ○ 98.7-100.3 is a low grade fever Raynauds (1) ● Manifestations of RA ● Response to cold is immediate and more exaggerated than normal ● Risk for ischemia and necrosis ● Causes SNS stimulation → vasoconstriction → vasospasm → necrosis from lack of oxygen Rheumatoid Arthritis (8) ● RA ○ Inflammatory condition + autoimmune component is likely (molecular mimicry) ○ Autoimmune etiology ○ Inflammation of synovial tissue (synovitis) → pannus formation (overgrowth of synovial tissue) → erosion of bones/joints/cartilage/ligaments ○ Altered anatomy → altered physiology ○ Fibrosis and scar tissue → loss of function in motion of joints → disability ● Symptoms and Manifestations ○ Bilateral involvement of the joints ○ Most often affecting the smaller joints in the fingers/toes/wrists but can also affect larger joints ○ Raynaud’s syndrome ○ Anemia ■ Inflammatory effects on bone marrow and reduce kidney production of erythropoietin →reduces bone marrow stimulation ■ Normochromic normocytic anemia ○ Fatigue ■ R/t chronic inflammation ■ Increased CRP and ESR ■ Increased # swollen and tender joints ○ Sjogren Syndrome ■ Systemic inflammatory disorder ■ Auto/self reactive antibodies produced → attack, inflame, and damage moisture producing glands (lacrimal and salary) ■ Risk for dry eyes, corneal abrasion, and dry mouth ● Diagnosis ○ Definitive diagnosis = ACPA anti cyclic citrullinated peptide antibodies ■ Non-essential amino acid in joints of patient with RA ■ Produce anti-CCP antibodies → inflammation ○ NOT definitive is the rheumatoid factor ○ ESR/CRP elevated ○ More than 10 joints (1+ smaller joints) ○ Symptoms chronic lasting 6 months ● Treatment ○ Reintroduce immunological tolerance ○ Relieve pain ○ Preserve joint mobility ○ Keep RA in remission ○ Anti-inflammatory drug ○ Anti-rheumatic drug to suppress autoimmune response ○ TB tests ○ All vaccines SLE (4) ● Systemic Lupus Erythematosus ○ Chronic, inflammatory, autoimmune disorder ○ Multiple tissues can be affected such as lungs, kidneys, heart, skin ○ Exact cause is unknown ○ More likely in women than men ○ Ages 15-40 ○ Triggered in unknown ways ■ Infection, stress, diet, rx ● Symptoms ○ Flare ups and remission ○ Fatigue,activity intolerance, discomfort ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ Fever Weight loss Skin: butterfly rash (red, itchy, painful), hair loss, light sensitivity Muscles and bones: bilateral soft tissue swelling, arthritis Kidneys: kidney failure, urine abnormalities Nervous system: seizures, headaches, mental health Pericarditis: sharp, knife like pain when cough/sneeze/laugh Visceral peritoneum: serositis Pleuritis: pleura compressed by chest wall Pulmonary fibrosis Pneumonitis Hypoxia → AEB, SOB, DOB Blood disorders: anemia, thrombocytopenia ■ Normochromic normocytic anemia ■ H/H and RBC decreased ■ MCV, size, and color same ● Diagnosis ○ 4/11 symptoms ○ ANA + lab test ■ Positive antinuclear antibody test ■ Anti-dna antibodies ● Treatment ○ Mild disease → symptomatic treatment ○ Sever → immunosuppressive therapy ○ Prognosis: 10 year survival exceed 85%; variable Module 2: Immunodeficiency and HIV HIV (4) ● Immune deficiency ○ HIV is a RNA virus that can progress to AIDS ○ HIV can survive in body as latent (hides in immune cells) ○ With tx, can hav 0 viral load having undetectable levels of the virus ○ Opportunistic infection: infections that occur in people with immunosuppression ○ Higher incidence among men ○ Mortality decreasing due to early diagnosis ■ HAART treatment ● Retrovirus ○ Viral replication ● ● ● ● ■ Dock on host cells CD4 receptor → enter cytoplasm and uncoated → reverse transcription to DNA copy → integrates its DNA into host cells DNA → host cell can reproduce virus → assembly of virus → release from cell by budding → repeated budding leads to cell death → virus can infect new cell ■ Stores genetic information as single strand of RNA ■ Reverse transcriptases = makes DNA version of its genes after entering the cell ■ Integrase = inserts newly formed DNA into host cell DNA ■ Protease = packages HIV virus T Lymphocytes ○ T lymphocytes express the CD4 antigen ○ If the CD4 lymphocytes are damages → function of lymphocytes decrease ■ Scan for foreign invades, kill infected cells/cancer cells, help cells phagocytosis, and help b cells make antibodies ○ HIV decrease the activity of t lymphocytes → risk for infection and malignancy Diagnosis ○ Day 0 = exposure ○ Day 7-14 = viral load detected ○ Day 16 = P24 antigen detected ○ Day 28 = antibodies detected ○ 4th generation test for HIV (combined antigen/antibody test) ■ ELISA tests for antibodies ■ Tests for p24 antigen ○ Home Access Express HIV Test →99% reliable blood test ○ Ora Quick → antibodies in saliva Transmission ○ Need # and virulence ○ Route: blood or body fluids ○ #1 risk factor is sex with men ○ Risks: unprotected sex and sharing needles with an infected person ○ Mom → baby transmission is now rare ■ Nucleic Acid Amplification Test → screening ■ Recommended HIV + moms do not breastfeed Prevention ○ Safe sex and do not share needles ○ Tenofovir = PREP ■ Up to 92% effective in high risk people ■ Must take consistently ○ N vaccine ○ PEP ■ 1-2 times a day for 38 days within 72 hours of exposure ● AIDS ○ CD4 or T lymphocyte count less than 200 ○ OR 1 of 26 conditions that affect people with advanced HIV; primarily opportunistic infection ■ Pneumonia, yeast infections herpes, NH lymphoma, TB, and HPV ■ Prevent from HPV with gardasil vaccine ○ Increased risk for liver failure and cancer from hep b and c ■ Vaccinate against hep b and c ● Wasting Syndrome ○ Unintended weight loss of 10% ○ Diarrhea, weakness, fever lasting 30 days ○ Etiologies in person with AIDS ■ Malabsorption ■ Decreased intake ■ Increased need Module 3: Diabetes Mellitus DM/Metabolic syndrome (17) ● Review ○ Insulin is produced by beta cells of the pancreas ■ Insulin receptors are found on muscle, liver, and adipose tissue ○ Glucagon is produced by alpha cells of the pancreas ○ Insulin and glucagon stabilize blood glucose levels ○ Low glucose → release glucagon → raises blood glucose levels ■ Glucagon = glycogen → glucose ○ High glucose → release insulin → lowers blood glucose level ■ Insulin also regulates movement of amino acids into cells, increases protein and adipose cell synthesis, and stores fat ■ Insulin opens up glucose transport channels in cell membrane allowing glucose to move into the cell by facilitated diffusion ■ Insulin stores excess glucose ● Excess glucose stored the liver is called glycogen ○ Normal blood sugar 70-99 ; 2 hour PP <140 ● Diabetes Mellitus ○ Endocrine disorder involving insulin ○ Production ■ Beta cells are destroyed → produce no insulin → Type 1 DM ■ Produce insufficient insulin → Type 2 DM ○ Cellular utilization ■ Cells can’t use available insulin = insulin resistance → Type 2 DM ○ Blood sugars are above normal ○ Type 1 vs Type 2 ■ Type 1: autoimmune, small vessel disease, requires insulin injections for life, no prevention ■ Type 2: insulin resistance, large vessel disease, might require insulin, prevented through weight loss/exercise ○ Prevalence ■ 5% T1 DM ■ 95% T2 DM ■ ½ adults are pre diabetic or diabetic ○ R/t concern = Hyperglycemia ■ High blood sugar fasting, postprandial, or both ■ Fasting BS = 126 or higher ■ 2 hr PP BS = 200 or higher ■ A1c = 6.5% or higher (diagnostic for T2 DM) ○ A1c ■ Glycosylated hemoglobin stays high for the life of the RBC = 90-120 days (3 to 4 months) … binding to RBC is irreversible ■ Normal A1c <5.7% ■ This can be checked at any time showing the average BS ■ More accurate than fasting ● Type 1 DM ○ Autoimmune disease, failure of self recognition ○ Genetic susceptibility + environmental trigger ○ Autoimmune beta cell destruction → no insulin secretion ○ Results of molecular mimicry where antigen on beta cell resembles antigen on the surface of a pathogen ■ Parts of the beta cell look like a virus to the immune system ■ Immune system generates antibodies to attack viral antigen and the beta cells → halted insulin production ■ T lymphocytes may attack the virus and beta cells → no insulin production ○ Progression ■ Trigger → immune response → lymphocytes begun infiltration of islet of Langerhans attacking beta cells → gradual loss of insulin release → normal BS → overt DM → c peptide present → no c peptide present ■ C-peptide is an amino acid chain formed as a byproduct of insulin ■ No insulin = no C-peptide ■ Latent autoimmune DM in adults … latent onset over the age of 30. Antibodies are present but insulin continue to be produced for months to years ○ S/S of T1 DM ■ Polyuria: excessive urination ● More glucose is filtered than can be reabsorbed → glucose in tubules exert a pull → glucose in urine excreted long with water ■ Polydipsia: excessive thirst ● Polyuria → dehydrated → increase blood osmolarity → osmoreceptors in hypothalamus → thirst ■ Polyphagia: excessive hunger ● Without insulin, glucose cant diffuse into cells → cells are starving → body thinks it needs to eat → increased food intake ■ Weight loss ● Polyuria → fluid depletion ● Cell starvation “Starvation in the face of plenty” → breakdown of body tissue to generate energy ○ Lipolysis (adipose tissue) ○ Protein catabolism (muscle tissue) ○ Acute complications of T1 DM ■ Hyperglycemia ● Cell starvation in the face of plenty: glucose can't move into the brain and cardiac cells without insulin ■ Diabetic Ketoacidosis ● No insulin → glucose can't move into cells → high BS outside cell → osmotic diuresis low glucose inside cell → cellular starvation → lipolysis (fat breakdown) → ketones and fatty acids generated → energy and H+ → metabolic acidosis → CNS depression → coma ● BS = 350 ● Ketones in blood and urine ● Hyperkalemia ● R/t beta cell loss T1 DM, failure to intake insulin as required to sustain life, and infection/stressors → fight or flight ○ Fight or flight → cells need more glucose → cells generate energy from fat → ketones and H+ → ph drops ● Treat with IV insulin and electrolytes ● R/t concern of hypovolemic shock: catastrophic because in perfusion AEB catastrophic decrease in BP ■ Hypoglycemia ● Most common etiology for hypoglycemia is insulin treatment for hyperglycemia ○ R/t too much insulin or too little glucose (failure to eat) ● Treat with rapid acting glucose, glucose tablets/other source of glucose ● Low BS → glucagon raises → glycogenolysis (glycogen → glucose) → BS rises ● Cortisol (from adrenal gland) rises → gluconeogenesis (amino acids → glucose) → BS rise ● S/S are shakiness, tachycardia, sweating, dizziness, and hunger ○ Chronic complications of T1 DM ■ Diabetic Nephropathy ● Diabetic Kidney Disease ● Hyperglycemia → increased growth factors (VEGF_ ⇒ hypertrophy of glomerular capillaries → more pressure to push blood through vessel → change in pressure → pushes albumin out of glomerulus to Bowman's Capsule ● Hypertrophy and HTN → glomerular capillaries continue to break down → risk for renal failure ● Albuminuria: rule out ● As nephrons are lost → GFR decrease → BUN/Cr increase ■ Diabetic Retinopathy ● Leading cause of blindness resulting from poor BS control and damage to the retina → floaters, flashers, blurry vision ● → cataracts (excessive sorbitol; r/t poor BS control) ■ Diabetic Neuropathy ● Sensorimotor and autonomic small vessel disease ● Basement membrane thickening → hypertrophy → narrow arteries → Ischemia → nerve degeneration → failure to conduct impulses ● Affect myelin sheath → impaired nerve conduction/slower more erratic ● Decreased vibratory sensation ● Monofilament test → Cant feel filament, makes a C ● → abnormal weight bearing and infections ● → gastroparesis and neurogenic bladder ○ Infections for T1 DM ■ UTI: r/t urinary retention and stasis secondary to autonomic neuropathy ■ Feet: r/t sensory neuropathy and vascular changes ○ T1 DM Treatment ■ Insulin is lifelong and life sustaining ■ Lowering A1c reduced risk for complications ● Metabolic Syndrome ○ Metabolic Syndrome: cluster of risk factors for T2 DM including insulin resistances ■ Increase IAF → inflammation→ insulin resistance → FBS 100-125 → Prediabetes → T2 DM ○ Metabolic Syndrome criteria 3 out of 5 ■ BP: 130/85 or higher ■ HDL: less than 40 for men; less than 50 for women ■ Triglycerides: greater than 150 mg/dL ■ Waist: 40+ for men; 35+ for women ● Visceral fat → inflammation → increased CRP ● Increased risk for atherosclerosis ■ BS: FBS 100-125 “pre-diabetes, insulin resistance” ○ Insulin resistance: the pancreas is producing insulin but the cells cant use it ○ Prevalence in US ■ Up to ⅓ of adults ○ Prevention and treatment ■ Diet, exercise, and weight control ■ 5-10% weight loss → 20% loss of visceral fat → increase insulin sensitivity ■ → FBS between 70-99 ■ → A1c less than 5.7% ■ → decrease inflammatory markers and improvise lipid profile ○ Pre-diabets and T2 DM ■ Prediabetes ● A1c 5.7 to 6.4% ● FBS 100-125 ● BS 2 hr 140-199 ■ Diabetes ● A1c 6.5%+ ● FBS 126+ ● BS 2 hr 200+ ● Type 2 DM ○ Insulin resistance: more insulin docks with recept → channel is resistant and does not open normally →fewer channels rise to the surface → not enough glucose moves into the cell ■ Someone with type 1 DM may have insulin resistance if they are overweight/obese ○ Fasting BS ≥ 126 ○ 2 hr PP ≥ 200 ○ A1c ≥ 6.5% ○ Screening for T2 DM ■ Overweight and 1 or more risk factors ● First degree relative with diabetes ● BP > 140/90 ● HDL < 35 ● Triglycerides > 200 ■ Everyone over 45 ○ Up to 70% of people with insulin resistance → T2 DM ○ Incretine ■ Eat → glucose enters