331 test 3 Flashcards
1
Q
what disease are considered obstructive lung diseases
A
Asthma, COPD, chronic bronchitis, and emphysema
2
Q
upper respiratory infection symptom relief
A
expectorants, antitussives, nasal decongestants, and anti-histamines
3
Q
upper respiratory infection symptoms
A
excessive mucus production and nasal congestion
4
Q
Empiric therapy
A
based on symptoms practitioner is making an educated guess with their knowledge and experiences
5
Q
when histamine attaches to H1 receptors
A
upper respiratory: Smooth muscle of airway Increased vasodilation Increased vascular permeability Constriction of the bronchioles in airway
6
Q
histamine does what to parietal cells
A
directly stimulate parietal cells to increaseacidsecretion
7
Q
when histamine attaches to H2 receptors
A
stomach (increases gastric secretions) and heart (increases HR)
8
Q
histamine is a true
A
neurohormone
9
Q
Pepsid targets
A
H2 receptors
10
Q
histamine is released in response to
A
antigen exposure
11
Q
what are found in the heart and known to release histamine
A
mast cells
12
Q
excessive histamine release can lead to
A
anaphylaxis
13
Q
histamine inflammatory responses
A
urticaria, angioedema, pruritus and fever
14
Q
urticaria
A
hives
15
Q
how does histamine produce both hives and agiokedema
A
dilating the small blood vessels in the skin causing fluid to leak
16
Q
constant itching can be associated with
A
high temperatures
17
Q
vasodilation and increased permeability =
A
increased body secretions and leads to hypotension and edema
18
Q
anaphylactic shock
A
lung constriction, increased body secretions, vasodilation everywhere except in the bronchioles which constrict, increased capillary permeability
19
Q
Palliative
A
relieving pain without dealing with the cause of the condition (treating symptoms)
20
Q
Antiemeticdrugs are
A
types of chemicals that help ease symptoms of nausea or vomiting. – typically for motion sickness
21
Q
contraindications of antihistamines
A
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.
22
Q
why do you want to give antihistamines as early as possible
A
as early as possible because it will not push already bound histamine off receptors. it competes for receptor sites
23
Q
when are antihistamines indicated
A
allergies, vertigo (anti-emetic), insomnia, cough
24
Q
what do antihistamines do
A
have anti-emetic effects - ease nausea, sedation, has anticholinergic effects of drying secretion, causes bronchodilator and prevents vasodilation
25
Diphenhydramine
Benadryl
26
where does diphenhydramine work
peripherally and centrally
27
what does diphenhydramine do
antihistamine, anticholinergic, sedative, and anti-emetic
28
anticholinergic
blocks the neurotransmitter acetylcholine (parasympathetic) in the central and the peripheral nervous system
29
why treat Parkinson's with diphenhydramine
its anticholinergic effects help relax the patient
30
what can diphenhydramine do to older adults
cause hangover effect which puts them at risk for falls
31
decongestants
shrink engorged mucosa and constrict nasal arterioles
32
expectorants
decrease the viscosity (thickness) of sputum and increase cough and spit to overall decrease cough in the end
33
antitussives
cough suppressant
34
two types of antitussives
opioid (watch for respiratory depression) and non-opioid (might feel numbness in throat of mouth
35
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)
36
example of decongestant
fluticasone (Flonase)
37
example of antitussive
codeine (opioid) and benzonatate (Tesselon)
38
example of expectorant
guaifenesin (mucinex)
39
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
40
Bacteremia
presence of bacteria in blood
41
most common nosocomial infection
UTI
42
risk factors of pneumonia
Immunosuppression
Sedentary – especially in elderly and post op
Underlying chronic heart or lung disease
43
Atelectasis
complete or partial collapse of the entire lung or area (lobe) of the lung
44
different things you can see in a chest x ray of the lungs
consolidation, interstitial, nodule, mass, atelectasis
45
malaise
A general sense of being unwell, often accompanied by fatigue, diffuse pain, or lack of interest in activities.
