Exam 3 (w5&6) Flashcards
Chest Tube: purpose
Drain whatever is causing lungs to be collapsed that is causing pneumothorax
Tube is placed into plural space
Assessments for chest tube
Go watch youtube video on slide 55/79 in powerpoint
Describe the movement of water in the chest tube
Inspiration = water goes up (water goes down with inspiration if patient on vent)
Expiration = water goes down; always bubbling (water goes up with expiration if patient is on vent)
What is happening if the water seal chamber is always bubbling
Water seal chamber should never constantly be bubbling; if it is, it could be a sign of an air leak, so make sure it is connected to the patient
If you clamp the tubing and the bubbling stops, the leak is coming from the patient. If you clamp the tubing and the bubbling does not stop, the leak of coming from the system
What part of the chest tube system is always bubbling?
suction control chamber (?)
What should the nurse do if the chest tube comes out of the patient?
Put sterile gauze dressing out the hole in the patients chest; only tape it down on 3 sides
What should the nurse do if the pluravac comes disconnected?
The tube coming out of the patient should be put in a bottle/container of sterile saline or water (SHOULD HAVE THIS AT BEDSIDE JUST IN CASE)
Sternal and rib fracture: common cause
MVA - most are benign and treated conservatively
What ribs have the highest mortality if they become fractured and why?
they are closest to the subclavian artery or vein - can lacerate –> bleeding
Sternal and rub fracture: clinical manifestations and assessment
Pain increases with breathing resulting in hypoventilation
crepitus
Sternal and rib fractures: medical and nursing management
Pain management
Do not decrease respiratory drive
Chest binder to decrease pain
What is a common complication of sternal and rub fractures?
Pneumonia related to hypoventilation (slow breathing because it is painful)
What is flail chest?
Blunt chest trauma
Three or more adjacent ribs are fractures in two or more sites resulting in free floating rib segments
Flail chest: clinical manifestations and assessment
Hypoxia and respiratory acidosis
Asymmetrical chest wall movement (no intercostal or diaphragm support)
Flail chest: medical and nursing management
Ventilatory support and pain management Rib plating (surgery; metal put in rib to put back together to decrease complications with ventilator)
Pulmonary contusion: patho
Damage to lung tissues resulting in hemorrhage and edema
Abnormal accumulation of fluid in the interstitial and intra alveolar spaces result from the inflammatory process (leaking proteins change osmotic pressure, capillaries leak fluid which then interferes with gas exchange
Pulmonary contusion: clinical manifestations and assessment
Constant ineffective cough, unable to clear secretions
Hypoxia, respiratory acidosis
Pulmonary contusion: medical and nursing management
Hydration to mobilize secretions
May need antibiotics to treat infection r/t fluid leaking into the interstitial tissue
How can we prevent pulmonary contusions?
Pulmonary hygiene / toileting to prevent
- cough, deep breath, incentive spirometry, chest
- physiotherapy, postural drainage (affected side up)
- Mobilize secretions
- Pain management
What is a cardiac tamponade?
Compression of the heart resulting from fluid or blood within the pericardial sac; compresses ventricles –> decreased CO (hypotension)
High mortality rate
painful
Cardiac tamponade: complications
Narrowing pulse pressure & hypotension (complications)
Cardiac tamponate nursing management
teach to lean forward - Might be able to breath better if they lean forward
cardiac tamponade: cause
direct assault to chest: air bag, baseball bat, etc.