duodenum → defective incretin response → pancreas release on insulin is not normal (does not get message to release insulin) → BS are higher (particularly after eating) ○ May not have the 3 P’s because the BS is only slightly elevated ○ Treatment of T2 DM ■ Reduce workload of beta cells and reduce insulin resistance ■ Control BS by reducing insulin resistance ■ Weight loss, diet, exercise ● 5-10% weight loss → 20% loss of visceral fat → increase insulin sensitivity ■ Surgery: roux en y gastric bypass; not cure helps with remission ■ Hypoglycemics make insulin more available ■ Artificial incretin response via medications ○ Goals are personalized ■ Maintain a1c less than 7% ○ HTN ■ Increase BP by decreasing the blood vessel ability to stretch, increasing amount of fluid in the body, and hyperinsulinemia ● Decrease nitric oxide vasodilation → vasoconstriction ○ Dyslipidemia ■ HDL are low and triglyceride are high → increase risk for atherosclerosis in person who are insulin resistant ○ Macrovascular complications of T2 DM (uncontrolled BS) ■ Visceral fat → atherosclerosis → macrovascular disease ■ Temporary and irreversible ischemia: acidity pain, rest relief ● Heart → angina ● Legs → claudication ○ 7 P’s ■ Total occlusion → necrosis (major cause of death in T2 DM) ● Coronary arteries → MI ● Brain → stroke ■ Ischemic myocardial tissue cannot pump out blood/oxygen to meet bodies needs ● CAD → heart failure ■ Ischemia distal → proximal ● Vascular ulcers are pale and non bleeding d/t low blood flow ● Risk for osteomyelitis ■ PAD ● Dry gangrene ● Poor blood flow → prolonged ischemia/necrosis Module 4: Hearing and Vision Disorders Vision (6) ● Glaucoma ○ 2nd leading cause of blindness in US ○ Open angle: angle is open but drainage is defective → increase volume and pressure of aqueous humor → no early symptoms ○ Aqueous humor cannot drain out of anterior chamber ○ Diagnosis ■ IOP tonometry ■ > 21 mmHg ○ Perimetry = click when you see flashing light ■ Pressure on the eye phishing against optic nerve “cupping” ■ Destruction of nerve → loss of peripheral visual field ○ Risk factors ■ AA > 40 ■ White > 65 ■ Family hx ● ● ● ● ■ Diabetes ■ Severe myopia ○ Goal ■ Decrease IOP, improve drainage, decrease formation of aqueous humor, decrease pressure on optic nerve ○ Treatment ■ Medication ■ Lasers ■ Trabeculectomy (sclera surgery) Macular Degeneration ○ Central visual field loss ○ AMSLER Grid: wavy lines = age r/t macular degeneration screening tool ○ Etiology ■ Drusen (retinol garbage) builds up → distorts vision ○ Diagnosis ■ Visually seen by eye doctor ○ Dry vs wet ■ Dry form can progress to wet in 10% of people with AMD ■ Accounts for 90% vision loss ■ Treatment for wet r/t risk for retinal bleeding ● Inject medication into the vitreous to block VEGF (vascular endothelial growth factor) Cataracts ○ Scattered light, glare, blurring → blurry vision ○ Clouding of lens ■ Lens crystalizes → light can’t pass through normally ○ Advanced age is #1 risk factor ■ Diabetes ○ Treatment ■ Surgery “phacoemulsification” Diabetic Retinopathy ○ Related to poor glycemic control ○ Flashers and floaters ■ Represents vitreous detachment = not sight threatening ■ Represents retinal detachment = is sight threatening Retinal Detachment ○ Curtain/veil coming across visual field ○ Flasher = traction of retina from choroid pulling ○ Floaters = bleeding ○ Diagnosis ● ● ● ● ■ Slit lamp to see fluid passing through the tear ○ Treatment ■ Reattach retina quickly to preserve visual field ■ Reattach retina to blood supply → reconnect with choroid → conduct electrical impulse to brain ■ Sclera blocking → push choroid back to retina ■ Lasers → push choroid back to retina; hold retina in place ■ Pneumatic retinopathy → seak retinal tear with cryotherapy injecting air bubble Vitreous Detachment ○ Normal process of aging ○ Vitreous shrink and dries ○ If vitreous pulls away from retina → flashes of light ○ Treatment ■ None ○ Complications ■ Retinal detachment Vitreous Hemorrhage ○ Proliferative diabetic retinopathy resulting in bleeding Presbyopia ○ Lens has lost accommodation and can’t bulge → loss of elasticity ○ Lens cannot shape to focus on near objects → blurry near object ○ Age r/t refractive error → farsightedness ○ Starts around 40 ○ Treatment ■ Glasses Refractive Errors ○ Myopia: nearsightedness → problem seeing at distance ■ In front of retina ○ Hyperopia: farsightedness → problem seeing up close ■ Behind retina ○ Astigmatism: change in curve of cornea → retina receives 2 images Hearing (3) ● Normals ○ Outer: pinna, external auditory canal ○ Middle: tympanic membrane, malleus, incus, stapes ○ Inner: cochlea, semicircular canals ● Conductive hearing loss ○ Vibration is not conducted through the outer and middle ear (only inner) ○ Earwax, otitis media, osteosclerosis, ruptured Tympanic Membrane ○ CLASS ACT ■ Noisy room → trouble isolating sounds ○ History: risk for damage to tympanic membrane ○ Age ■ Young = infection of middle ear, otitis media ■ Old = impacted cerumen ○ Physical ■ Start with inspection of the ear for cerumen ○ Diagnostic test ■ Weber = tuning fork in the middle of the head ● Normal is equal ● Conductive lateralized to affected side ● Sensorineural lateralized to unaffected side ■ Rinne = tuning fork is placed on the side of the head ● BC > Ac ■ Audiogram ● Clicks and frequency identification which creates a graph ● Cerumen ○ Vibration does not get to tympanic membrane ○ Older people, nursing homes ○ Goal: restore ability vibration to conduct from outer to inner ear ● Ruptured Tympanic Membrane ○ Blocks/blunts tympanic membrane → less vibration to middle ear ○ History of ear infection trauma to membrane (slap, explosion) ○ Treatment ■ ATB ■ Analgesics ■ Warmth ■ Tympanoplasty close hole with graft ● Otosclerosis ○ Stapes is fused to the oval wall → low quality vibration of lymph and les bin gog hair cells → muffled sounds ○ Risk factors ■ White adults ■ Women ■ Pregnancy ■ Genetics ○ Diagnosis ■ Tympanogram ● ● ● ● ○ Treatment ■ More vibration frome incus → oval window → inner ear Sensorineural hearing loss ○ Defective or absent hair cells in the cochlea (inner ear) ○ Noise, presbycusis, ototoxic drugs, meniere's disease, benign paroxysmal positional vertigo (BPPV) ○ History ■ Single exposure to 140 DBA + ■ Prolonged exposure to 85-90 DBA ■ Brief exposure to 100-130 DBA ○ Red flag is shouting to be heard 2 feet away or the person next to you can hear your headset ○ Diagnosis ■ Both AC and BC are reduced ○ Etiologies ■ Shaken baby syndrome → subdural hemorrhage ■ Ototoxic drugs → damage hair cells ○ Treatment ■ Cochlear implants behind ear Congenital Deafness ○ Autosomal recessive condition = connexin 26 mutation ○ Otoacoustic emission test ■ Stimulus → vibrates cochlear fluids → stimulate organ and tissues → vibrations form Organ of Corti bounce back to the air of the external auditory canal → can be registers by microphone Presbycusis ○ The aged ear ○ Loss of hearing that gradually occurs as an individual ages ○ Loss of function and number of hair cells ○ Etiologies ■ Unknown ○ CLASS ACT ■ Mumbles sounds ■ Annoying noises ■ High pitched sounds are hard to tell apart ○ Treatment ■ Hearing aids to increase vibrations to hair cells that are still working Meniere Disease ○ Result of excessive buildup of fluid in the inner ear chamber →increase pressure in the ends of lymph → increase the pressure on the hair cells an acoustic nerve → impaired hearing ○ If endolymph chamber rupture → spinning or dizziness “vertigo” ○ Prevention ■ Avoid salt, caffeine, alcohol ● BPPV ○ Risk for falling r/t dizziness secondary to reposition of otoliths in the inner ear ○ Otoliths →messages to brain to balance ○ Defective otolith movements → send altered messages –. Vertigo ○ Treatment ■ Epley maneuver to float otoliths back to their correction location using positions Otitis media (1) ● Inflammation/infection of the middle ear ● Caused by bacteria/virus → fluid and pus → blocks vibrations of the small bones in the middle ear → less vibration into the inner ear ● Risk: children r/t shorter eustachian tube ● Ear pain (otalgia) ● Tx: antipyretics, pain control, ATB ○ 70% resolve spontaneously in 3 months ● Chronic ○ 5+ infections in 1 year; 3+ infection in a year over a two year period ○ Persistent ear pain, ear drainage, or healing loss over 3 months ○ Treatment ■ Tympanotm or myringotomy to open up the tympanic membrane ○ Prevention ■ Vaccines Module 5: Thyroid, Parathyroid, Adrenal, and ABG Adrenal gland (5) ● Adrenal Insufficiency ○ Most often due to medication → secondary adrenal cortical insufficiency ■ Long term corticosteroid use ○ Steroid therapy → raise serum cortisol levels → reduce hypothalamus CRF → reduce pituitary ACTH → adrenal cortex atrophy without stimulation from ACTH ○ Addison’s like signs and symptoms ■ Low cortisol levels ■ Hypotension and dizziness ■ Hyponatremia ■ Hyperkalemia ■ Hypoglycemic ■ Weight loss ■ Perpetual tan (hyperpigmentation) ○ Because cortisol is low, ACTH is high ( pituitary trying to jump start the adrenal cortex) ● Autoimmune etiology ○ Concern: adrenal insufficiency during times of stress (physical or psychological) ● If a person is steroid dependent, what do you do during stressful events ○ Take additional glucocorticoid (prednisone) by mouth ○ Give IV med before surgery or NPO patient ● Withdrawing weaning steroid therapy ○ Gradually reduce dose, decrease prednisone → reproduce CRF ○ CRF → anterior pituitary → ACTH → reactivate adrenal cortex Cushing’s ● Hypercortisolism ○ Exaggerated cortisol ○ Most common cause is therapeutic use of cortisol (steroids… iatrogenic) ● Cushing’s s/s ○ Moon face ○ Fat pad between shoulder blades ○ Abdominal fat ○ Stretch marks (striae) ■ Protein metabolism → Purple striae ○ Increased mobilization of fatty acids ○ Altered fat metabolism ○ Osteoporosis ○ Hyperglycemia ○ Hypertension ○ Risk for infection ○ Mood swings ● Hypercoagulation ○ Increased cortisol → increase fibrinogen (more clots) ○ Increase von willebrand factor (increase platelet activity) ○ Increased plasminogen activator inhibitor ■ TPA → plasminogen → fibrinolysis (lyse clots) ■ Inhibit TPA → clot formation ● Iatrogenic Cushing’s Syndrome ○ Steroid use ○ S/S related to dose and length of time ○ High dose, long time → cushing’s s/s ○ High dose, short time → fewer s/s ● Diagnosis ○ If serum cortisol levels are low ■ ACTH stimulation test: ACTH increase = adrenal insufficiency, no increase in cortisol ○ If serum cortisol levels are high ■ Dexamethasone suppression test (high cortisol dose) = body production does not decrease = Cushing’s Syndrome Thyroid gland (2) ● Basics ○ Thyroid hormone acts on body cells to regulate metabolism ○ Parathyroid acts on bones, kidneys, and GI tract to regulate calcium ○ Negative feedback of thyroid hormone ■ T3 and T4 drop → hypothalamus → TRH → anterior pituitary → TSH → thyroid → produce T3 and T4 ○ An increase in TSH suggest low T3 and T4 ○ When the T3 and T4 drop, TRH from the hypothalamus stimulates the anterior pituitary to secrete TSH ○ The end results is that the thyroid gland is stimulated to produce more T3 and T4 ○ Negative feedback: decrease thyroid hormones → increase TSH .. increase thyroid hormones → decrease TSH ○ Thyroid Gland: produces 3 hormones T3, T4, and calcitonin ○ When the serum calcium levels rise, calcitonin is released from the thyroid gland more calcium is moved from the blood and into the bones ○ The body can try and compensate for hypercalcemia by releasing calcitonin from the thyroid gland ● Hypothyroidism ○ Low T3 and T4 increased TSH ○ Fatigue and cretinism (congenital hypothyroidism – all newborns are checked) ○ Low T3 and T4 → TRH increases → TSH increases → thyroid gland can’t respond (T3 and T4 never rise) ■ Lower the T3 and T4 gets higher TSH levels (shouting at the thyroid gland) ■ TSH rises as pituitary tries to stimulate the diseased thyroid → TRH and TSH cannot be shut off ● Hashimoto’s Thyroiditis (hypothyroidism) ○ An autoimmune disorder ○ Most common etiology for hypothyroidism ○ Primary hypothyroidism thyroid cells have been destroyed ○ Inflammatory autoimmune → failure to recognize self → antibodies against ■ T3 and T4 → apoptosis (cell death) of thyroxine producing cells ○ Slow onset, at first because of inflammation will have hyperthyroidism until cells die ○ At risk ■ Middle aged women, family history ○ Signs and Symptoms ■ Hypo-metabolism ■ Intolerance to cold ■ Weight gain ■ Low energy ■ Constipation ■ Dry skin ■ Hair loss ■ Slow thought process ○ CLASS ACT ■ Fatigue ■ Past history: S/S ■ Physical exam: goiter (enlarged thyroid gland) ● Decrease T3 and T4 → increased TRH from hypothalamus → increased TSH from pituitary → gland undergoes hyperplasia (increase volume of tissue) in an attempt to produce more thyroid hormone ○ Diagnosis of hashimoto’s hypothyroidism ■ Low T3 and T4 ■ High TSH ■ Hypothyroidism r/t Hashimoto’s Antibodies present ○ Treatment ■ Replace thyroid hormones – restore physiology ● Expect T3 and T4 to rise to normal ● Expect TSH to decline to normal ● Expect energy levels to rise to normal ● Hyperthyroidism ○ Most common reason: overtreatment of hypothyroidism ■ Dose of thyroid medication was too high → increase in T3 and T4 → excessive metabolic rate ○ High T3 and T4 ○ Low TSH ● Grave’s Disease (autoimmune etiology for hyperthyroidism) ○ Antibodies bind to TSH receptor sites (irreversible binding) on thyroid gland → thyroid hormone production is always on/always accelerated so T3 and T4 levels rise ○ Signs and Symptoms ■ Hyper-metabolism ■ Weight loss ■ Increased appetite ■ Tremors ■ Restlessness ■ Heat intolerance ■ Palpitations: tachycardia, atrial dysrhythmias ■ Diarrhea ■ Exophthalmos: fibroblasts behind eye → bulged out eyes ■ Maybe goiter ○ Diagnosis ■ High T3 and T4 ■ Low TSH (trying to shut down production of thyroid hormones) ■ Radioactive scanning of thyroid: iodine radioactive increased uptake ○ Treatment ■ Radioactive iodine ■ Surgery to remove thyroid ■ Antithyroid medications ■ Complications: person becomes hypothyroid unless hormone replacement therapy is given (HRT) ■ As a result of treatment for hyperthyroidism, a person does start to become hypothyroid …. What do we do now?? ● Restore thyroid hormones ● Restore physiology as result of treatment for hypothyroidism ○ Expect T3 and T4 to rise ○ Expect TSH to drop ● Hyperthyroid and CAD ○ Hyperthyroid → increase HR and force → increase oxygen demand → increase risk of angina in an at risk person ■ Chest pressure/squeeze/burn less than 20 minutes, activity pain rest relief ○ Hyperthyroid → increase in irritability of the heart → increase risk for dysrhythmias in an at risk person ■ Irregular HR, dizziness, drop in BP and CO ● Hypothyroid and CAD ○ Low thyroid function → decrease rate and force of contraction→ risk for heart failure in an at risk person. ■ Activity intolerance, fatigue, SOB ○ Hypothyroid and the elder: risk for injury r/t confusion ■ Drop in BP, dizziness ● Thyroid disorders in someone with T2DM ○ Hyperthyroidism → hyperglycemia ○ Hypothyroidism → hypoglycemia ABG (1) ● Normal Values ○ pH = 7.35 to 7.45 ○ pCO2 =35 to 45 ○ pO2 = 80 to 90 ○ HCO3- = 22 to 26 ● Basics ○ Ventilation: movement of air in and out of alveoli ○ Hyperventilation: increased amount of air into and out of alveoli ○ Hypoventilation: decreased amount of air into and out of alveoli ○ Alveolar minute ventilation: amount of air moved into and out of alveoli over 1 minute ○ CO2 is an acid ○ Retain CO2 = retain acid → acidosis so hypoventilation tend to be acidotic ■ High pCO2 = hypoventilation ○ Blow off CO2 = blow off acid → alkalosis so hyperventilation tend to alkalotic ■ Low pCO2 = hyperventilation ● Acidosis ○ Decrease in pH ○ Too much respirator acid = high pCO2 ○ Too little base = low HCO3 ● Alkalosis ○ Increase in pH ○ Too little respiratory acid = low pCO2 ○ Too much base = high HCO3 ● Pulse Oximetry ○ Indirectly measure the amount of pO2 = % hemoglobin combined with oxygen ○ 60-90 Rule: pO2 of 60 provides enough pressure to combine 90% of hemoglobin with oxygen ○ Hypoxia = less than 90% ● If pCO2 is abnormal think respiratory ● If HCO3 is abnormal think metabolic ● Compensation: a change in the opposite system is needed ● ABG Analysis Steps ○ Oxygenation: what is pO2? ○ Acid Base: what is pH? ○ Cause: what caused the change in acid-base? ○ Compensation: is there compensation from the opposite system? Module 6: Urological Disorders UTI (1) ● Urinary Tract Infection ○ Cystitis = lower “bladder infection” ○ Pyelonephritis = upper “kidney infection” ● Urinalysis is diagnostic for UTI ○ WBC + ○ LE + ○ Nitires + ■ Enteric coated bacteria converts nitrates → nitrites ● Urine culture ○ More than 100k colony forming units is diagnostic for UTI Cystitis (1) ● Lower UTI ● Bladder infection most often caused by the bacteria e coli ● Most caused by bacteria that enter through the urethra ● Signs and symptoms r/t inflammation ○ Pain = dysuria ○ Tenderness = suprapubic ○ Fever ● ● ● ● ○ Leukocytosis CLASS ACT ○ Dysuria ○ Burning ○ Urethral tip of urethra ○ Fever r/t inflammation and infection ○ Cloudy urine ○ Foul smelling urine ○ Urgency in elderly → incontinence and it smells awful ○ Elderly = cognitive and ADL issues ■ Mental confusion, fatigue, tiredness, loss of appetite ■ UTI is a common cause of fevers in elderly Risk Factors ○ Sexually active females ○ Post menopausal or older women ■ Mucin/mucus layer in the bladder acts as a protective layer to keep bacteria from adhering to the bladder wall. Post menopausal and older women produce less mucin as a result of lower estrogen. ○ Diabetes Mellitus ■ Normal bladder function = urge to void at 150 to 300 ml ■ DM → risk for autonomic neuropathy → stretch but limited snap → urine is retained and bacteria is not flushed out ○ Self care deficit ■ Hygiene issues, perineal care Risk for infection related to instrumentation of the bladder ○ Infection can occur during insertion of catheter ○ Infection can occur because bacteria clings to the outside wall of the catheters and migrates into the bladder ○ Prevent catheter acquired UTIs by removing them as quickly as possible and providing proper care. ○ Cystoscopy – procedure that has a risk for infection Diagnosis ○ Urine culture and sensitivity ■ Healthy urine is sterile ■ UTI = contaminated with bacteria ○ Colony count of 100,000 colony forming units per milliliter ○ Urinalysis diagnostic for UTI ■ WBC + ■ Leukocyte esterase + ● Released from WBC in presence of infection ■ Nitrites + ● Enteric bacteria converts nitrates to nitrites ● WBC and band count often present with infections ○ If WBC were drawn, expect the levels to be elevates and the predominant cell type to be neutrophils (non specific phagocytic cells) ○ The band count could also be elevated ● Treatment ○ Choose an antibiotic to which the organism is sensitive (S) ● Goals ○ S/S of cystitis monitored and managed as evidence by absence of symptoms and signs ○ Nitrate and LE ○ Lower UTI recurrence ■ Culture and Sensitivity followed by treatment plan ○ Further investigation could be needed if recurrence is happening ■ Bladder scan to determine post void residual (PVR) ■ Cystometrics to measure the bladder tone and capacity Pyelonephritis (2) ● Upper UTI ● Inflammation or infection of the nephrons of the kidney and pelvis of the kidney ● Most are acute some can be chronic ● Etiology ○ Common etiology: ascends from bladder (cystitis) ○ Vesicoureteral reflux: reflux from the bladder up into the ureters and on to the kidney ● CLASS ACT ○ Triangle: N/V, CVA tenderness, and fever ○ Inflammation → fluid shifts out of the capillaries and into the tissue spaces of the kidney → stretch the renal capsule → flank pain (ache) ○ Nausea and vomiting ○ Fever, chills, diaphoresis ○ Malaise ○ Elderly: confusion, changes in ADLs ○ History of recent cystitis ○ Past history of pyelonephritis ○ Presence of risk factors: (DM) autonomic neuropathy, vesicoureteral reflux ○ CVA tenderness – costovertebral angle tenderness ○ Increase temperature ○ Skin appear red and moist ● Diagnosis ○ CT or MRI to confirm diagnosis (swollen kidney) ○ Urinalysis ■ Increases casts RBC/WBC shaped like tubules ● Casts = RBC or WBC (pyuria “pus in urine”) ■ Leukocyte Esterase + ■ Nitrite + ○ Urine