331 test 3 Flashcards
what disease are considered obstructive lung diseases
Asthma, COPD, chronic bronchitis, and emphysema
upper respiratory infection symptom relief
expectorants, antitussives, nasal decongestants, and anti-histamines
upper respiratory infection symptoms
excessive mucus production and nasal congestion
Empiric therapy
based on symptoms practitioner is making an educated guess with their knowledge and experiences
when histamine attaches to H1 receptors
upper respiratory: Smooth muscle of airway Increased vasodilation Increased vascular permeability Constriction of the bronchioles in airway
histamine does what to parietal cells
directly stimulate parietal cells to increaseacidsecretion
when histamine attaches to H2 receptors
stomach (increases gastric secretions) and heart (increases HR)
histamine is a true
neurohormone
Pepsid targets
H2 receptors
histamine is released in response to
antigen exposure
what are found in the heart and known to release histamine
mast cells
excessive histamine release can lead to
anaphylaxis
histamine inflammatory responses
urticaria, angioedema, pruritus and fever
urticaria
hives
how does histamine produce both hives and agiokedema
dilating the small blood vessels in the skin causing fluid to leak
constant itching can be associated with
high temperatures
vasodilation and increased permeability =
increased body secretions and leads to hypotension and edema
anaphylactic shock
lung constriction, increased body secretions, vasodilation everywhere except in the bronchioles which constrict, increased capillary permeability
Palliative
relieving pain without dealing with the cause of the condition (treating symptoms)
Antiemeticdrugs are
types of chemicals that help ease symptoms of nausea or vomiting. – typically for motion sickness
contraindications of antihistamines
include narrow-angle glaucoma, cardiac disease, kidney disease, hypertension, bronchial asthma, chronic obstructive pulmonary disease, peptic ulcer disease, seizure disorders, benign prostatic hyperplasia, and pregnancy.
why do you want to give antihistamines as early as possible
as early as possible because it will not push already bound histamine off receptors. it competes for receptor sites
when are antihistamines indicated
allergies, vertigo (anti-emetic), insomnia, cough
what do antihistamines do
have anti-emetic effects - ease nausea, sedation, has anticholinergic effects of drying secretion, causes bronchodilator and prevents vasodilation
Diphenhydramine
Benadryl
where does diphenhydramine work
peripherally and centrally
what does diphenhydramine do
antihistamine, anticholinergic, sedative, and anti-emetic
anticholinergic
blocks the neurotransmitter acetylcholine (parasympathetic) in the central and the peripheral nervous system
why treat Parkinson’s with diphenhydramine
its anticholinergic effects help relax the patient
what can diphenhydramine do to older adults
cause hangover effect which puts them at risk for falls
decongestants
shrink engorged mucosa and constrict nasal arterioles
expectorants
decrease the viscosity (thickness) of sputum and increase cough and spit to overall decrease cough in the end
antitussives
cough suppressant
two types of antitussives
opioid (watch for respiratory depression) and non-opioid (might feel numbness in throat of mouth
three types of nasal decongestants
adrenergics (sympathomimetics), which are the largest group; anticholinergics (parasympatholytics), which are somewhat less commonly used; and selected topical corticosteroids (intranasal steroids)
example of decongestant
fluticasone (Flonase)
example of antitussive
codeine (opioid) and benzonatate (Tesselon)
example of expectorant
guaifenesin (mucinex)
different categories of pneumonia
- CAP - community-acquired pneumonia – out in the community anywhere
- HCAP - healthcare-associated pneumonia – pt has extensive interactions with healthcare community – constant contact with healthcare workers
- HAP - Hospital-acquired pneumonia – show signs within 48 hrs of admission into hospital
- VAP - Ventilator-associated pneumonia – pt in ICU who require ventilator support (happens in 9-27% of people on ventilators) – proper oral care of patients can decrease risk immensely
Bacteremia
presence of bacteria in blood
most common nosocomial infection
UTI
risk factors of pneumonia
Immunosuppression
Sedentary – especially in elderly and post op
Underlying chronic heart or lung disease
Atelectasis
complete or partial collapse of the entire lung or area (lobe) of the lung
different things you can see in a chest x ray of the lungs
consolidation, interstitial, nodule, mass, atelectasis
malaise
A general sense of being unwell, often accompanied by fatigue, diffuse pain, or lack of interest in activities.