Pneumothorax: patho
Parietal or visceral pleura punctures and pleural space exposed to positive atmosphere pressure
Pneumothorax: clinical manifestations and assessment
Respiratory distress varies
Tracheal alignment (tension: trachea shifts Away from affected side)
Pneumothorax: medical and nursing management
Chest tube
Simple pneumothorax
Spontaneous: rupture of bleb on surface of lung or emphysema
Traumatic pneumothorax
Air escapes from a laceration in lung itself and enters the pleural space
May occur during a procedure (lung biopsy)
Barotrauma from mechanical ventilation
May be accompanied with a hemothorax
Tension pneumothorax
Air that enters the chest can not escape
Each breath increases pressure in the chest
May need decompressed emergently with a needle
Might see trachea deviateion
Put in needle and re-expand that lug
What should the nurse keep in mind about ABC with pneumothorax
circulation trumps airway and breathing because there is bleeding occurring in chest
(IV in, ready for fluid and blood replacement before we fix that airway)
Subcutaneous emphysema: what?
Air escapes into the subcutaneous tissue
Not an emergency unless enters neck area and airway may become compromised (then patient will need trach)
Can happen with any chest trauma
Aspiration: patho
Stomach contents into lung
Ph of stomach destructive to alveoli and capillaries
Aspiration risk factors
Altered level of consciousness
Ng feeding
dysphagia
Aspiration: medical and nursing management
Compensating for absent reflexes
Assessing feeding tube placement
- Xray placement and document where the tube exits the nose and checked every medication or feeding
- Air auscultation & ph EBP remains inconclusive
- Must follow institution protocol
Where should the nurse listen if she believes someone has aspirated?
Right lower lobe
Aspiration: prevention
Prevention = key
Unconscious people –> on side
Tube feed –> bed 35 degrees or higher at all times
COPD: emphysema
abnormal enlargement of the airspaces (alveoli) beyond the terminal bronchioles with destruction of the walls of the alveoli
COPD: chronic bronchitis
presence of cough and sputum production for at least 3 months in each of 2 consecutive years (chronic infection)
What should we keep in mind about tracheostomy suctioning?
only apply suction coming out; sterile; only when needed;
COPD: risk factors
Alpha1-antitrypsin deficiency (genetic link)
Smoking
COPD: diagnosis
hx physical exam PFT
FEV1 lower
How do you calculate pack years?
packs per day x years smoked = pack years
COPD: teaching
Get to quit smoking
Modify teaching around their decision to quit or not
– not going to get 70 year old to quit
COPD (emphysema / chronic bronchitis): clinical manifestations and assessment
a. Easily fatigued
b. Frequent respiratory infections
c. Use of accessory muscles
d. Orthopneic
e. Cor Pulmonale (late in disease)
f. Thin appearance
g. Wheezing
H. Pursed-lip breathing
I. Chronic cough
j. Barrel chest
k. prolonged expiratory time
l. bronchitis - increased sputum
m. nail clubbing
COPD: tripod position
Promotes getting rid of CO2
COPS: RR high 20s-30
patient is in trouble
COPD: management
Education Bronchidilators 1st Inhaled corticosteroids 2nd Pulmonary rehabilitation O2 Surgery
COPD: Bronchodilators
laba (long acting beta adrenergic) lama (long acting muscarinic agent) saba (short acting beta adrenergic) sama ( short acting muscarinic agent) MDI
COPD: corticosteroids
inhaled or Iv
COPD: Roflumilast
?
Go look at slide 71
Tells about bronchidilators for COPD
COPD: IV steroids and steroids in general
Chronic problems –> increase risk of adrenal insufficiency, not abruptly stop
COPD: nutritional concerns
Eating can be very tiring for these individuals
Frequent, small meals that are high in protein
No carb intake because byproduct of carb is co2
COPD: resting energy expenditure
10-15%
COPD: physical activity
Simple, small goals
Minimize weight loss d/t low lung reserve
Asthma: patho
complex and characterized by recurring and variable symptom and airflow obstruction and hyper-responsiveness
Asthma: inflammation is key in underlying feature - how?