46
objective findings with pneumonia
tachycardia, fever, cyanosis, dullness to percussion, inspiratory crackles, and elevated WBC
47
CXR
chest xray
48
ABX
antibiotics
49
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
50
what do you need to watch out for in a person with pneumonia
bacteremia and sepsis
51
what needs to be ordered for a person with pneumonia
Chest xray, antibiotics, blood/sputum culture, and supportive therapy
52
supportive therapy
treat symptoms and prevent organ hypoxia
53
hypoxia
decreased oxygenation of tissue - An absence of enough oxygen in the tissues to sustain bodily functions.
54
what can hypoxia lead to
anaerobic metabolism which will increase lactivist acid levels
55
what does sepsis present as
systemic inflammatory response, vasodilation which leads to low BP, and increased vascular permeability which leads to edema
56
SIRS
systemic inflammatory response syndrome
57
pulmonary vascular disorder
disorders that occlude vessels, increase pulmonary vascular resistance, and destroy vascular bed
58
pulmonary embolism
occlusion of vascular bed in lungs usually from a DVT but can be from foreign body or fat
59
Pulmonary embolism can be either
embolus with/without infarction
60
infarction
tissue death due to inadequate blood supply to the affected area
61
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
62
obstruction leads to
pulmonary vasoconstriction which causes pulmonary hypertension
63
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
64
pulmonary embolism without infarction
embolism still there, fibrinolytic system can still dissolve clot, but getting circulation from other area – such as bronchiole arteries
65
how can you test for a PE
D-Dimer, BNP, CT scan
66
D- Dimer
test for pulmonary embolism. less than 250 – if high then we have thrombus (blood clot) formation
67
BNP
looks at right ventricular pressure
68
CT scan
help visualize a pulmonary embolism
69
high V/Q ratio
alveoli are ventilated but not perfused. = dead space
70
normal V/Q ratio
0.8, 4 (ventilation) / 5 (perfusion) = 0.8
71
high V/Q ration numbers
V/Q > 0.8, about 4 (ventilation) / 3 (perfusion) = 1.3 - dead space - pulmonary embolus
72
V/Q low
V/Q < 0.8. 2 (ventilation) / 5 (perfusion) = 0.5 perfusion without ventilation = shunt - atelectasis, asthma, pulmonary edema &PNA
73
what is the V/Q ration during a pulmonary embolism
high
74
risk factors of PE
genetics, venous stasis, hyper-coagulability, oral contraceptives
75
hypoxemia
decreased oxygenation of arterial blood - A low level of oxygen in the blood, inadequate exchange
76
what can PE cause
SOB, tachypnea, hypoxemia, tachycardia
77
pulmonary embolism prevention
bed exercises, early ambulation, pneumatic calf compression, prophylactic low-dose anticoagulation
78
what medication can you give for anticoagulation
low dose lovinox
79
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
80
PAH
pulmonary artery hypertension
81
cor pulmonale
Right ventricular enlargement. can be hypertrophy, dilation, or both
82
hypertrophy
the wall itself is enlarged
83
dilated
stretched chamber
84
idiopathic pulmonary artery hypertension
endothelial dysfunction due to increase production of vasoconstrictors and decrease production of vasodilators
85
why does pulmonary artery hypertension occur
increase pressure from LHF, chronic lung disease or hypoxia, chronic thromboembolism
86
what happens during pulmonary artery hypertension
hypoxic pulmonary artery vasoconstriction and increased pulmonary artery pressure
87
why does cor pulmonale occur
pulmonary artery hypertension and chronic pressure overload
88
what happens with cor pulmonale
pulmonic valve murmur and increase systemic venous pressure which causes JVD, hepatosplenomegaly, peripheral edema
89
how does PAH manifest
fatigue, chest discomfort, tachypnea, and dyspnea
90
most common post/op pulmonary problems
atelectasis, PNA, pulmonary edema, and PE
91
hypercapnia
inadequate alveolar ventilation
92
what can you do to prevent clots on post op patients
early ambulation
93
acute respiratory "failure"
inadequate gas exchange will be a little acidic with over 50 mm Hg CO2 and less than 60 mmHg of O2
94
acute respiratory "failure" can either be
hypercapnia or hypoxemia
95
hypercapnia acute respiratory "failure"
inadequate alveolar ventilation - use ventilator support
96
hypoxemia acute respiratory "failure"
