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85 Cards in this Set
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Neurologic Control of Bladder function
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Spinal cord reflex centers help control bladder
Micturition center in the pons help control bladder Cortical and subcortical centers help control bladder |
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Storage & Emptying of Urine
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Involves involuntary (autonomic nervous system) and voluntary control (somatic nervous system)
Parasympathetic nervous system promotes bladder emptying by contracting detrusor muscle and relaxing internal sphincter. Causes detrusor muscle to contract and relaxes internal sphincter so the bladder can be emptied. Sympathetic nervous system promotes bladder filling by relaxing detrusor muscle and contracting internal sphincter. Relaxes detrusor to bladder has bigger capacity and causes internal sphincter to contract with the idea of keeping you from leaking urine during fight or flight. Striated muscles in the external sphincter and pelvic floor provide for voluntary control of urine. So when external sphincter and pelvic are relaxed urine is released. |
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Urinary incontinence and its causes
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Urinary Incontinence
Involuntary loss of urine severe enough to cause social or hygiene problems. Not a normal consequence of aging or childbirth General Causes Structural changes in the bladder, urethra, or surrounding organs. During certain situations the bladder can be stretched and if bladder loses support it changes position in pelvic cavity. Urethra can get inflamed and cause urethritis, which allows sphincter to open. If problem with movement of uterus then the bladder can drop out of place. Rectum can also drop out of normal location. Impairment of neurologic control of bladder function. Neurologic is usually problem with nerve transmission like MS. |
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Types of Incontinence
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Stress incontinence
Urge incontinence/Overactive bladder Reflex/Overflow incontinence Mixed incontinence Functional incontinence |
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Stress incontinence
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•Involuntary loss of urine during coughing, laughing, sneezing, or lifting (increases in intra-abdominal pressure)
•Inability to tighten the urethra enough to overcome the pressure from the bladder detrusor muscle. •Unable to contract sphincters correctly so urine leaks out. More common in women. •Can be corrected •Results in small amounts of leaking usually •More common in females |
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Stress incontinence causes
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•Childbirth may weaken muscles that support the bladder neck
•Urethral sphincter deficiency caused by epispadias (urethra is on top of penis, so urine exits at the top) or myelomeningocele (opening in the spinal cord that causes weakness of the sphincters) •Damage to the urethral sphincter from multiple incontinence surgeries, prostatectomy, radiation therapy, trauma. |
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Stress incontinence clinical manifestations
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•Small amounts of urine lost
•Retains normal voiding habits. •Do not feel urgency or frequency •Post-void residuals should be less than 50 ml. •Do a straight cath after they void to see how much urine is left over. |
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Stress incontinence treatments
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•Diet - cut caffeine out because it irritates the bladder
•Kegel – pelvic floor muscle exercise Men can do Kegels. •Strengthen pelvic floor muscle. Teach by have them stop and start the flow of urine to know which muscles to use. •Surgical repair- When bladder has dropped out of position, you can surgically repair this •Medication Postmenopausal women- estrogen meds will help, low estrogen causes tissues to thin out, so take estrogen or use topically to thicken tissues. •Also estrogen is low during breast feeding. When giving estrogen need to also give progesterone so the uterun lining will shed to prevent cancer. •Estrogen PO daily or intravaginally every other day Improves pelvic muscle tone Can increase risk of endometrial cancer & thrombophlebitis |
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Urge incontinence/Overactive bladder
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•Involuntary loss of urine associated with a strong desire to void (urgency).