objective findings with pneumonia
tachycardia, fever, cyanosis, dullness to percussion, inspiratory crackles, and elevated WBC
CXR
chest xray
ABX
antibiotics
if pt presents with pneumonia what type of antibiotics would you start them on?
broad spectrum until blood/sputum cultures come back and pathogen is identified
what do you need to watch out for in a person with pneumonia
bacteremia and sepsis
what needs to be ordered for a person with pneumonia
Chest xray, antibiotics, blood/sputum culture, and supportive therapy
supportive therapy
treat symptoms and prevent organ hypoxia
hypoxia
decreased oxygenation of tissue - An absence of enough oxygen in the tissues to sustain bodily functions.
what can hypoxia lead to
anaerobic metabolism which will increase lactivist acid levels
what does sepsis present as
systemic inflammatory response, vasodilation which leads to low BP, and increased vascular permeability which leads to edema
SIRS
systemic inflammatory response syndrome
pulmonary vascular disorder
disorders that occlude vessels, increase pulmonary vascular resistance, and destroy vascular bed
pulmonary embolism
occlusion of vascular bed in lungs usually from a DVT but can be from foreign body or fat
Pulmonary embolism can be either
embolus with/without infarction
infarction
tissue death due to inadequate blood supply to the affected area
what you need to know during a pulmonary embolism
Extent of Blood flow obstruction
Size of vessel
Why is it there
What is the clot doing
obstruction leads to
pulmonary vasoconstriction which causes pulmonary hypertension
pulmonary embolism with infarction
if its there long enough has the ability to cause tissue death, and the fibrinolytic system does not have the ability to dissolve clot
pulmonary embolism without infarction
embolism still there, fibrinolytic system can still dissolve clot, but getting circulation from other area – such as bronchiole arteries
how can you test for a PE
D-Dimer, BNP, CT scan
D- Dimer
test for pulmonary embolism. less than 250 – if high then we have thrombus (blood clot) formation
BNP
looks at right ventricular pressure
CT scan
help visualize a pulmonary embolism
high V/Q ratio
alveoli are ventilated but not perfused. = dead space
normal V/Q ratio
0.8, 4 (ventilation) / 5 (perfusion) = 0.8
high V/Q ration numbers
V/Q > 0.8, about 4 (ventilation) / 3 (perfusion) = 1.3 - dead space - pulmonary embolus
V/Q low
V/Q < 0.8. 2 (ventilation) / 5 (perfusion) = 0.5 perfusion without ventilation = shunt - atelectasis, asthma, pulmonary edema &PNA
what is the V/Q ration during a pulmonary embolism
high
risk factors of PE
genetics, venous stasis, hyper-coagulability, oral contraceptives
hypoxemia
decreased oxygenation of arterial blood - A low level of oxygen in the blood, inadequate exchange
what can PE cause
SOB, tachypnea, hypoxemia, tachycardia
pulmonary embolism prevention
bed exercises, early ambulation, pneumatic calf compression, prophylactic low-dose anticoagulation
what medication can you give for anticoagulation
low dose lovinox
steps to massive PE
starts with venous stasis, vessel injury, or hyper coagulability which leads to thrombus formation-dislodgment of portion of thrombus- occlusion of part of pulmonary circulation - hypoxic vasoconstriction, decrease surfactant, release of inflammatory substance, pulmonary edema, and atelectasis - signs and symptoms
PAH
pulmonary artery hypertension
cor pulmonale
Right ventricular enlargement. can be hypertrophy, dilation, or both
hypertrophy
the wall itself is enlarged
dilated
stretched chamber
idiopathic pulmonary artery hypertension
endothelial dysfunction due to increase production of vasoconstrictors and decrease production of vasodilators
why does pulmonary artery hypertension occur
increase pressure from LHF, chronic lung disease or hypoxia, chronic thromboembolism
what happens during pulmonary artery hypertension
hypoxic pulmonary artery vasoconstriction and increased pulmonary artery pressure
why does cor pulmonale occur
pulmonary artery hypertension and chronic pressure overload
what happens with cor pulmonale
pulmonic valve murmur and increase systemic venous pressure which causes JVD, hepatosplenomegaly, peripheral edema
how does PAH manifest
fatigue, chest discomfort, tachypnea, and dyspnea
most common post/op pulmonary problems
atelectasis, PNA, pulmonary edema, and PE
hypercapnia
inadequate alveolar ventilation
what can you do to prevent clots on post op patients
early ambulation
acute respiratory “failure”
inadequate gas exchange will be a little acidic with over 50 mm Hg CO2 and less than 60 mmHg of O2