inadequate exchange - use supplemental oxygen
97
ventilation
gas/air into and out of the lungs
98
respiration
exchange of CO2 and O2 during cellular metabolism
99
what do you need to oxygenate
both adequate ventilation and pefusion
100
tidal volume
amount of air coming in and going out should be 400-800 ml
101
is dyspnea subjective or objective
subjective
102
dyspnea
air hunger and labored breathing
103
dyspnea turns into objective when you see
pulmonary, cardiac, pain, psychogenic effects
104
psychogenic
anxiety or disorder
105
DOE
dyspnea on exertion
106
orthopnea
Discomfort when breathing while lying down flat
107
cough
protective reflex can be chronic or acute
108
acute cough
2-3 weeks
109
chronic cough
4-6 weeks - chronic bronchitis or lung cancer
110
kussmauls breathing
when you are trying to compensate when you are metabolic acidosis. increase rate, increase volume, no pause
111
gasping or agonal breathing
irregular quick inspiration, expiratory pause, severe cerebral hypoxia
112
cheyne-strokes
when you are dying. alternating deep, shallow, apnea- associated with decrease blood flow to brainstem
113
apnea
cessation of breath
114
labored breathing
can either by obstructive or restrictive
115
large airway labored breathing
decrease rate, increase volume, increase effort, prolonged inspiration and expiration, stridor or audible wheeze
116
small airway labored breathing
increased rate, decrease volume, increase effort, prolonged expiration and wheezing
117
hypoventilation
inadequate alveolar ventilation
118
potential causes of hypoventilation
respiratory depression, neuromuscular disease, trauma or pain, physiological dead space
119
hypercapnia
air sacs not ventilating properly leads to CO₂ retention, more CO2 production than CO2 removal
120
hypoventilation can lead to
hypercapnia, respiratory acidosis which can lead to hypoxemia and Altered level of consciousness
121
neuromuscular disease
conditions that impair the functioning of the muscles. can impact ability to ventilate
122
physiological dead space
where ventilation should be occurring but its not and example is pulmonary embolism
123
hyperventilation
excessive alveolar ventilation - blowing off too much CO2- leads to hypocapnia
124
potential causes of hyperventilation
pain, anxiety, head injury
125
hypocapnia
more CO2 removal than CO2 production
126
what can hypocapnia lead to
respiratory alkalosis
127
hypoventilation and hyperventilation is all based off
metabolic demand
128
deoxy hemoglobin
desaturated hemoglobin
129
lack of cyanosis
does not mean oxygenation is normal
130
O2 sat =
% of Hgb binding sites carrying oxygen
131
PaO2=
oxygen content of blood
132
O2 Sat of 90%=
PaO2 of 60 mmHg
133
clubbing
nail bed hypertrophy due to chronic hypoxemia
134
cyanosis
desaturated hemoglobin can show peripheral (finger tips) or central (face/mouth)
135
special circumstance of cyanosis
anemia, carbon monoxide, polycythemia
136
anemia
not enough Hgb - they will be pale
137
carbon monoxide cyanosis
Hgb saturated with wrong gas - will have a cherry hue
138
polycythemia
too many RBC- increased blood viscosity (increase risk of clot) and decreased tissue perfusion
139
hypoxemic manifestations
cyanosis, confusion, tachycardia, edema, decreased urinary output
140
FiO2
fraction of inspired air = 21%
141
if you have hypoxemia that you have
pulmonary issue
142
mechanism of oxygenation
oxygen delivery to alveoli and diffusion of oxygen from alveoli to blood
143
how is oxygen delivered to alveoli
inspired air and adequate ventilation
144
diffusion of oxygen from alveoli to blood
includes V/Q - alveolar ventilation and alveolar perfusion
145
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
146
widespread tissue dysfunction leads to
organ infarction
147
two types of shunting
right and left shunting. can be anatomic or ventilation issues
148
shunt - anatomic issue
deoxygenated blood bypasses the lung and goes right back into the circulation
149
shunt - ventilation issues
alveoli collapsed - structural issue
150
most common cause of hypoxemia
an abnormal ventilation perfusion ration
151
more effort to expand the lungs =
increase work of breathing
152
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
153
restrictive lung disease is expected in
geriatric population
154
will restrictive lung disease have low or high V/Q?