•“Overactive bladder” – inability to relax bladder detrusor muscle and overcome urge to urinate •Detrusor muscle is hyperexcitable. Not able to relax, so small amount of urine can trigger urgency, when usually it takes 400ml to feel this •May have overactive bladder without incontinence. •Can have feeling of urgency, but may not have incontinence •Large amount of urine leaking if incontinent, if they are incontinent they will lose a large amount of urine. |
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Urge incontinence causes
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Cause may be unknown
•Neurologic – stroke, Parkinsons’ disease, multiple sclerosis, spinal disease •UTI – chronic or acute. Constant inflammation can cause problem with detrusor muscle. Acute UTI is like not being able to urinate. •Benign prostatic hypertrophy. •Enlarged prostate, more prob with retention •Bladder irritability from ingested substances - caffeine •Diuretics, nicotine travels with mucous membranes causing problems •Atrophic vaginitis causes tissues of urethra and vagina to atrophy |
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Urge incontinence treatment
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•Diet Get rid of things that irritate the bladder
•Behavioral interventions Training pt to go to the bathroom on schedule •Surgery not recommended |
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Urge incontinence medications
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•Anticholinergics – *relax smooth muscle* detrusor(sympathetic) ; most effective drug treatment
•Probantheline, Oxybutynin PO qid Contraindicated for patients with narrow angle glaucoma Food interferes with absorption Causes dry mouth and constipation •Dicyclomine PO tid •Tolterodine PO bid or daily •Tricyclic antidepressant – imipramine This relaxes the bladder muscle, side effect is urinary retention Administer at bedtime May causes postural hypotension, dizziness Anticholinergic, alpha-adrenergic side effects •Use of other types of drugs not yet proven effective |
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Reflex/Overflow incontinence
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•Involuntary loss of urine that occurs when intravesicular pressure exceeds the maximal urethral pressure because of bladder distention in the absence of detrusor activity – cause may be unknown
•Bladder detrusor muscle does not contract and bladder fills to the point where it must leak or rupture •May also be caused by urethral obstruction like: BPH prostate has squeezed off the urethra Fecal impaction large amount in rectum pressing on the urethra |
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Reflex/Overflow incontinence treatment
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•Surgery to remove urethral obstruction
•For detrusor muscle weakness bladder compression and intermittent self-catheterization •Medication only used short-term for post op urinary retention •Bethanechol chloride increases pressure inside bladder to promote urination |
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Mixed incontinence
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•Combination of stress and urge incontinence. Stress and Urge seem to go together
•Treatment and medications will also be combined •More common in perimenopausal or postmenopausal women |
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Functional Incontinence
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•Bladder function itself is normal, but decreased access to bathroom facilities, impaired mobility, or decreased cognitive function leads to incontinence.
•If this person is under nursing care, this should not happen. •They have mobility problem or change in LOC. |
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Urinary Tract Infection
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•Bacteria ascend into urinary bladder – easier in female due to shorter urethra
•Contamination with feces wipe front to back •Catheters sterile technique •Sexual Intercourse pee after sex •Diabetes increased sugar in urine can cause bacteria to grow and never damage to bladder |
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UTI Clinical Manifestations
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•Frequency
•Urgency •Hesitancy Cant get pee flow started •Dysuria Pain with urination •Cloudy urine •UA – nitrite positive, WBCs, RBCs. nitrite means infection because when your killing bacteria in body nitrite is used to kill off infection. |
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UTI Treatment
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•Antibiotics
Sulfa drugs (Bactrim, Septra), Penicillins, Macrolides (Macrodantin) •Pyridium – short term (2-3 days) for pain relief. Can get in drug store and only relieves pain, turns urine orange and make sure people know this is not a treatment and they need something to kill the bacteria •Increase fluids- to flush out system •Sterile technique for catheter insertion •Patient teaching •Hygiene •Urination after intercourse •Control of blood sugar |
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Complications of UTI
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•Urolithiasis- bacteria can travel up into the kidneys and cause an infection and is very serious and can cause damage to nephrons and chronic kidney disease