acute respiratory “failure” can either be
hypercapnia or hypoxemia
hypercapnia acute respiratory “failure”
inadequate alveolar ventilation - use ventilator support
hypoxemia acute respiratory “failure”
inadequate exchange - use supplemental oxygen
ventilation
gas/air into and out of the lungs
respiration
exchange of CO2 and O2 during cellular metabolism
what do you need to oxygenate
both adequate ventilation and pefusion
tidal volume
amount of air coming in and going out should be 400-800 ml
is dyspnea subjective or objective
subjective
dyspnea
air hunger and labored breathing
dyspnea turns into objective when you see
pulmonary, cardiac, pain, psychogenic effects
psychogenic
anxiety or disorder
DOE
dyspnea on exertion
orthopnea
Discomfort when breathing while lying down flat
cough
protective reflex can be chronic or acute
acute cough
2-3 weeks
chronic cough
4-6 weeks - chronic bronchitis or lung cancer
kussmauls breathing
when you are trying to compensate when you are metabolic acidosis. increase rate, increase volume, no pause
gasping or agonal breathing
irregular quick inspiration, expiratory pause, severe cerebral hypoxia
cheyne-strokes
when you are dying. alternating deep, shallow, apnea- associated with decrease blood flow to brainstem
apnea
cessation of breath
labored breathing
can either by obstructive or restrictive
large airway labored breathing
decrease rate, increase volume, increase effort, prolonged inspiration and expiration, stridor or audible wheeze
small airway labored breathing
increased rate, decrease volume, increase effort, prolonged expiration and wheezing
hypoventilation
inadequate alveolar ventilation
potential causes of hypoventilation
respiratory depression, neuromuscular disease, trauma or pain, physiological dead space
hypercapnia
air sacs not ventilating properly leads to CO₂ retention, more CO2 production than CO2 removal
hypoventilation can lead to
hypercapnia, respiratory acidosis which can lead to hypoxemia and Altered level of consciousness
neuromuscular disease
conditions that impair the functioning of the muscles. can impact ability to ventilate
physiological dead space
where ventilation should be occurring but its not and example is pulmonary embolism
hyperventilation
excessive alveolar ventilation - blowing off too much CO2- leads to hypocapnia
potential causes of hyperventilation
pain, anxiety, head injury
hypocapnia
more CO2 removal than CO2 production
what can hypocapnia lead to
respiratory alkalosis
hypoventilation and hyperventilation is all based off
metabolic demand
deoxy hemoglobin
desaturated hemoglobin
lack of cyanosis
does not mean oxygenation is normal
O2 sat =
% of Hgb binding sites carrying oxygen
PaO2=
oxygen content of blood
O2 Sat of 90%=
PaO2 of 60 mmHg
clubbing
nail bed hypertrophy due to chronic hypoxemia
cyanosis
desaturated hemoglobin can show peripheral (finger tips) or central (face/mouth)
special circumstance of cyanosis
anemia, carbon monoxide, polycythemia
anemia
not enough Hgb - they will be pale
carbon monoxide cyanosis
Hgb saturated with wrong gas - will have a cherry hue
polycythemia
too many RBC- increased blood viscosity (increase risk of clot) and decreased tissue perfusion
hypoxemic manifestations
cyanosis, confusion, tachycardia, edema, decreased urinary output
FiO2
fraction of inspired air = 21%
if you have hypoxemia that you have
pulmonary issue
mechanism of oxygenation
oxygen delivery to alveoli and diffusion of oxygen from alveoli to blood
how is oxygen delivered to alveoli
inspired air and adequate ventilation
diffusion of oxygen from alveoli to blood
includes V/Q - alveolar ventilation and alveolar perfusion
what do the V and Q stand for in V/Q ratio and what does V/Q overall stand for
V=air entering alveoli (alveolar ventilation)
Q= blood reaching capillaries (alveolar perfusion)
V/Q = ventilation perfusion
widespread tissue dysfunction leads to
organ infarction
two types of shunting
right and left shunting. can be anatomic or ventilation issues
shunt - anatomic issue
deoxygenated blood bypasses the lung and goes right back into the circulation
shunt - ventilation issues
alveoli collapsed - structural issue
most common cause of hypoxemia
an abnormal ventilation perfusion ration
more effort to expand the lungs =
increase work of breathing
restrictive lung disease
decrease lung compliance due to stiff chest wall this causes increase effort to fill lungs, increase respiratory rate, and decrease tidal volume
restrictive lung disease is expected in
geriatric population
will restrictive lung disease have low or high V/Q?