low - can't get air in - less ventilation - hypoxemia
155
aspiration most common in
right lung, especially right lower lung
156
PNA
pneumonia
157
surfactant
keeps lungs with surface tension - if its disrupted lung can collapse
158
what does CO2 do to the vessels
vasodilation which causes hypotension
159
risks that can lead to aspiration
ALOC, seizures, dysphagia, NG tube
160
what can aspiration lead to
pneumonia, damage to alveolocapillary membranes, surfactant production disrupted and lung collapsed, hypoventilation which can lead to hypercapnia and hypotension
161
PEEP
positive and expiratory pressure (through ventilation)
162
prevention of aspiration
semi-fowlers, assessment of swallowing/NG tube, promotility agents, avoid excessive sedation
163
promotility agents
keep GI mobile
164
aspiration pneumonitis presentation
choking, cough, dyspnea, fever, wheezing
165
aspiration pneumonitis treatment
oxygen, PEEP, corticosteroids
166
aspiration pneumonitis always has the risk of turning into
bacterial pneumonia
167
atelectasis
collapse of lung tissue
168
cause of atelectasis
lack of air to hyperventilated alveoli due to surfactant impairment or compression
169
decrease surfactant production =
increased surface tension
170
compression
tumor or fluid
171
atelectasis treatment
deep breathing exercises, IS, position changes, early ambulation, NIPPV
172
NIPPV
non invasive positive pressure ventilation device
173
how does atelectasis present
dyspnea, cough, fever, leukocytosis
174
pulmonary edema
excess water in lung, pink frothy sputum, hypoventilation, hypercapnia
175
what keeps lungs dry
lymphatic drainage
176
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
177
ARDS
acute respiratory distress syndrome
178
causes of pulmonary edema
heart failure, toxic gas, tumor, lung fibrosis, and ARDS
179
what toxic gases can cause pulmonary edema
chloride, nitrogen dioxide, ammonia
180
clinical manifestations of pulmonary edema
dyspnea, hypoxemia, increased work of breathing, hypercapnia, crackles and dull percussions
181
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
182
type 1 diabetes
t-cell mediated autoimmune - pancreas failure to produce insulin - secretion - insulin deficiency
183
type 2 diabetes
you have insulin but insulin receptors do not work. you have a tolerance - action problem - resistance of tissue
184
FPG
fasting plasma glucose
185
tests of high risk for diabetes
FPG of 100-125 mg/dL, 2 hr PG 140-199, hgbA1C- 5.7%-6.4%
186
glycogenolysis
glycogen to glucose
187
insulin is secreted when
after a meal
188
the glucose that does not get used up goes to where
the liver
189
t-cells do what
identify and kill a target, beta cell antigens
190
insulin
suppresses glucagon secretion
191
glucagon
promotes glycogenolysis and gluconeogenesis
192
amylin
beta cell hormone - suppresses glucagon secretion
193
lack of insulin and lack of glucagon suppression =
hyperglycemia
194
there is ______ amylin production during type 1
less
195
t-cell mediated autoimmune
destruction of insulin secreting beta cells, macrophages infiltration of islets, t-cells
196
what happens when there is a destruction of insulin secreting beta cells
decreased insulin synthesis, hypoinsulinemia, hyperglycemia
197
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
198
when water moves from inside cells into bloodstream following osmotic pull of large glucose molecules what happens
cellular dehydration and increase in plasma volume
199
what happens when renal threshold for glucose is exceeded and glucose and water starts spilling out
polyuria and polydipsia
200
polyphagia
lost nutrients
201
weight loss with DM1 is due to
initial weight loss is due to osmotic dieresis (fluid loss) and tissue loss
202
insulin can cause
weight gain through lipogenesis - converts glycogen to fat stores
203
weight gain from DM1 can cause chronic complications associated with
DM2 such as MI/CVA
204
diabetes type 1 patient will get what if they do not control their diabetes
metabolic syndrome
205
warning signs of DM2 linked to increased
CV complications
206
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
207
insulin resistance
during DM II. action problem- suboptimal receptor response to insulin in the liver, muscle, and adipose tissue.