culture ■ More than 100,00 colones in the urine is diagnostic for UTI ■ Sensitivity reports will tell you which organism is in the blood and what antibiotic to give the patient. ● Related Concerns ○ Bacteremia: failure to localize ■ Immunosuppressed or elderly patients ○ Most cases of pyelonephritis resolves with treatment however pyelonephritis can be etiology for renal failure ● Treatment ○ Antibiotics to which the organism is S ○ Treat underlying pathophysiology if known ■ Control BS in DM ■ Control effects of bladder neuropathy ● Impact of pyelonephritis or cystitis on a person with T1DM or T2DM ○ T2DM: risk for increase BS r/t fight or flight response ■ Increase dose of hypoglycemic agents likely needed ○ Risk for DKA in T1DM ■ Increase dose of insulin is likely needed ● Risk for adrenal insufficiency in person who are steroid dependent ○ Cortisol issues in persons who are steroid dependent ■ increase the dose of cortisol is likely needed ○ Risk for adrenal insufficiency when the need for cortisol is greater than the supply ■ BP drops ■ Complains of dizziness Nephrolithiasis (1) ● “Kidney stones” ● Obstructive disorder: obstruct the flow of urine ● Occur in proximal ureter, vesicoureteral junction, or urethra (neck of bladder) ● CLASS ACT ○ Stones → ureteral stretch → pain (colic, sharp cramping pain) ● ● ● ● ● ■ Pain originates in flank of back and refers from the back to the front of the labia or testicles ○ Nausea and vomiting r/t fight or flight response ○ Past history or family history of kidney stones ○ Malabsorptive conditions: dehydration → crystalized urine ○ Abdominal tenderness r/t inflammation ○ Fever r/t inflammation ○ Hematuria: blood in urine Diagnosis ○ CT (MRI) Analysis of Stones ○ Strain the 1st urine of the morning to catch the stones ○ See under a microscope: calcium oxalate stones (most common) Treatment goals ○ Relieve the obstruction ○ Many small stones pass without treatment ■ Fluids to flush out and keep urine dilute ○ Pain medications ○ Crush the stone to more easily urinate ■ ESWL “Extracorporeal Shock Wave Lithotripsy” ● Sends shock waves outside the body to break up the stone ■ Intracorporeal lithotripsy = ureteral lithotripsy ● Laser therapy to break up stones ● Need general anesthesia ● R/t concern: risk for ureteral obstruction r/t inflammation so a stent is placed Prevention of recurrence ○ Fluid intake = 8 standard 8 ounce cups of water daily Concept of volume and pressure to an obstructing kidney stone ○ Kidney stone obstructing ureter → increased volume and pressure proximal to or above the stones → increased volume and pressure in the pelvis of the kidney → increased volume and pressure in calyces → increase pressure on nephrons → risk for nephron loss ○ Obstructing kidney stones → hydronephrosis (urine backing up in the kidney) → loss of nephrons Renal Failure (6) ● As a result of: reduced nephron function → renal failure ● Acute: rapid onset ● Chronic: long standing, progressive poorly treated or untreated hypertension and diabetes mellitus ○ Stages ■ Kidney damage with normal GFR ■ Kidney damage with mild GFR ■ Moderate decrease in GFR 30-59% of normal ■ Severe reduction in GFR 15-29% of normal ■ Kidney failure less than 15% GFR ● Types of Acute Renal Failure ○ Prerenal – prior to the kidney; decrease renal blood flow ■ RAS, HF, Shock, Dehydration ○ Intrarenal – in the kidney; intrinsic/damage to kidneys structure ■ HTN, DM, infection, inflammation ○ Postrenal – after the kidney; obstruction of urine outflow ■ BPH, stones ○ Reduced GFR → signs and symptoms can be the same → can move to stages of chronic renal failure ● Pre-Renal clinical scenario ○ Reduced blood supply to kidney, but nephrons are still healthy ○ Examples: diuretics and dehydration ■ BUN above 20 ○ Diminished renal reserve (elderly) + pre renal issue (such as dehydration) = reduced renal failure (increase BUN/CR, decrease GFR ● How to preserve renal function in an older individual ○ Control underlying disease ○ Prevent UTI ○ Control blood pressure ● Renal failure: lose ability to perform functions → S/S ○ Glomerular Filtration Rate (GFR) ○ Measure serum creatinine ■ Calculation considerations: age, race, gender ○ Serum creatinine is used to determine % renal failure because creatinine is only filtered ■ If creatinine is not being filtered → serum creatinine levels rise ○ Regardless of etiologies → decreased BP, decreased GFR, increased BUN, increased creatinine ● Acute kidney injury (acute tubular necrosis) ○ An etiology for acute renal failure ○ Ischemia r/t shock and drop in BP ○ Toxic Insult r/t contrast nephropathy/ use of fye and nephrotoxicity ● ● ● ● ● ● ■ Lower GFR → increase BUN and creatinine ○ S/S based on number of nephrons lost ■ Chronic renal failure: # of nephrons lost, GFR determines the stage ○ Accumulation of waste is an early sign of renal failure ■ Increase BUN and creatinine ■ Age, gender, race → creatinine clearance → convert to % renal function = GFR Fluid balance ○ Normally, 99% of filtrate is reabsorbed → 1% is urine ○ Renal failure → gradual decrease in urinary output (oliguria) → anuria when kidneys completely shut down ○ Rationale for diuretics: volume overload r/t renal failure ○ Low urinary output → increase in blood volume → heart can't pump it all → blood backs up around lungs → pulmonary edema Electrolyte balance ○ Potassium (life threatening) ■ 90% potassium is excreted through the kidney ■ Decrease GFR → increase K+ is possible ● Hyperkalemia → EKG flat line ○ Sodium ■ 99% reabsorbed by kidney ■ Decrease GFR → increase Na+ and water → serum Na levels will be normal (total body Na+ will increase) Blood pressure ○ Renin released by the ischemic kidney ○ Aldosterone → Na+ and water retention → increased BP ○ Renal failure → renin → hypertension → increased workload on the heart → heart failure Acid Base Balance ○ Excretes acid such as hydrogen ○ Produces and reabsorbs bicarbonate ○ Too little bicarbonate ○ Hyperventilation to get rid of respiratory acid ○ Acidosis worsens with hypokalemia because hydrogen into cell pushes out potassium Anemia and hypocalcemia ○ Not seen in acute renal failure due to time ○ Kidney activates vitamin D → can’t be absorbed by the GI tract Anemia in person with chronic renal failure ● ● ● ● ○ Low H/H or low O2 → stimulate kidney to release erythropoietin → stimulates bone marrow to produce more RBC →normalize H/H ○ Stop producing erythropoietin → less bone marrow stimulation → less RBC produced → anemia ○ Normochromic normocytic anemia (normal size, normal color, too few cells) Hypocalcemia in persons with chronic renal failure ○ Low serum calcium due to inability of kidney to activate vitamin D ○ Phosphorus levels ise (can't be filtered) → low calcium ■ Inverse relationship with