low - can’t get air in - less ventilation - hypoxemia
aspiration most common in
right lung, especially right lower lung
PNA
pneumonia
surfactant
keeps lungs with surface tension - if its disrupted lung can collapse
what does CO2 do to the vessels
vasodilation which causes hypotension
risks that can lead to aspiration
ALOC, seizures, dysphagia, NG tube
what can aspiration lead to
pneumonia, damage to alveolocapillary membranes, surfactant production disrupted and lung collapsed, hypoventilation which can lead to hypercapnia and hypotension
PEEP
positive and expiratory pressure (through ventilation)
prevention of aspiration
semi-fowlers, assessment of swallowing/NG tube, promotility agents, avoid excessive sedation
promotility agents
keep GI mobile
aspiration pneumonitis presentation
choking, cough, dyspnea, fever, wheezing
aspiration pneumonitis treatment
oxygen, PEEP, corticosteroids
aspiration pneumonitis always has the risk of turning into
bacterial pneumonia
atelectasis
collapse of lung tissue
cause of atelectasis
lack of air to hyperventilated alveoli due to surfactant impairment or compression
decrease surfactant production =
increased surface tension
compression
tumor or fluid
atelectasis treatment
deep breathing exercises, IS, position changes, early ambulation, NIPPV
NIPPV
non invasive positive pressure ventilation device
how does atelectasis present
dyspnea, cough, fever, leukocytosis
pulmonary edema
excess water in lung, pink frothy sputum, hypoventilation, hypercapnia
what keeps lungs dry
lymphatic drainage
how does pulmonary edema occur (steps)
left sided heart failure creates backup into lung, pulmonary capillary injury causes increase capillary permeability and decrease surfactant, and lymphatic obstruction causes no removal of excess fluid
ARDS
acute respiratory distress syndrome
causes of pulmonary edema
heart failure, toxic gas, tumor, lung fibrosis, and ARDS
what toxic gases can cause pulmonary edema
chloride, nitrogen dioxide, ammonia
clinical manifestations of pulmonary edema
dyspnea, hypoxemia, increased work of breathing, hypercapnia, crackles and dull percussions
diagnostic criteria from diabetes
HbgA1C more than 6.5%, fating glucose more than 126 mg/dL, 2-hr glucose tolerance above 200 mg/dL, or in crisis with signs and symptoms of hyperglycemia with random glucose above 200 mg/dL
type 1 diabetes
t-cell mediated autoimmune - pancreas failure to produce insulin - secretion - insulin deficiency
type 2 diabetes
you have insulin but insulin receptors do not work. you have a tolerance - action problem - resistance of tissue
FPG
fasting plasma glucose
tests of high risk for diabetes
FPG of 100-125 mg/dL, 2 hr PG 140-199, hgbA1C- 5.7%-6.4%
glycogenolysis
glycogen to glucose
insulin is secreted when
after a meal
the glucose that does not get used up goes to where
the liver
t-cells do what
identify and kill a target, beta cell antigens
insulin
suppresses glucagon secretion
glucagon
promotes glycogenolysis and gluconeogenesis
amylin
beta cell hormone - suppresses glucagon secretion
lack of insulin and lack of glucagon suppression =
hyperglycemia
there is ______ amylin production during type 1