208
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
209
risk factors for DMII
genetic factors, sedentary lifestyle, smoking, and poor diet
210
what do you end up with if you have insulin resistance
hyperglycemia and hyperinsulinemia
211
insulin deficiency
decrease response of beta cells to hyperglycemia because they are fatigued and less responsive after trying to compensate during insulin resistance
212
#1 contributor to DM2
obesity
213
what does obesity do to leptin and adiponectin
increases leptin and decreases adiponectin
214
leptin resistance
promotes over eating and insulin resistance
215
intra abdominal cytokines
toxic to beta cells and contribute to insulin resistance
216
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
217
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
218
consequences of hyperglycemia
decreased cognition, neuropathy, cataracts, hypertension, stroke, heart disease, gastroparesis, nephropathy, chronic kidney disease, oxidative stress, infection, cancer, immunosuppression
219
acute complications of diabetes
hypoglycemia, DKA, and HHNKS
220
somogyi effect
hypoglycemic episodes during the night and causes a rebound hyperglycemic period in the morning. more common in type 1 DM.
221
insulin counter regulator hormones
growth hormone, glucagon, epinephrine, cortisol
222
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
223
diabetic ketoacidosis
profound deficiency of insulin with increased stress hormones
224
characteristics to DKA
acidosis, ketonuria, ketonemia, hyperglycemia over 250 mg/dL, tachycardia, dehydrated
225
what will someones breath smell like if they are in DKA
juicy fruit due to ketones
226
what type of breath do you usually see in DKA patents
kussmaul
227
what should you do for someone in DKA
they need hydration, insulin, electrolyte replacement
228
ketone bodies
produced in liver when fat is broken down for an energy source
229
gluconeogenesis
metabolic pathway that results in the generation of glucose for the break down of fats
230
without insulin
fat catabolism occurs and thus ketone bodies develop
231
what do the accumulation of ketones do to ph
drop it
232
insulin normally stimulates
lipogenesis and inhibits lipolysis
233
diabetic ketoacidosis symptoms
Kussmauls, postrural dizziness, decreased CNS, N/V, abdominal pain, polyuria, polydipsia, anorexia, weight loss
234
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
235
HHNKS is common in what population
geriatric
236
what is the number one cause of HHNKS
infection
237
high osmolarity
volume depletion with high concentration
238
what do you need to do first for people in HHNKS
start on IV fluids then insulin
239
main goal for pt in HHNKS
rehydration, electrolyte replacement, correct hyperglycemia, treat underlying disease, monitor cardio/pulmonary, renal, and CNS
240
symptoms of HHNKS
hypotension, hypovolemia, hypoperfusion
241
glucose toxicity over time does what to our bodies
cataracts, damage nerve conduction, and inhibits perfusion
242
AGEs
advanced glycation end products
243
what are AGEs
harmful compounds that are formed when protein or fat combine with sugar in the bloodstream
244
decrease tissue perfusion can lead to _______ of the capillaries
occlusion of the capillaries which causes hypoxia and ischemia
245
leading cause of blindness
diabetic retinopathy
246
macular edema
blurred vision
247
stages of diabetic retinopathy
1. micro aneurysm formation 2. poor perfusion and ischemia 3. neovascularizaition and fibrous tissue formation within retina which may cause retinal detachment
248
diabetic retinopathy increases your risk for
glaucoma and cataracts
249
ESRD
end stage renal disease
250