calcium and phosphorus ■ PTH less effective when phosphorus levels are high ○ Low calcium → stimulate parathyroid gland ○ Increase PT hormone ○ Calcium pulled from bones into the blood ■ If this process is not stopped, bones with demineralize ■ This process is called secondary hyperparathyroidism Dialysis ○ Monitor estimated GFR ○ If GFR < 15 ml/min ○ Accompanied by: uremia, fluid overload, refractory hyperkalemia ○ Then need to start dialysis or transplant Can you live without your kidneys? ○ Yes, but you need to replace function ○ Dialysis ■ Diffusion: movement of waste products into dialysis solution ■ Filtration: movement of excess water into dialysis solution ■ Need arteriovenous fistula shunt for dialysis ○ Peritoneal dialysis ■ Dialysis fluid in the peritoneum then drained ■ Drained fluid contains waste products ad excess water ○ Kidney transplant ■ Option for a lucky few Effects of aging on the kidneys and bladder ○ Reduce # of nephrons: half by the age of 70-80 ○ Reduced ability to concentrate urine ○ Reduced bladder size and reduced tone of detrusor muscle ■ Increased frequency of voiding ■ Increased residual → increased risk for UTI ■ No real impact on kidney’s ability to control acid base or electrolyte balance unless disease sets in ● HF or severe dehydration → low renal blood flow and pressure → worsen renal function in person with reduced reserve (BUN/Cr rises above normal until underlying disease is fixed) ○ Reduced ability to response to drugs with neurotoxic side effects HF (1) ● Related to renal failure ○ ○ ○ ○ HF diagnosed on increased BNP MI diagnosed on increased troponin Age decreases GFR Heart failure → decreased cerebral [perfusion → decreased GFR → increased BUN/Creatinine ○ Treat: ■ Increase CO → increase renal blood flow and pressure → increase GFR → decrease BUN/Creatinine Module 7: Fluid and Electrolyte Electrolyte issues (3) Calcium ● Hypocalcemia ○ Low calcium ○ Etiologies ■ Failing kidney can’t activate vitamin D → can’t absorb calcium ■ Surgery on parathyroid glands → fail to sense drop in calcium → PTH not released → calcium falls ■ Diet is low in calcium ■ Related to low magnesium ● Low magnesium → low parathyroid hormone release ● Or bones less responsive to PT ● Or kidneys less able to absorb calcium ○ Concerns ■ Osteoporosis: low bone density → increase risk for fractures ■ Muscle contractions less effective ■ Decrease threshold stimuli from loss of calcium as sodium channel gate keeper ● Na+ channels not stable … ○ In muscle → cramping, twitching ○ In brain → seizure activity ○ S/S ■ Depends on the levels and and on the amount of ionized calcium ■ Numbness and tingling ■ Trousseau’s ● Exaggerated with ischemia – pressure on nerve (BP cuff) ● Ischemia → cells more permeable to Na+ → swell → increased neuronal excitability ● Muscle contracture wrist hyperflexion ■ Chvostek's ● When tap the facial nerve, on cheek → one eye wink ● Spontaneous neuron firing ○ Lab ■ Measure calcium in the blood ■ 1% of body calcium is found in the blood ○ Treatment ■ Treat the underlying problem – aggravating factor ■ Etiology drives treatment ■ Activate vitamin D (renal disease) ■ Diet instructions (low calcium diet) ■ Replace calcium (post thyroidectomy) Sodium ● Hypernatremia ○ r/t dehydration as evidence by serum Na+ levels > 145 ○ Na+ increased ○ BUN, WBC, BS, hct, are all elevated ■ Loss of plasma → concentrated in smaller plasma volume ○ S/S ■ Confusion ■ Dry mucous membranes ■ Low blood pressure ■ Low and concentrated urinary output ○ Treatment ■ Replace fluids slowly to prevent r/t concern of volume overload ● Crackling, SOB, pulmonary edema ● Hyponatremia ○ Serum Na+ levels less than normal < 135 ○ Serum osmolarity drops below 300 … plasma has fewer particles → fluid pulled into the cells → cells swell ○ CLASS ACT ■ Low sodium diet ■ Na+ wasting diuretics (furosemide) ■ HF ○ S/S ■ Fluid shifts intracellular → fingerprint edema ■ Fluid shifts into muscles → cramps and weakness ■ Fluid shifts into GI tract → anorexia, nausea, vomiting, abdominal cramps, diarrhea ■ Fluid shifts into brain → brain death ● Increasing volume in a container that cannot stretch → increased intracranial pressure and arteries are compressed → brain deprived of oxygen → prolonged ischemia → death of brain cells → pressure on brain stem → brain death ○ Treatment ■ Sodium containing IV solutions to restore osmolarity and put particles back ■ Fluid restriction if has adequate plasma volume ● Dehydrate plasma → sodium concentrates in the plasma → returns plasma to isotonic state ● Increase sodium diet Potassium ● Hyperkalemia ○ Serum levels of potassium above normal ○ Etiologies ■ Renal Failure ● 90% of K+ regulated by the kidneys ● Reduced renal function → risk for hyperkalemia ● The serum K+ goes up because GFR decreased and body is acidotic ■ Acidosis ● pH less than 7.35 → hydrogen moves intracellular to raise serum pH → potassium pushed extracellular: the damaged kidney cannot excrete excess in serum K+ ■ Complications of K+ replacement with elevated creatinine ● 90% of K+ regulated by the kidneys ● Reduced renal function → decrease excretion of potassium ● Diuretic → replace potassium loss → risk for hyperkalemia ■ Aldosterone reabsorbs positive ion sodium → positive ion potassium excreted ● Decrease aldosterone → less Na+ reabsorbed → more K+ reabsorbed ● Spironolactone (blocks aldosterone) → raise K+ ● Renin block (in treatment of hypertension) ○ Complications ■ Cardiac conduction depending on severity → dysrhythmias ● T wave repolarization issues ○ EKG staters to flatline = asystole ● Dysrhythmias originating from ventricles are most life threatening, affect heart's ability to pump out sufficient volume to maintain BP and perfusion ○ Treatment ■ ECG changes → treatment ■ Mild hyperkalemia ● Discontinue drugs causing hyperkalemia ● K+ wasting diuretic (furosemide) ■ Severe hyperkalemia ● Insulin and glucose → force K+ into cell ● Increase GI losses of K+ → diarrhea high in potassium ● Drug bind to K in GI tract ■ Limit consumption of high potassium foods ■ Dialysis ● Hypokalemia ○ Low serum potassium ○ Alters membrane potential ○ Etiologies ■ Potassium wasting diuretics (most common) ■ Malabsorption ● Diarrhea related to : c. diff, crohn’s, any malabsorptive state ■ Upper GI losses → lose acids (alkalosis) → absorb H- and lose K+ ■ Damaged liver (cirrhosis) ● Doesn’t breakdown aldosterone → high aldosterone → high Na+ and water retention → increase blood volume → edema ● Increase Na+ decrease K+ ○ Complications ■ Cardiac conduction depending on severity → dysrhythmias ■ Less than 3 associated with significant dysrhythmias ○ Other associated S/S ■ Muscle weakness ■ Fatigue ■ Muscle cramping ■ Anorexia, nausea, vomiting ○ Treatment ■ Depends on