leads to recurrent episodes
Asthma: clinical manifestations and assessment
cough, chest tightness, wheezing, dyspnea
Asthma: prevention
Patients should ID triggers and avoid them
Asthma: continuous attack
wheezing not breathing well tight – status asthmaticus (corticosteroids, bronchodilators, IV zanthene such as theophylline (10-20 is correct range)
Function and regulation of hormones
Directly released into blood and go to target tissue to initiate function of that target tissue
hypothalamus - connection
The hypothalamus is the connection between the nervous system and endocrine system. It controls the pituitary system gland which secretes stimulating hormones
Anterior pituitary gland releases what hormones
Growth hormone Follicle stimulating hormone Lutenizing hormone Prolactin Andrenocorticotropic hormone Thyroid stimulating hormine Melanocyte stimulating hormone
Growth hormone
Growth Hormone releasing hormone secreted from hypothalamus to stimulate pituitary to secrete growth hormone (somatotropin) (causes pain
Prolactin
Released by anterior pituitary gland
Control breast milk secretion
Adrenocorticotropic hormone
Controlled by anterior pituitary gland
adrenal stimulating
Melanocyte stimulating hormone
controlled by anterior pituitary glan
skin color
Posterior pituitary gland releases what hormones?
- Vasopressin (ADH) - when released, decrease UOP
2. Oxytocin - uterine contractions during labor
Thyroid gland releases what hormones?
a. TSH (thyrotropin) = pituitary, then to thyroid to release the hormones thyroxing, triiodothyonine, calcitonin
Thyroxine (t4)
released by TSH (thyrotropin) - metabolism
Calcitonin
released by TSH (thyrotropin) - lowers blood calcium and phosphate by pushing calcium back into the bone when someone is hypocalcemic
Where are the parathyroid glands?
Sit on thyroid
Parathyroid hormone releases what hormone?
PTH - regulates serum calcium and phosphate levels
secreted when someone is hypocalcemic
What hormones are released from adrenal cortex
Androgens, mineralcorticoids, glucocorticoids
Androgens
Released by adrenal glands; Sex hormones (mainly male)
Mineralcorticoids
Released by adrenal glands - ex. is aldosterone; regulates electrolytes and metabolism
Glucocorticoids
Released by adrenal glands; example is cortisol - regulates inflammation and glucose metabolism
What hormones are released by the adrenal medulla
Catecholamines (epinephrine and NE)
- fight or flight response
Insulin
Hormone released by the pancreas
Facilitates glucose transport INTO the cells
Glucagon
Released by pancreas
increases BG
stimulates gluconeogenesis
Somatostatin
Released by pancreas
Reduced rate food is absorbed from GI tract
Gerontological considerations: thyroid
Decreased metabolic rate (not as hungry, cold)
Gerontological considerations: parathyroid
Decreased absorption of vitamin D leading to..
Osteoporosis
Gerontological considerations: adrenals
Decreased androgens Decreased glucocorticoids (decreased inflammatory response)
Gerontological considerations: pancreas
Decreased insulin secretion
Decreased cell sensitivity
Gerontological considerations: pituitary
Decreases TSH, ACTH, FSH, LH (stimulating hormones)
What is the main issue with DM
hyperglycemia - goal is to prevent complications by controlling hyperglycemia
Type I Diabetes
Onset any age
Cause: genetics, environmental, immunologic
Pancreas producing little to no insulin
Will need life-long insulin
aka ketosis, DKA
Why are most people diagnosed with Type I diabetes
patient goes to hospital because they developed DKA
Characteristics of type II diabetes: patho
Decrease insulin production
Decrease cell sensitivity
Type 2 diabetes cause
Obesity, genetics and environmental
pancreas = tired
type 2 diabetes management
Oral antidiabetic agents may help
May need insulin (does not require)
May improve with weight loss and diet
Ketosis uncommon
Type 2 diabetes: Hyperglycemic Hyperosmolar Non Ketotic Syndrome
idk
Secondary diabetes: pancreatic diseases
Cancer of pancreas can lead to diabetes dx
medications such as corticosteroids and estrogen containing meds can lead to DM dx
Gestational diabetes
Usually 2 or 3 trimester
Due to hormones secreted by placenta that inhibit the action of insulin
Macrosomia (unusually large babies)
30-40 % of mothers may develop DM II later
All women should be screened 24-28 weeks gestation
Impaired glucose tolerance: oral glucose tolerance