•Pyelonephritis – ascent of bacteria into upper urinary tract- kidney stones due to inflammation and sitting urine |
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Disorders of the Pancreas
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Diabetes Mellitus
•Acini Secrete digestive enzymes into the duodenum •Islets of Langerhans Secrete hormones into the blood Composed of beta cells that secrete insulin, alpha cells that secrete glucagon •Insulin – anabolic action Increases glucose transport into skeletal muscle and adipose tissue Increases glycogen synthesis Decreases gluconeogenesis Slows making of new glucose •Glucagon – catabolic action Promotes glycogen breakdown Increases gluconeogenesis Problem in Beta Cells, Excess glucose is stored as glycogen |
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Types of Diabetes Mellitus
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Problem with any nutrients
•Prediabetes: impaired fasting plasma glucose and impaired glucose tolerance •Disorder of carbohydrate, protein, and fat metabolism Results from an imbalance between insulin availability and insulin need •Can represent: An absolute insulin deficiency Impaired release of insulin by the pancreatic beta cells Inadequate or defective insulin receptors Production of inactive insulin or insulin that is destroyed before it can carry out its action •Type 1 results from: Loss of beta cell function An absolute insulin deficiency Beta cells are not producing insulin properly •Type 2 results from: Impaired ability of the tissues to use insulin A relative lack of insulin or impaired release of insulin in relation to blood glucose levels Lack of insulin there is none to use |
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Type 1A
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More Common
•Genetic predisposition (diabetogenic genes) •A hypothetical triggering event involving an environmental agent that incites an immune response •Immunologically mediated beta cell destruction •Triggering events: sickness, coxsackie, cold temps may be a trigger, because diagnosis happens in the winter and more people in cold areas have it. The trigger makes an immune response which then attacks beta cells |
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Type 1B
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Idiopathic diabetes
Those cases of beta cell destruction in which no evidence of autoimmunity is present Only a small number of people with type 1 diabetes fall into this category; most are of African or Asian descent. Type 1B diabetes is strongly inherited. People with the disorder have episodic ketoacidosis due to varying degrees of insulin deficiency with periods of absolute insulin deficiency that may come and go. DONT NEED TO KNOW THIS Beta Cells get wore out and cannot produce insulin Strongly inherited, NO autoimmunity |
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Type 2
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•Impaired beta cell function and insulin secretion. Relative insulin deficiency. Ex: Beta cell may make insulin that is inactive, or insulin does not get secreted, or beta cells die faster and cannot be replaced 1 for 1.
•Peripheral insulin resistance. Insulin cannot attach to cell membrane, it cannot bind. Liver takes stored glycogen, starts producing glucose when you don’t need it, because the body thinks you need it. •Increased hepatic glucose production •An initial decrease in the beta cell mass •Increased beta cell apoptosis/decreased regeneration •Long-standing insulin resistance, leading to beta cell exhaustion. Beta cells burn out •Chronic hyperglycemia can induce beta cell desensitization (“glucotoxicity”). Beta cells do not respond to increased blood sugar •Chronic elevation of free fatty acids can cause toxicity to beta cells (“lipotoxicity”). Fatty Acids are toxic to beta cells causing betas not to make insulin •Amyloid deposition in the beta cell can cause dysfuncti |
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Metabolic Syndrome in Type 2 DM
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Metabolic syndrome
•Triglycerides •HDL: Good Cholesterol •Hypertension •Systemic inflammation: Within the blood vessels •Fibrinolysis: Unable to break down blood clots •Abnormal function of the vascular endothelium: Problem with lining of blood vessels leading to athlersclerosis •Macrovascular disease: Problem with large vessels, the vessels thicken •Obesity and insulin resistance Increased resistance to the action of insulin •Impaired suppression of glucose production by the liver |
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Clinical Manifesations of metabolic syndrome in Type 2 DM
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•Polyuria - Excessive urination: Due to excess glucose excretion, glucoes takes H2o with it
•Polydipsia - Excessive thirst •Polyphagia - Excessive hunger: •Their cells are not able to use the glucose take in •Weight loss: Type 1 DM •Recurrent blurred vision: From increased glucose •Fatigue: Due to inability to use glucose •Paresthesias: Numbness, abnormal pain, this is when diabetics are unable to feel rubbing that can lead to infection •Skin infections: Due to extra glucose. Mostly yeast infections •Labs and other tests – Fasting blood glucose test - >126 mg/dl x 2: Over 126, two times means diabetes •Casual blood glucose test - >200 mg/dl: Need more testing to confirm •UA – presence of acetone: •Acetone from fatty acid breakdown, not necessarily uncommon •Glycosylated hemoglobin testing - 7% or less is goal: Hgb ALC, looking for % of glucose in a RBC, However RBC do not need insulin to get glucose in. Normal is 5%, but with diabetes it will be 7% or higher for at leas |