less
t-cell mediated autoimmune
destruction of insulin secreting beta cells, macrophages infiltration of islets, t-cells
what happens when there is a destruction of insulin secreting beta cells
decreased insulin synthesis, hypoinsulinemia, hyperglycemia
how does renal overload happen in type 1 DM
water moves from inside cells into bloodstream following osmotic pull of large glucose molecules, renal threshold for glucose is exceeded and glucose and water spill out, and nutrients are lost
when water moves from inside cells into bloodstream following osmotic pull of large glucose molecules what happens
cellular dehydration and increase in plasma volume
what happens when renal threshold for glucose is exceeded and glucose and water starts spilling out
polyuria and polydipsia
polyphagia
lost nutrients
weight loss with DM1 is due to
initial weight loss is due to osmotic dieresis (fluid loss) and tissue loss
insulin can cause
weight gain through lipogenesis - converts glycogen to fat stores
weight gain from DM1 can cause chronic complications associated with
DM2 such as MI/CVA
diabetes type 1 patient will get what if they do not control their diabetes
metabolic syndrome
warning signs of DM2 linked to increased
CV complications
labs with metabolic syndrome
HDL less than 40 in men or less than 50 in woman, trig over 150 mg/dL, BP over 130/85, FBS over 100, waist bigger than 40 inches men and 35 inches in woman
insulin resistance
during DM II. action problem- suboptimal receptor response to insulin in the liver, muscle, and adipose tissue.
what cells try to compensate during insulin resistance
beta cells try to compensate by producing more insulin . once they are fatigued they will stop working at good which leads to insulin deficiency
risk factors for DMII
genetic factors, sedentary lifestyle, smoking, and poor diet
what do you end up with if you have insulin resistance
hyperglycemia and hyperinsulinemia
insulin deficiency
decrease response of beta cells to hyperglycemia because they are fatigued and less responsive after trying to compensate during insulin resistance
1 contributor to DM2
obesity
what does obesity do to leptin and adiponectin
increases leptin and decreases adiponectin
leptin resistance
promotes over eating and insulin resistance
intra abdominal cytokines
toxic to beta cells and contribute to insulin resistance
incretins
released from GI tract in response to food - increase insulin secretion, decrease glucagon secretion, delay gastric emptying, produce new beta cells, and get broken down by DPP-4
what can intracellular deposits of triglycerides and cholesterol do
changes cellular insulin signaling which decreases tissue’s response to insulin, promotes inflammation, and alters incretins
consequences of hyperglycemia
decreased cognition, neuropathy, cataracts, hypertension, stroke, heart disease, gastroparesis, nephropathy, chronic kidney disease, oxidative stress, infection, cancer, immunosuppression
acute complications of diabetes
hypoglycemia, DKA, and HHNKS
somogyi effect
hypoglycemic episodes during the night and causes a rebound hyperglycemic period in the morning. more common in type 1 DM.