cause ■ Replace K+ either IV or PO ■ Replace K+ cautiously in persons who are elderly (diminished renal reserve) or i persons who have increased creatinine (decrease GFR) ● Cant handle potassium Magnesium ● Hypermagnesemia ○ Mg is filtered in the glomeruli. When the kidney fails, Mg is not filtered and the serum levels rise. Dialysis makes this electrolyte imbalance rate. ○ Etiologies ■ Most common is replacing magnesium IV r/t concern hypermagnesemia ○ Concerns ■ Respiratory insufficiency → stops release of ACTH → respiratory muscles don’t get the message to contract and high levels of magnesium block effects of calcium so that muscle can’t contract ● Hypomagnesemia ○ Etiologies ■ Diuretics (flush out magnesium) ■ Alcohol ■ Small bowel malabsorption ■ Laxative ○ Concerns ■ Cardiac conduction – ventricular dysrhythmias ○ Treatment ■ MgCl oral replacement or IV replacement Diabetes Insipidus (1) ● Problem with antidiuretic hormone (ADH) vasopressin ● Increase amount of urine of low specific gravity ● Causes ○ Damage to the hypothalamus or pituitary ○ Surgery or head injury ● S/S ○ Polyuria ■ ADH levels are low, can't hold urine ■ Unable to concentrate urine ○ Polydipsia ○ Weight loss ● Complications ○ Hypovolemic shock: low BP increased HR ○ Dehydration ● Treatment ○ Vasopressin (ADH) ○ Fluid replacement ○ If unsuccessful, urinary output drops to normal … ADH → hold onto fluids ○ Desmopressin: nasal drops 1-2 times a day ● Diagnosis ○ Diagnosed when short term fluid restriction does not result in decreased urine output. ○ No water for 6 to 8 hours → wait to see if urinary output drop ■ If it does not drop = confirm diagnosis ○ Injection of vasopressin → urine flow should stop Module 8 Orthopedic Disorders Osteomyelitis (1) ● Inflammation in the bone or bone marrow related to infection ● Risk factors ○ Downward extension: vascular ulcer with PAD or infected surgical wound ■ Decubitus ulcer: downward extension of bone ○ Open fractures: break in nonspecific immune barrier of skin ● Signs and Symptoms ○ Not manly early manifestations ○ Increase temperature ○ Increase WBC ○ Increase neutrophils ○ Pain ○ Swelling ○ Skin = red and warm ○ Elevated ESR and CRP ○ Inability to bear weight ○ Pain, bone tender to palpation, reduced joint movement ○ Soft tissue swelling (late) ○ Suspicious X ray ○ Positive blood culture ● Definitive diagnosis ○ Bone biopsy ● Treatment ○ Antibiotics based on specific organism (sensitive) ○ Local debridement: removal of infected tissue ○ Surgical treatment: limited amputation Osteoarthritis (3) ● Bone/joint inflammation ● Wear and tear condition involving cartilage and bone ● Degenerative joint disease ● Most affect joints: larger joints that carry the most weight and most repetitive action (injury) ● X-Ray ○ Joint space narrowing ■ Thinning or loss of cartilage ○ Subchondral bone erosion ■ Bone erosion below cartilage ● OA → break down joint cartilage → inflammation → irregular growth of new bone (bone spurs, osteophytes) → pain when they grind on other bones and sensory nerves → may restrict range of motion for joint ● Early cartilage swelling = reflects an effort by cartilage to repair itself ● Late cartilage loses elasticity → flaking or shredding of cartilage ● OA in the knee begins medially then progresses laterally ● Increased inflammation → swelling, pain, stiffness ● Change in weight bearing = disuse → muscular atrophy on the opposite side (unaffected side) ● Person at risk for secondary OA ○ Mechanical injury: repeated joint stress, wear and tear, athletes, runners ● Person at risk for primary OA ○ Age + … ○ Decreased cartilage volume, cartilage thins ○ Decreased vascular supply to cartilage ○ Decreased proteoglycans ■ Compound that holds water in the cartilage → able to give rather than crack ○ DNA/genetics ● CLASS ACT ○ Chief complaint: worsening chronic pain ○ A: “gel phenomenon” = stiffness r/t thickening of synovial fluid r/t inactivity ■ Crepitus (bone grinding on bone) ○ T: morning/sedentary lasting less than 30 min (gel phenomenon) ○ Tx: get up + more ○ Physical exam: impaired physical mobility r/t loss of muscle mass and strength association with abnormal weight bearing and disuse. Decreased ROM. ● Treatment ○ Goal: correct altered anatomy to restore physiology ○ Weight control ■ Take stress off joints ○ Analgesia ■ NSAIDs, cushioning w/ hyaluronic acid injections ○ Platelet Rich Plasma ■ Inject into the knee to activate growth factors ○ Knee replacement = arthroplasty Osteoporosis (4) ● Thinning of bones … Demineralization ● Bones become porous because osteoclasts > osteoblasts ● High Risk ○ Post menopausal women ■ Decreases estrogen → osteoclasts > osteoblasts ● Men ○ ¼ men over the age of 50 have or at risk for osteoporosis ○ Men generally have a greater bone density than women; bone loss begins later and advances more slowly ○ Highest risk: thin white males over the age of 65 ○ Pathological fracture r/t osteoporosis ○ Visceral obesity in men ■ Visceral fat → adipokines (weaken bones) → inflammation → osteoclast activity ● Related Concerns ○ Pathological fracture caused by thinning of bone matrix primarily spongy bone ○ Fractures: ■ vertebrae, wrists, hips (intertrochanteric area) ○ Kyphosis: ■ Stooped posture, loss of height, collapse change in contour, fracture in vertebral bodies ● Prevention ○ Screening for osteopenia (small deficient bone) ○ Routine osteoporosis screening of all women over 65 or postmenopausal under 65 with risk factors ○ No recommended screening for men (unless they have risk factors) ○ Ultrasound bone density screen (ankle) ○ Bone Mineral Density Scan (DEXA scan) → T score ■ Lumbar Vertebrae and femoral neck ■ Normal > -1 (best is 0) ■ Osteopenia - 1 to 2.5 ■ Osteoporosis < 2.5 ○ Resistance exercises to build bone as muscle pulls ○ Dietary calcium and Vitamin D ● Treatment ○ Goal is to remineralize ○ Calcium and Vitamin D ○ Resistance exercises ○ Decrease osteoclast activity with medication (alendronate) ● Special cases of bone demineralization ○ Renal failure ■ Decrease in active Vitamin D + increase in serum phosphorus (does not get filtered) → decrease in calcium ○ Long term high dose of glucocorticoids ■ Less formation of bone r/t absorption of calcium from GI tract ○ Chronic malabsorption ■ Doesn’t absorb Vitamin D + calcium ■ Roux en Y Module 9: Muscles and Ligaments Carpal tunnel (1) ● Etiologies ○ Congenital predisposition ■ Smaller than normal carpal tunnel (decrease size) → increased pressure → compression of median nerve → thumb, index finger, long finger, and lateral ring finger ○ Contributing factors ■ Repetitive injury ● Cumulative trauma injury ● Work stress ■ Abnormal wrist alignment ■ Wrist sprain or fracture ● Swelling ■ Rheumatoid arthritis ● Synovial tissue swelling