leading cause of end stage renal disease
diabetes
251
what four things contribute to kidney injuries
hyperglycemia, advanced glycation end products (AGEs), activation of metabolic pathways, and inflammation
252
hyperglycemia and high renal blood flow (hyper filtration) lead to
glomerulosclerosis
253
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
254
first manifestation of diabetic renal dysfunction
microalbuminuria
255
microalbuminuria
protein in urine
256
Hypoproteinemia
Hypoproteinemia is a condition where there is an abnormally low level of protein in the blood
257
when seeing microalbuminuria what is happening in our blood
decreasing the amount of protein in out blood - Hypoproteinemia
258
laster signs of diabetic renal dysfunction
Hypoproteinemia, decrease oncotic pressure, fluid overload, anasarca, HTN
259
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
260
a pt with nerve ischemia and demyelination will have
delayed nerve conduction
261
amyotrophy
weakening of the hip joint and muscle
262
diabetic neuropathy sensory deficits
footdrop, amyotrophy, temp, and pain
263
diabetic autonomic neuropathy deficits
delayed gastric emptying, altered bladder function, impotence, orthostatic hypotension, HR variability
264
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
```
265
68% of diabetics die from
CAD - coronary artery disease
266
prevalence of CAD in diabetic patients increase with
the duration but the the severity of diabetes
267
risk factors for macrovascular disease
HTN, hyperglycemia, hyperlipidemia, and thrombosis
268
what happens during CAD
increased platelet adhesion, decreased fibrinolysis, and accelerated atherosclerosis
269
decreased fibrinolysis
more likely to clot
270
claudication
pain from reduced blood flow during exercise
271
peripheral vascular disease can lead to what in diabetic patients?
claudication, ulcers, gangrene, osteomyelitis, amputation, and increased morbidity
272
risk factors or peripheral vascular disease in diabetics
age, duration with DM, genetics, smoking, hyperlipidemia, HTN
273
important nursing actions for diabetics
teaching, persevere skin integrity, promote nutrition vaccinations and exercise
274
acute complications of diabetes
extreme fluctuations of blood glucose levels. examples: hypoglycemia, hyperglycemia, DKA, HHNKS
275
chronic complications of diabetes
damage occurs from hyperglycemia over time. examples: microvascular (eyes, kidneys, and nerves), macrovascualr (CVA,CAD,PVD), and infection
276
decreased insulin production is a characteristic of
type 1 DM
277
alpha cells release what?
glucagon
278
metabolic syndrome is a component if type 1, 2 or both
both
279
first line drug for type 2 diabetes
metformin (Glucophage)
280
can metformin be combined with insulin
yes
281
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
282
black box warning of metformin
lactic acidosis and renal disease. renal kidney disease
283
adverse effects of metformin
GI, weight loss, hypoglycemia
284
signs and symptoms of lactic acidosis
tachypnea, cold/clammy, pain, dizziness, irregular HR
285
metformin contraindicated in
renal disease. slows down GFR - drug can build up which can lead to lactic acidosis so check creatine levels before
286
if you have a CT scan with contrast media you should not have
metformin for 48 hrs
287
sulfonylureas
binds to receptors on beta cells to stimulate release of insulin and decreases glucagon secretion. need a working pancreas for these to work
288
when should sulfonylureas be given
30 minutes before breakfast. has a rapid onset of action
289
can you use sulfonylureas in renal patients
yes
290
can you use sulfonylureas with insulin? what about metformin?