insulin counter regulator hormones
growth hormone, glucagon, epinephrine, cortisol
dawn phenomenon
blood sugar rises with the sun with no hypoglycemia during the night. due to growth hormone released during the night and decreases peripheral glucose uptake
diabetic ketoacidosis
profound deficiency of insulin with increased stress hormones
characteristics to DKA
acidosis, ketonuria, ketonemia, hyperglycemia over 250 mg/dL, tachycardia, dehydrated
what will someones breath smell like if they are in DKA
juicy fruit due to ketones
what type of breath do you usually see in DKA patents
kussmaul
what should you do for someone in DKA
they need hydration, insulin, electrolyte replacement
ketone bodies
produced in liver when fat is broken down for an energy source
gluconeogenesis
metabolic pathway that results in the generation of glucose for the break down of fats
without insulin
fat catabolism occurs and thus ketone bodies develop
what do the accumulation of ketones do to ph
drop it
insulin normally stimulates
lipogenesis and inhibits lipolysis
diabetic ketoacidosis symptoms
Kussmauls, postrural dizziness, decreased CNS, N/V, abdominal pain, polyuria, polydipsia, anorexia, weight loss
HHNKS
server dehydration with loss of electrolytes and high glucose over 600 with enough insulin to prevent ketoacidosis. High osmolarity over 320. normal ph and bicarb
HHNKS is common in what population
geriatric
what is the number one cause of HHNKS
infection
high osmolarity
volume depletion with high concentration
what do you need to do first for people in HHNKS
start on IV fluids then insulin
main goal for pt in HHNKS
rehydration, electrolyte replacement, correct hyperglycemia, treat underlying disease, monitor cardio/pulmonary, renal, and CNS
symptoms of HHNKS
hypotension, hypovolemia, hypoperfusion
glucose toxicity over time does what to our bodies
cataracts, damage nerve conduction, and inhibits perfusion
AGEs
advanced glycation end products
what are AGEs
harmful compounds that are formed when protein or fat combine with sugar in the bloodstream
decrease tissue perfusion can lead to _______ of the capillaries
occlusion of the capillaries which causes hypoxia and ischemia
leading cause of blindness
diabetic retinopathy
macular edema
blurred vision
stages of diabetic retinopathy
- micro aneurysm formation 2. poor perfusion and ischemia 3. neovascularizaition and fibrous tissue formation within retina which may cause retinal detachment
diabetic retinopathy increases your risk for
glaucoma and cataracts
ESRD
end stage renal disease
leading cause of end stage renal disease
diabetes
what four things contribute to kidney injuries
hyperglycemia, advanced glycation end products (AGEs), activation of metabolic pathways, and inflammation
hyperglycemia and high renal blood flow (hyper filtration) lead to
glomerulosclerosis
glomerulosclerosis
changes in the glomerular basement membranes that becomes permeable to proteins which starts to spill out into the urine leads to decrease in filtration and blood flow to kidneys
first manifestation of diabetic renal dysfunction
microalbuminuria
microalbuminuria
protein in urine
Hypoproteinemia
Hypoproteinemia is a condition where there is an abnormally low level of protein in the blood
when seeing microalbuminuria what is happening in our blood
decreasing the amount of protein in out blood - Hypoproteinemia
laster signs of diabetic renal dysfunction
Hypoproteinemia, decrease oncotic pressure, fluid overload, anasarca, HTN
as GFR decreases to less than 10 what type of signs occur
uremic signs - nausea, lethargy, acidosis, anemia, and HTN from having high levels of urea in the blood
a pt with nerve ischemia and demyelination will have
delayed nerve conduction
amyotrophy
weakening of the hip joint and muscle
diabetic neuropathy sensory deficits
footdrop, amyotrophy, temp, and pain
diabetic autonomic neuropathy deficits
delayed gastric emptying, altered bladder function, impotence, orthostatic hypotension, HR variability
steps from healthy tissue to infection in pt with diabetic peripheral neuropathy
healthy tissue capillary damage nerve damage and loss of sensation injury circulation problem and infection
68% of diabetics die from
CAD - coronary artery disease
prevalence of CAD in diabetic patients increase with
the duration but the the severity of diabetes
risk factors for macrovascular disease
HTN, hyperglycemia, hyperlipidemia, and thrombosis
what happens during CAD
increased platelet adhesion, decreased fibrinolysis, and accelerated atherosclerosis
decreased fibrinolysis
more likely to clot
claudication
pain from reduced blood flow during exercise
peripheral vascular disease can lead to what in diabetic patients?
claudication, ulcers, gangrene, osteomyelitis, amputation, and increased morbidity
risk factors or peripheral vascular disease in diabetics
age, duration with DM, genetics, smoking, hyperlipidemia, HTN
important nursing actions for diabetics
teaching, persevere skin integrity, promote nutrition vaccinations and exercise
acute complications of diabetes
extreme fluctuations of blood glucose levels. examples: hypoglycemia, hyperglycemia, DKA, HHNKS
chronic complications of diabetes
damage occurs from hyperglycemia over time. examples: microvascular (eyes, kidneys, and nerves), macrovascualr (CVA,CAD,PVD), and infection
decreased insulin production is a characteristic of
type 1 DM
alpha cells release what?