test value between 140 mg/dL (7.7 mmol/L) and 200 mg/dL (11 mmol/L)
Impaired glucose tolerance: impaired fasting glucose
a fasting plasma glucose between 110 mg/dL (6 mmol/L) and 126 mg/dL (7 mmol/L)
Describe what happens to glucose tolerance is someone is on corticosteroids
Glucose tolerance is going to be artificially elevated if someone on corticosteroids
Pathophysiology of diabetes
Insulin produced by the pancreas secreted by the beta cells
Transports and metabolizes glucose for energy
Stimulates storage of glucose as glycogen in the liver and muscle cells
Signals liver cells to stop the release of glucose
Enhances storage of dietary fat in adipose tissue
Accelerates transport of amino acids into cells
Facilitates the transport of potassium into the cells
Inhibits the breakdown of stored glucose, protein, and fat
Insulin secretion
Approximately 50% of the total insulin secreted daily by the pancreas is secreted under basal conditions, and the remainder is in response to meals.
The estimated secretion rate of basal insulin in the average adult (assume a weight of 70 kg) ranges from 18 to 32 units/24 hours
Minutes after eating, the serum insulin level rises, peaking in 3 to 5 minutes and returning to baseline within 2 to 3 hours
To attain glycemic control, nurses may be required to manage insulin drips based upon the secretion rate of basal insulin.
What does the body do if BG gets too low
glucagon, is secreted by the alpha cells
Glucagon stimulates the liver to release stored glucose, thereby increasing the blood sugar.
How do insulin and glucagon work together
insulin promotes hypoglycemia; glucagon promotes hyperglycemia. They work in tandem to maintain a constant level of glucose in the blood.
Why do we get confused when we are hypoglycemic?
Brain does not store supply of glucose for us
We have to have a constant steady supply of BG because our brain does not store it for us why we get confused when we are hypoglycemic
Liver role in diabetes
The liver assists with glucose control by storing glucose in the form of glycogen.
As the level of glucose in the blood begins to drop, the liver produces glucose through the breakdown of glycogen (glycogenolysis)
After 8 to 12 hours without food, the liver forms glucose from the breakdown of noncarbohydrate substances, including amino acids (gluconeogenesis)
Clinical manifestations of diabetes
Polyuria (most common w type 1) Polydipsia (most common w type 1) Polyphagia (most common w type 1) Dehydration Weight loss Fatigue and weakness Numbness and tingling hands and feet (type 2) Vision changes (type 2) Dry skin Wounds that are slow to heal Recurrent infections (particlarily yeast)
Complications of hyperglycemia
Impairs immune function (decreases white blood cell function)
promotes inflammation
increases blood viscosity (increase risk for blood clot)
favors the growth of yeast organisms
associated with changes in the blood vessel walls
- resulting in increased risk for infection
- microvascular and macrovascular complications (eyes –> blind, kidney failure)
- foot ulcers (neuropathy, cant feel)
Criteria for diagnosis of DM
A1c of 6.5% or greateror
Symptoms of diabetes plus casual plasma glucose concentration equal to or greater than 200 mg/dL (11.1 mmol/L). “Casual” is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss.or
Fasting plasma glucose greater than or equal to 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 hours.or
Two-hour postload glucose equal to or greater than 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test. The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.
Gerontological considerations for DM
Almost 27% of people over 65 years of age have diabetes
Older patients with diabetes are likely to have coexisting illnesses
the goals of diabetes treatment may need to be altered when caring for elderly patients
- Quality not quantity
Focus is on quality of life
DM medical management
Nutrition Exercise Monitoring Medication Education
Stress and BG
The stress response results in hyperglycemia because it activates the sympathetic nervous system. The ensuing increase in catecholamines, systemically derived from the adrenal gland or released locally at the level of the liver, increases hepatic glycogenolysis and the release of large quantities of glucose into the bloodstream while inhibiting the release of insulin. Thus, all patients who are stressed are at risk for hyperglycemia.