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Acute Complications
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•Diabetic ketoacidosis: Usually type 1, due to fat breakdown leading to ketones
•Hyperglycemia •Ketosis •Metabolic acidosis •Hyperosmolar hyperglycemic state: Type 2 •Hypoglycemia: Type 2, too much insulin |
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Diabetic Ketoacidosis (DKA) TYPE 1
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•Hyperglycemia (blood glucose levels >250 mg/dL) Increased glucose
•Low bicarbonate (<15 mEq/L) Decreased Bicard •Low pH (<7.3) Lowers PH •Ketonemia Increases Ketones in the Blood •Moderate ketonuria Ketones in urine |
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Characteristics of Hyperosmolar Hyperglycemic state (HHS) TYPE 2
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Hyperglycemia (blood glucose >600 mg/dL): High glucose contributes to hyperosmolarity
Hyperosmolarity (plasma osmolarity >310 mOsm/L) •Dehydration The absence of ketoacidosis: Not breaking down Fats Depression of the sensorium: Increase glucose level changes LOC and can lead to a coma |
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Chronic Complications
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Disorders of the microvasculature
•Neuropathies, nephropathies, and retinopathies •Thickening of the walls of the nutrient vessels that supply the nerve. Microvascular walls thickens and becomes inflamed. Ex: nerves in feet not supplying good oxygen needs to numbness. Ex: nephron’s in kidneys do not get enough oxygen and they die •Leading to the assumption that vessel ischemia plays a major role in the development of neural changes •Segmental demyelinization process that affects the Schwann cell. Myelinsheath starts to break down and schwann cells break down and signals do not conduct like they are supposed to •Accompanied by a slowing of nerve conduction •Distal symmetric neuropathy and foot ulceration Macrovascular complications •Athelrosclerosis |
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Impact of Osteoporosis
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•850,000 to 1.5 million fractures yearly among persons 65 or older: Accounts for a lot of fractures, 25 to 28 million at increased risk of fracture because of low Bone Mineral Density (BMD)
•Lifetime risk of osteoporosis fracture at age 50 is 40% for women, 13% for men: •More in women •Mortality in the 6 months following hip fracture is 10% to 20%: if elderly fall and have osteoporosis they have a high risk for hip fracture and then mortality, Neck of femur usually breaks and the ball breaks off, so they are immobile, in pain, pneumonia, blood clots. Need to do fall risk assessment. |
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Economic Impact
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Direct costs attributable to osteoporosis have risen from $7-10 billion in 1986 to $14-20 billion currently in the U.S.
Projected that by 2050 the annual cost of hip fractures in the U.S. will be $240 billion |
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Risk Factors
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•Genetic factors
•Caucasian or Asian •Family history •Female gender •Small body frame |
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Risk Factors
OB/Gyn |
•Late menarche
•Early Menopause before age 51 •Nulliparity not ever having kids or being pregnant, high estrogen levels are protective |
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Risk Factors
Lifestyle |
•Lifetime low dietary calcium intake
•Sedentary lifestyle •Tobacco and alcohol use contribute to loss of bone density |
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Risk Factors
Medical conditions |
•Previous osteoporotic fracture
•Hyperparathyroidism •Cushing Syndrome sterioids are high and that causes bone loss •Cancer metastasis as cancer metastisses to bone it takes up room so calcium goes into the blood •Gonadal dysfunction ovaries are not producing estrogen and testes are not produing testosterone and testosterone also helps prevent osteoporosis in a big way which is prob why men have it less. |
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Greatest RISK FACTOR IS for osteoperosis
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Greatest RISK FACTOR IS POSTMENOPAUSE- 80% of osteoporosis can be attributed to this*** Regardless of stature
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Physiology of Bone Formation
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•Bone is constantly undergoing remodeling
•Osteoclasts are bone-resorbing cells •Osteoblasts are bone-forming cells •Osteoporosis results from an imbalance in the two that creates bone with a lower BMD •Trabecular bone - 20% of skeletal mass, 80% of the turnover (spine, hip, forearm, ribs) most of the probs with osteoporoses have to do with trabecular bone •Cortical bone - 80% of skeletal mass, 20% of the turnover |
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Type 1- Postmenopausal
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•Age - 55-70