glucagon
metabolic syndrome is a component if type 1, 2 or both
both
first line drug for type 2 diabetes
metformin (Glucophage)
can metformin be combined with insulin
yes
what does metformin do?
decreases hepatic production of cholesterol, glucose intestinal absorption, and glucose production in liver and increases peripheral glucose uptake and insulin receptor sensitivity
black box warning of metformin
lactic acidosis and renal disease. renal kidney disease
adverse effects of metformin
GI, weight loss, hypoglycemia
signs and symptoms of lactic acidosis
tachypnea, cold/clammy, pain, dizziness, irregular HR
metformin contraindicated in
renal disease. slows down GFR - drug can build up which can lead to lactic acidosis so check creatine levels before
if you have a CT scan with contrast media you should not have
metformin for 48 hrs
sulfonylureas
binds to receptors on beta cells to stimulate release of insulin and decreases glucagon secretion. need a working pancreas for these to work
when should sulfonylureas be given
30 minutes before breakfast. has a rapid onset of action
can you use sulfonylureas in renal patients
yes
can you use sulfonylureas with insulin? what about metformin?
cannot be used with insulin but can be used with metformin
adverse effects of sulfonylureas
hypoglycemia and weight gain
what is an example of a sulfonylureas
glipizide (glucotrol)
Dipeptidyl peptidase IV inhibitors
DPP-IV - inhibits breakdown of incretins
Dipeptidyl peptidase IV inhibitors indication
improve glycemic control for type 2 diabetes
Dipeptidyl peptidase IV inhibitors are associated with
pancreatitis
common side effects of Dipeptidyl peptidase IV inhibitors
URI, headache, and diarrhea
can you use Dipeptidyl peptidase IV inhibitors with insulin
yes
example of Dipeptidyl peptidase IV inhibitors
sitagliptin (Januvia)
incretin mimetics
stimulate insulin production, suppress glucagon, slows gastric emptying, and increased satiety
satiety
declining satisfaction generated by the consumption of a certain type of food
how and when do you give incretin mimetics
subcutaneous injection 60 minutes before meal. once daily
adverse effect of incretin mimetics
thyroid tumors, N/V/D, hemorrhagic/necrotizing pancreatitis
black box warning of incretin mimetics
thyroid carcinoma
example of incretin mimetics
liraglutide (Victoza)
FSBS
finger stick blood sugar
what do you want to watch for with insulin and what do you want to check before hand
watch for hypoglycemia and check figure stick blood sugar (FSBS) before administration
insulin is given
sub cut only! besides regular (can be given IV) fat absorbs chemicals slower than muscle
insulin restores patient’s ability to
metabolize nutrients and convert glycogen to fat stores
insulin onset and duration times
rapid: 15 minutes onset of 3-5 hr duration
short: 30-60 minutes onset with 6-10 hr duration
long: 1-2 hour onset with 24 hr duration
insulin sliding scale
basic and basal bolus
basic sliding scale
FSBS several times a day, delays treatment until hyperglycemia occurs, no research supports it
basal bolus scale
mimics healthy pancreas, basal = long acting, bolus= meal coverage and corrections
severe sign and symptoms of hypoglycemia
hypothermia, seizure, brain damage, and death
hypoglycemia blood glucose level
less than 70 mg/dL
less sever signs on hypoglycemia
shaking, sweating, dizziness, hunger, fast HR, headache, weakness, irritable
no IV access with someone in hypoglycemia
give them sugar tablets
what do you do for a patient with hypoglycemia
give simple carbs, oral glucose, or IV dextrose (D50W)
obstructive lung disease
difficulty exhaling
restrictive lung disease
difficulty getting air in
during asthma what happens to activate immune response
IgE binds to mast cells and crosslinks to antigen
asthma
constriction and obstruction of airways
eosinophils play a role in what with asthma
early (direct tissue injury) and late (release of toxic neuropeptides) inflammatory response
activation of immune response during asthma
vasodilation, mucosal swelling, bronchocontriction
what immunity is involved in asthma
cellular and humoral
what happens with mast cell degranulation