BG and eating / nutrition
It is important to assess the patient’s blood sugar BEFORE meals when insulin coverage is ordered since the patient’s blood sugars will rise after ingesting food.
Promote eating patterns that help improve glucose, blood pressure, and lipid control.
Tailor therapy to each person’s individual cultural and behavioral needs.
Emphasize the pleasure of eating while changing eating
habits.
Provide practical tools for healthy eating.
Caloric requirements
Carbohydrates
Protein
Alcohol and BG
Alcohol is absorbed before other nutrients
Large amounts can be converted to fats, increasing the risk for DKA
Hypoglycemia and drunk can mask each other
What should the nurse do if she cannot tell if someone is drunk or hypoglycemic
Treat patient like they are hypoglycemic until she knows for certain
Misleading food labels
Foods labeled “sugarless” or “sugar-free” may still provide calories equal to those of the equivalent sugar-containing products if they are made with nutritive sweeteners
Foods labeled “dietetic” still may contain significant amounts of sugar or fat
Read the labels of “health foods”—especially snacks—often contain carbohydrates, such as honey, brown sugar, and corn syrup
Exercise benefits and education for DM
Exercise uses glucose, caution for hypoglycemia (teach about ss)
Should not get implement a big exercise regime after being diagnosed
SS hypoglycemia
Tachycardia, agitation, confusion
Monitoring glucose and keytones
Self Monitoring of Glucose Continuous monitoring (phone apps) Measuring Glycated Hemoglobin Urine Glucose Ketone testing
Insulin therapy: rapid
Meal coverage
Onset = 15 minutes
insulin therapy: short
Regular is the only insulin that can be given IV (regular insulin is a form of short acting)
used for meal coverage
slide 36/50
brush up on insulin types
Insulin sites
Rotate sites but keep in same area
SQ is fastest absorbed because high vol. of vessels
Do not massage sites
Complications from insulin therapy: Local vs systemic allergy
Local = usually NBD Systemic = not allergic to insulin by allergic to the preservatives in it
Insulin lipodystrophy
no clue
Fasting hyperglycemia: Dawn phenomenon
someone who wakes w hyperglycemia
Intervention = give insulin later at night, no snacking before bed
Fasting hyperglycemia: Somogyi effect
morning hyperglycemia because hyperglycemic episode in middle of the night (at 2 or 3 am BG is really low, body responds then you become hyperglycemia.
Intervention = giving long acting or insulin coverage earlier in evening, snack b4 bed
Dawn phenomenon and somogyi effect require what?
middle of night BG checks
Fast hypoglycemia: insulin waning
no idea
Non-insulin anti diabetic agents: sulfonylureas
Sulfonylureas (glipazides)
Stimulate insulin release from pancreas, can cause hypoglycemia
Effective for type II only
These will sulfur antibiotics together increase risk of hypoglycemia
Non Insulin Anti Diabetic Agents: Biguanides
Metformin Nephrotoxic Can cause lactic acidosis Does NOT cause hypoglycemia Discontinue in response to needing contrast dye for diagnostic testing
Non Insulin Anti Diabetic Agents: GLP-1 Agonists SGLT-2 Inhibitors Thiazolidinediones Alpha-Glucosidase Inhibitors Non sulfonylurea Insulin Secretagogues
Did not talk about these not sure if i need to know
What does someone require if they have a pancreas transplant
Lifelong immunosuppressants = at risk for infection
Diabetes: nursing management
Develop a Diabetic Teaching Plan
- Assess readiness to learn
- Determine teaching methods
Implementing the teaching plan
- Teaching experienced patients
- Teaching patients self care
Providing Continuing Care
Acute complications of DM: hypoglycemia
we can over correct hyperglycemia and cause this. We need to know ss and hypoglycemia
Acute Complications of DM: DKA
Causes metabolic acidosis
- body can not use sugar and uses fat instead (?)