•Years past menopause - 5-15 •Sex ratio: F/M - 20:1 •Fracture site - Spine fracture, pt will get shorter, kyphosis, very painful in spine •Bone loss - Mostly trabecular bone loss •Contributing factor - Mostly menopause |
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Type 2 Senile
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•Age - 75-90 age is the greatest contributer
•Years past menopause - 25-40 •Sex ratio: M/F - 2:1 •Fracture site - Hip, spine, pelvis, humerus •Bone loss - Both cortical and trabecular •Contributing factor - Age affects more than menopause |
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Clinical Presentation
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•Shortened stature
•Dorsal kyphosis •Cervical lordosis •Pulmonary and cardiovascular complications because it is hard to breath •Back pain •Fracture |
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Assessment and Diagnosis
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•Thorough history and physical
•Dual energy x-ray absorptiometry (DEXA)- If symptomatic (prior to pharmacotherapy) or with several risk factors for baseline BMD. Take xray of hip and spine to look at bone density. •May recommend baseline xray at 35 if there is high family history |
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Treatment and Prevention
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•Decrease caffeine-contributes to bone density loss
•Stop Smoking- bone density loss •Reduce alcohol intake- bone density loss •Increase exercise cautiously- may break something or pull muscles •Fall prevention •Calcium and Vitamin D take simultaneously •Estrogen (females) protective against bone loss, this is why osteop is big after menoupase •Medications |
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Calcium
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•Premenopausal adult women – 1000 -1200 mg/day of calcium
•Postmenopausal, pregnant, lactating women - 1500 mg/day •Males less than age 65 – 1000 mg/day •All adults age 65 and older – 1500 mg/day •Average diet provides 500 mg/day Milk has 300mg per cup, some milk has 500mg skim extra |
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Dietary Sources
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Dairy products - if lactose intolerant, consider yogurt and hard cheese
Collard, mustard, turnip greens Sardines, broccoli Some foods, such as orange juice are now fortified with calcium |
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Calcium Supplements
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•Absorbed best if given with food
•Requires adequate amounts of Vitamin D •Absorption of different products varies •Calcium carbonate (Oscal, Tums): 40% •Calcium gluconate: 9% •Calcium lactate: 13% •Dibasic calcium phosphate: 23% •Increases risk of kidney stones Some stones are formed from calcium, so teach pt’s drink a lot of water |
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Vit D
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Increases absorption of calcium
Up to age 50 - 200 IU/day 51-70 yrs - 400 IU/day >70 yrs - 600 IU/day Vit D Sources Diet: eggs, liver, butter, fatty fish, vitamin D fortified milk and cheese Sun exposure: 5-15 minutes 2-3x per week Supplements: 400-800 IU/day for osteoporosis, Rocaltrol is one brand name |
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Estrogen Replacement
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•Decreases bone resorption decreases the break down of bone, this is good
•Increases calcium absorption and retention •Greatest effect in first five years after menopause and if continued for 10 years |
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Bisphosphonates
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•Decrease bone resorption help body absorb and use calcium better, but biphosphonates have low absorption rate
•First generation - Etidronate: increases BMD, not proven to reduce fractures, not approved by FDA for osteoporosis •Alendronate (Fosamax): once weekly Poorly absorbed, only water 30 min side effects: upper GI (ulcers, esophagitis) •Ibandronate (Boniva): monthly, only water 60 mins must sit up right Same effects as Alendronate |
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Patient Education
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•Alendronate (Fosamax)
Take on an empty stomach with a full glass of water No other medications, food, or liquids may be taken for at least 30 minutes Remain upright for at least 30 minutes after taking, remain upright so there is no reflux •Ibandronate (Boniva) Same as above, but must wait 60 minutes |
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Osteomylitis (infection of the bone)
Osteo-Myelo-Itis
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Bone-Marrow cavity- Inflammation
•There are a variety of opportunistic pathogens that can cause osteomyelitis •Most Common infection microorganism is Staphylococcs aureus •Sticky: Able to produce a collagen-binding adhesion molecule that adheres to connective tissue elements of the bone • Sneaky: Has the ability to be internalized and survive in osteoblasts, making the microorganism more resistant to antibiotic therapy(Porth, 2005). |
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It will either break in or be let in through your bloodstream to your bone home.
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It will either break in or be let in through your bloodstream to your bone home.