leukotriene synthesis, histamine release, and bradykinin release
what can happen to airways with untreated inflammation
airway remodeling
hyperinflation
alveoli getting bigger from CO2 getting trapped
asthma attack
sudden onset, severe wheezing occurs with inspiration and expiration, dyspnea, nonproductive cough, tachycardia
if asthma attack is not resolved
status asthmaticus
status asthmaticus
decrease expiratory volume, increased hypoxemia and CO2, respiratory acidosis
silent chest
can not hear air movement in lungs. PaCO2 greater than 70 = impending death
most common lung disease
COPD - 4th leading cause of death
risk factors for COPD
smoking, air pollutants, genetic components
COPD characteristics
prolonged expirations, air trapping and pursed lip breathing
chronic bronchitis
hyper secretion of mucus leads to chronic productive cough and ciliary function impaired so mucus in not moving
presentation of chronic bronchitis
bronchospasm, cough, air trapping, decrease tidal volume, hypoventilation, hypercapnia, V/Q mismatch, hypoxemia
chronic bronchitis treatment
bronchodilators, expectorants, antibiotics, steroids, oxygen, and chest physiotherapy
what receptors tell use to breathe
chemoreceptors
chest physiotherapy
airway clearance technique (ACT) to drain the lungs, and may include percussion (clapping), vibration, deep breathing, and huffing or coughing.
chronic bronchitis patients
blue bloaters
pulmonary emphysema
pink puffer
what med is used to treat neuropathy in diabetes patients
gabapentin
long term control of obstructive lung disease
long acting beta 2 agonists, anticholinergics, and leukotriene receptor antagonists
quick relief meds for obstructive lung disease
IV corticosteroids, short acting beta 2 agonist, and anticholinergics
bronchodilating medications
short acting beta 2 agonist, long acting beta 2 agonist, and anticholinergics
immune suppressant medications
leukotriene receptor antagonist and corticosteroids
short acting beta 2 agonist example
albuterol
short acting beta 2 agonist
Relax and dilate airways by stimulating the beta 2- adrenergic receptors located throughout the lungs. Cardiac stimulation and increases diuresis and gastric acid secretion . Dose dependent
short acting beta 2 agonist indication
exercise-induced asthma, acute bronchospasm, bronchitis, emphysema, and other airway obstructions
if albuterol is used too much can
lose beta 2 affinity and stimulate beta 1
side effects of short acting beta 2 agonist
tremors, anxiety, restlessness, hypo/hypertension, dizziness
Long acting beta 2 agonist example
Advair (Fluticasone)
anticholinergic bronchodilator example
Ipratropium (atrovent)
anticholinergic bronchodilator MOA
Block acetylcholine receptors to prevent bronchoconstriction which indirectly causes airway relaxation and dilation.
anticholinergic bronchodilator indication
prevents bronchospasms in chronic bronchitis or emphysema
Leukotriene Receptor Antagonist (LTRAs) example
Montelukast (Singulair)
Leukotriene Receptor Antagonist (LTRAs) MOA
Alleviates asthma symptoms in the lungs by reducing inflammation, prevent smooth muscle contraction of the bronchial airways, decrease mucus secretion, and reduce vascular permeability
most important guardians of the lung
alveolar macrophages
what do alveolar macrophages do?
activate t and B cells, plasma protein systems (inflammation), and pattern recognition receptors (PRRs)
widespread inflammation during pneumonia
damage to bronchial mucosa and capillary membranes which cause neutrophil infiltration which causes lung consolidation
during pneumonia accumulation of exudate (consolidation) leads to
V/Q mismatch, hypoxemia, and hypercapnia
treatment for anaphylactic shock
diphenhydramine, famotidine (Pepsid), epinephrine
emphysema
loss of elastic recoil, decrease expiration, enlargement of acini, alveolar destruction without fibrosis, changes in lung tissue cause obstruction, air trapping
air trapping leads to
V/Q mismatch, hypoxemia, hypercapnia
bull and blebs
air blisters from alveolar destruction without fibrosis in emphysema patients - decreases ventilation
treatment for emphysema patients
inhaled anticholinergics, beta 2 agonist, and avoid steroids until late/severe