- goal = gets BG down
- losing a lot of fluid –> replace (fluids, IV, and hyperkalemia treatment)
Acute Complications: Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)
Type II
Hyperglycemia that is not spilling ketones
Long term complications of DM
Macrovascular Microvascular Diabetic Neuropathy - peripheral and autonomic neuropathies - complications of legs and feets
Renal failure, blindness
What is an example of autonomic neuropathy? And what is a treatment
Gastroparesis - stomach does not mTing
Metaclopromide can promote gastric mTing
Adverse side effect of metaclopromide
Extrapyramidal symptoms
Gigantism
Pituitary tumor
during puberty, our epiphysis on end of bones close NORMALLY - here, they stay open and grow LONGER
Growth hormone issues
Exessive secretion
Occurs pre-puberity
Acromegaly
Pituitary tumor
Occurs post puberty
during puberty, our epiphysis on end of bones close NORMALLY - here, they stay open (?) and grow WIDER
Diabetes insipidus
Pituitary disorder
Not enough ADH (large UOP, hypernatremia, dehydrated)
Diabetes insipidus treatment
vasopressin (should see decrease in UOP), Na restriction, high fluids
SIADH
Pituitary disorder
Syndrome of Inappropriate ADH (decrease UOP, edema, hyponatremia)
SIADH intervention
Declamyacin – increase UOP
Increase NA and strict fluid restriction
Most common surgery for when someone has pituitary tumor? What are important considerations before and after this surgery?
Most common surgery is hypophysectomy (incision in mouth above teeth, clip tumor, put face back to tumor) – MUST KEEP CLEAN TO DECREASE INCISION or patient could get meningitis
After surgery - no oral care bc they will break surgical scar (more opportunity for bacteria) and CSF can leak potential
Hypothyriodism: what? treatment? complication?
Thyroid disorder - cold, fat, slow
Treatment: thyroid replacement
Complication: Myedema –> progress to coma
Priapism
Hypothyroid as infant (mental delays / mentally challenged)
Hyperthyroidism: what, treatment, goal, complication
Thyroid disorder - hot, fast, skinny
Treatment: PTU – suppress thyroid hormone until they get to surgery (will most likely need it)
Goal: get TSH down
Complication: thyroid storm – hypertensive, tachycardic, hot
Considerations for Synthroid
can cause cardiac arrhythmia’s (monitor HR, esp. geriatric); most common A fib
- do not administer when someone having MI (increase metabolic rate, release of catecholamines)
Hyperparathyroidism
Parathyroid Disorders - causes hypercalcemia
Hypoparathyroidism
Parathyroid Disorders
causes hypocalcemia
Things to consider with thyroidectomy
If we take out thyroid gland, parathyroids are disrupted because parathyroid sits on top of it, so after surgery asses pt for hypocalcemia (?)
Assess neck incision and back (blood and gravity)
Assess tracheal is midline (blood can move it)
Pheochromocytoma
adrenal disorder
tumor of adrenal glands, benign take it out
PHEOCHROMOCYTOMA: considerations b4 surgery
- before surgery, get HR and BP under control (Beta blocker, anti htn meds)
PHEOCHROMOCYTOMA: s/s
- causes excessive catecholamine release, HTN, headache , tachycardia
PHEOCHROMOCYTOMA: post op considerations
- in post-op , going to have significant HYPOTENSION problem (fluid replacement, vasopressors)
Addison’s disease
Adrenal disorder
Hypoadrenalism
Not enough cortisol
Cause – daily steroid
Addison’s disease: s/s
hypoglycemia, hypotension, hyperkalemia
Addison’s disease: treatment
IV cortocosteroids
Cushing Disease
Primary Aldosteronism
Adrenal disorders
Go look at these in the endocrine work document