•Break in: DIRECT (Contiguous spread) Break in Skin,Break in Bone, Or BOTH!!! Fracture, surgery, •Let in: INDIRECT (Hematogenous) Pathogens from another infection site travels through the bloodstream to the bone. spreads through the blood, can come from another site of infection |
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Risk Factors: Direct (Contiguous spread)
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Risk Factors: Direct (Contiguous spread)
• SURGICAL: implanted orthopedic prosthetic device •ANY AGE: anybody any age •WOUNDS: Open, Penetrating wounds, Fractures |
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After entering body
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After entering body
• After gaining entrance to the bone by way of the blood, the pyogenic (pus-producing) microorganisms then lodge in an area of bone in which circulation slows, usually the metaphysis. •Then they multiply and produce purulent exudate. •Bone marrow is very moist and dark and have things to feast on |
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Multiply fast, need more oxygen, move to bone marrow
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Multiply fast, need more oxygen, move to bone marrow cavity
•Increased pressure beneath the periosteum creating ischemia and vascular compromise. •Eventually the infection passes through the bone cortex and marrow cavity, ultimately resulting in cortical devascularization and necrosis. •Once ischemia occurs, the bone dies. (F.A. Davis, 2005) It is difficult to treat |
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The dead bone
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The dead bone eventually separates from surrounding living bone, forming sequestra
• Necrotic and surrounded by pus, infected sequestrum is difficult for blood borne antibiotics or WBCs to reach. •Sequestrum can enlarge and become a site for microbes to spread to other sites (i.e. lungs, brain) •Sequestrum can move into the soft tissue and develop a sinus tract, which creates chronic purulent drainage. (Porth,2005) |
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Signs and symptoms
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look for localized signs
• Redness and Swelling, •Tendr to the touch, •If the infection is in the lower extremities, there maybe pain on movement or loss of movement |
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Diagnostic Tests
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•Bone scan:Bone changes from inflammation and infection
•Bone biopsy: Positive for infecting organisms •Blood culture & sensitivity: Identify organisms and sensitivities and antibiotics • Other Tests: Complete blood count, erythrocyte sedimentation rate, C reactive protein (an acute-phase protein), renal, bone, and hepatic blood profiles, x-rays, computed tomography (CT) scan, magnetic resonance imaging (MRI) |
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Complications if not treated
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•Spreading and infecting other sites like the brain and lungs.
•Sepsis •Chronic Osteomyelitis -New sheath of bone called involucrum forms around a sequestrum. •Site continues to release pus and bacteria into vascular system. -Sx Low grade fever -Process of exacerbations and remission. •Involucrum forms around dead bone, it is soft and spongy |
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Osteoarthritis
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•Progressive deterioration and loss of cartilage in the joints
•Primary (idiopathic): cause may be unknown •Secondary: wear & tear, trauma Cartilage thins, becomes soft, cracked; underlying bone deteriorates •Damage occurs faster than body can repair •Synovitis (inflammation) occurs later** in disease process |
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Causes of Osteoarthritis
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•Post-inflammatory diseases - RA
•Post-traumatic disorders - fracture •Anatomic or bony disorders – avascular necrosis: blood leaves the tissues •Metabolic disorders – calcium crystal deposition |
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Risk Factors for OA
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Age - >60 y/o
Family history Female Athletes obesity |
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Clinical manifestations
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•Joint & pain stiffness that improve with rest early in the disease process
•Crepitus: Crunchiness while palpating the joint •Heberden’s nodes – distal interphalangeal joints of fingers further out nodes •Bouchard’s nodes – proximal interphalangeal joints of fingers further in nodes •Ballottement of fluid under patella Bounces from fluid under the knee cap •Decreased function of affected joints |
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Preventing Knee and Hip Osteoarthritis
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•Losing weight: decreases wear and tare
•Preventing injury: Do fall assessment •Strengthening the muscles bridging joints: to take stress of the joints •Modifying job tasks: •Treatment – early in disease when inflammation is not present: Acetaminophen: good for pain, fever, no anti-inflammatory, if they have inflammation use NSAIDS |
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Alterations in Sensory Function
Glaucoma |
•Intraocular pressure
•Aqueous humor: maintains pressure in eye to stay in shape and provide nutrients to the eye and mediates the exchange of resp gases, so the eye gets oxygen. Also has protein, ascorbic acid, glucose, and amino acids. Produced in posterior camber of eye and flow through iris to anterior chamber of eye. Once it gets to anterior in order to maintain pressure if flows through trabecular mesh work then canals of schlemm and drains into the venous system. •Tears: Come from lacrimal glands. look in book to expand •Definition Problem with optic nerve. The optic disc becomes cup shaped. •Causes degeneration of the retina, optic nerve, edema in the eye. Eventually develop an opac cornea. Causes: Could be too much Aqueous humor, or drainage problem, usually drainage problem |
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Classifications of Glaucoma
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•Angle-closure (narrow angle) vs. Open-angle (wide angle)
•Open angle: More common, chronic problem. Risk Factors: over age 40, African American, Family History, Myopia (nearsidedness), HTN, Type 2 Diabetes, Trauma or inflammation that can block outflow. •The angle between the iris and cornea are normal, the problems is in trabechelar mesh work or cacals of schlemm We use meds to treat |
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classification of glaucoma
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•Angle closure: Acute onset is and an emergency,
•Shallow anterior chamber. The space between iris and cornea are not as deep as normal. Farsided. When pupils dilate it thickens the iris closes of trabecular mesh work causing pressure. Sharp stabbing Eye pain, poor vision, Nausea & Vomit, Headaches. To relieve pressure we use meds to constrict the pupil. We want parasympathetic response, so anticholerginic meds, or Beta antagonist, or Beta blocker. Surgery can be done and use laser to make holes in trabecular meshwork. Congenital or Infantile Glaucoma: Look for excessive lacrimation (tearing) photo-phobia (sensitive to light), fussy and do not eat well and rub eyes. Edema of cornea leading to a grayish white appearance. Ultimate result is Blindness |
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Cataracts
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Structure of the lens:
•Shape is Biconvex, the posterior side is more convex than the interior side, •supposed to be transparent, •It is avascular so no blood vessels and very elastic. •Has tiny ligaments attached to it that suspend it in place and attach to muscles in the eye, and the lend must change shape to see far away or focus up close, •Up close the lens is more rounded •With cataracts the lens is Opac , •over age 75 75% have cataracts. •When lens is Opac, light cannot get through it which means you cannot see. •As you age lens becomes thicker, and proteins, minerals and pigments accumulate and contributes to cataracts, |
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Cataracts,Causes:Diagnosis Treatment
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Causes:
•hereditary influence, •drugs like Amiodarone is a cardiac drug given for arrhythmia. Thorosine. •Miots increase risk for cataracts which is used to treat glaucoma. •Highly Associated with diabetes, and smoking, trauma, long term exposure to UV radiation. Diagnosis : •Red reflex is diminished and turns Opac, •look for changes on Snellen chart and do different light levels, •increased light makes it harder to see. Treatment : •no medical treatment, only surgical by removing the lens and get a lens implant |
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Hearing Disorders
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•External and middle ear: Main function is to capture and transmit sound
•Inner ear: Has organs that are stimulate by the sound, and helps maintain equilibrium •Eustachian tube: Ventilate the ear, so they equalize pressure from inner to outer,so secretion can drain from ear to nasal pharynx and also protect from unwanted noises. When you assess for tympanic up and back on adult down and back on kid (more horizontal and bigger round) |
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External ear Disorders
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External ear Disorders
•External ear disorders: Build up of wax (cercums) can get impacted and cause conductive hearing loss. If impacted do not use Q-tips. •Inflammation called “swimmers ear”. Middle ear and Eustachian tube disorders -Otitis media: Don’t lay kid down with bottle because it can flow into eustachian tube and increase ear infection. More common in kiddos. Crying, pull on ears, pink or red tympanic membrane or bulging from fluid behind it, may even rupture, sometimes can see line of fluid behind ear drum. fever, may have drainage, -Otosclerosis : 3 bones behind ear drum that conduct sound may form new spongy bone around ear to prevent moving and then you can’t hear. This is progressive hearing loss. Can be hereditary, don’t really have treatment; can create pressure causing tinnitus and vertigo |
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Inner Ear Disorders
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Tinnitus: high pitched ringing that doesn’t go away. Constant
Hearing loss Conductive: Conductive is a problem with transmission, like build up of wax, usually temporary. Sensorineural: Problem with auditory pathways of the brain, or hair cells in the ear, or cochlea (looks like a sea shell) Mixed : combo of 2 above |
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Hearing loss etiologies
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•Conductive : Caused by wax or a bug. Otitis media (if can cured your in good shape), otosclerosis, and tumors.
•Sensorineural : Head injury, loud music, work environment, meningitis, Gentacicym it ototoxic and can cause damage to nerve. Lasix (furosemide). Aspirin can cause tinitis which is a sensorineural loss. Tumor can be both conductive or sensor |
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Diagnosis
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•History : what led up to loss, characteristics, infections, family
•Testing : measure brain activity in response to sound with electrodes or tiny microphones. It is measuring sound waves. Weber- equal hearing in both ears, with conductive loss can hear better on the side with out loss, i think. and Rinne put on mastoid process first)- AC>BC 2:1, if you have conductive loss bone will be greater than ear. |
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Treatment
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Treatment
Obstructions: don’t stick things in your ear Hearing aids Cochlear implants: mechanical type of hearing, only for sensoryneural i think Other : can reconstruct bursting of ear infection, can lead to hearing problems is not corrected. |
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Acid Base Imbalance
Copd, renal, diabetes (DiabeticKetoAcidosis), liver problems |
Basics of acid-base balance
•Ratio of bicarbonate (HCO3-) to carbonic acid (H2CO3) = pH; ratio is 20:1:This is blood PH the normal ratio is 20:1 •Chemical buffer systems: Help keep correct ratio. •H2CO3 /HCO3- •Intracellular (protein) systems: Albumin immunglobumns help with hydrogen ions (hydrogen is an acid) protein binds to H to make PH go back to nornal, if you need acid, the proteins can release them. •H+/K+: If too many hydrogens floating you can have potassium come out of the cell and hydrogen will go in making it less acidic in the body. They can switch places. •Respiratory system regulates H2CO3: Regulates carbonic acid Kidneys regulate HCO3- by: absorbing bicarb so excrete less or retain bicarb (base) it can even out base to make it less alkalotic. Resorption of HCO3- Making new HCO3- Excretion of H+ ions |
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Which acts fastest?
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•Chemical buffer systems - instantaneously
•Respiratory systems – Can help compensate quickly by increased or decreasing resp rate by depth. •If you increase resp rate then you blow off the CO2 (acid) so more likely to become alkalotic. •Resp slows down you increase acid, so PH decreases and becomes more acidic. •Within minutes •Increase or decrease respiratory rate and depth •Does not completely correct imbalance •Kidney systems – Can make PH normal or close to normal Make take several days Continues until pH is normal or nearly normal |
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Lab values for acid-base balance
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•ph 7.35-7.45
•PaCO2 35-45 mm •PaO2 80-100mm •HCO3 22-26meq •O2 Saturation (% of heme that O2 is attached to) 95-100% •Base Excess or Deficit +/- 2 •Anion gap (Na total &add to total of cl &HCO3 to find anion gap) 8 - 12 mEq/L •Na+ minus (Cl- and HCO3-) •Big gap = problem •Useful in pinpointing cause of imbalance • CO2 is an inverse measurement of BiCarb •Potassium decreases acidity by leaving the cell so hydrogen can go into the cell |
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Imbalances
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Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis |
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Causes
Respiratory acidosis |
Causes
Respiratory acidosis – hypoventilation (too much acid due to resp problems, like COPD because to retain CO2) •Primary respiratory problems- COPD, Any obstruction of airway, pneumonia •Secondary respiratory problems-Drug over dose, by slowing resp rate, or head injury •Clinical manifestations- Confusion, lethargy, headache, dysrythmias, seizures, coma |
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Causes
Respiratory alkalosis – |
Respiratory alkalosis – hyperventilation (breathing fast, become alkalotic
•Primary- Asthma attack, pneumonia, •Secondary- anxiety, salicylate (aspirin) overdose •Clinical manifestations- dizziness, confusion, dysrythmias, seizures, coma: Need to look at resp rate and blood gases and lab values to distinguish between the two. |
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Causes
Metabolic acidosis |
Causes
Metabolic acidosis - being diabetic can cause meta acid from the ketones, breaking down fat because they cannot use the glucose in their body. Also renal failure because kidneys control absorbing bicarb etc.., if they are on hemodialysis there is fluid that will help clean. Another cause of metabolic acidiosis is diarrhea High anion gap don’t worry about Normal anion gap Clinical manifestations- headache, lethargy, confusion, dysrythmias, seizure, coma |
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causes Metabolic alkalosis-
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Metabolic alkalosis- Vomiting can cause because your vomiting up your bodies acid,
also gastric suctioning Clinical manifestations: same |
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Arterial blood gas interpretation
Is pH normal, acidotic, or alkalotic? |
Assess respiratory involvement – PaCO2
Assess metabolic involvement – HCO3- Assess for compensation First look at PH, is is acidotic (below normal range), alkalotic (above normal range?) Next is there resp involvment so look at PaCO2, is it normal? high?(acidotic cuz you are holding on to carbondioxide) Low? (alkalotic) Look at Bicarb, if it is high (it is alkalotic) Look for compensation the body has compensated in some way to bring the body back to normal. |