cannot be used with insulin but can be used with metformin
291
adverse effects of sulfonylureas
hypoglycemia and weight gain
292
what is an example of a sulfonylureas
glipizide (glucotrol)
293
Dipeptidyl peptidase IV inhibitors
DPP-IV - inhibits breakdown of incretins
294
Dipeptidyl peptidase IV inhibitors indication
improve glycemic control for type 2 diabetes
295
Dipeptidyl peptidase IV inhibitors are associated with
pancreatitis
296
common side effects of Dipeptidyl peptidase IV inhibitors
URI, headache, and diarrhea
297
can you use Dipeptidyl peptidase IV inhibitors with insulin
yes
298
example of Dipeptidyl peptidase IV inhibitors
sitagliptin (Januvia)
299
incretin mimetics
stimulate insulin production, suppress glucagon, slows gastric emptying, and increased satiety
300
satiety
declining satisfaction generated by the consumption of a certain type of food
301
how and when do you give incretin mimetics
subcutaneous injection 60 minutes before meal. once daily
302
adverse effect of incretin mimetics
thyroid tumors, N/V/D, hemorrhagic/necrotizing pancreatitis
303
black box warning of incretin mimetics
thyroid carcinoma
304
example of incretin mimetics
liraglutide (Victoza)
305
FSBS
finger stick blood sugar
306
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
307
insulin is given
sub cut only! besides regular (can be given IV) fat absorbs chemicals slower than muscle
308
insulin restores patient's ability to
metabolize nutrients and convert glycogen to fat stores
309
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
310
insulin sliding scale
basic and basal bolus
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basic sliding scale
FSBS several times a day, delays treatment until hyperglycemia occurs, no research supports it
312
basal bolus scale
mimics healthy pancreas, basal = long acting, bolus= meal coverage and corrections
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severe sign and symptoms of hypoglycemia
hypothermia, seizure, brain damage, and death
314
hypoglycemia blood glucose level
less than 70 mg/dL
315
less sever signs on hypoglycemia
shaking, sweating, dizziness, hunger, fast HR, headache, weakness, irritable
316
no IV access with someone in hypoglycemia
give them sugar tablets
317
what do you do for a patient with hypoglycemia
give simple carbs, oral glucose, or IV dextrose (D50W)
318
obstructive lung disease
difficulty exhaling
319
restrictive lung disease
difficulty getting air in
320
during asthma what happens to activate immune response
IgE binds to mast cells and crosslinks to antigen
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asthma
constriction and obstruction of airways
322
eosinophils play a role in what with asthma
early (direct tissue injury) and late (release of toxic neuropeptides) inflammatory response
323
activation of immune response during asthma
vasodilation, mucosal swelling, bronchocontriction
324
what immunity is involved in asthma
cellular and humoral
325
what happens with mast cell degranulation
leukotriene synthesis, histamine release, and bradykinin release
326
what can happen to airways with untreated inflammation
airway remodeling
327
hyperinflation
alveoli getting bigger from CO2 getting trapped
328
asthma attack
sudden onset, severe wheezing occurs with inspiration and expiration, dyspnea, nonproductive cough, tachycardia
329
if asthma attack is not resolved
status asthmaticus
330
status asthmaticus
decrease expiratory volume, increased hypoxemia and CO2, respiratory acidosis
331
silent chest
can not hear air movement in lungs. PaCO2 greater than 70 = impending death
332
most common lung disease
COPD - 4th leading cause of death
333
risk factors for COPD
smoking, air pollutants, genetic components
334
COPD characteristics
prolonged expirations, air trapping and pursed lip breathing
335
chronic bronchitis
hyper secretion of mucus leads to chronic productive cough and ciliary function impaired so mucus in not moving
336
presentation of chronic bronchitis
bronchospasm, cough, air trapping, decrease tidal volume, hypoventilation, hypercapnia, V/Q mismatch, hypoxemia
337
chronic bronchitis treatment
bronchodilators, expectorants, antibiotics, steroids, oxygen, and chest physiotherapy
338
what receptors tell use to breathe
chemoreceptors
339
chest physiotherapy
airway clearance technique (ACT) to drain the lungs, and may include percussion (clapping), vibration, deep breathing, and huffing or coughing.
340
chronic bronchitis patients
blue bloaters
341
pulmonary emphysema
pink puffer
342
what med is used to treat neuropathy in diabetes patients
gabapentin
343
long term control of obstructive lung disease
long acting beta 2 agonists, anticholinergics, and leukotriene receptor antagonists
344
quick relief meds for obstructive lung disease
IV corticosteroids, short acting beta 2 agonist, and anticholinergics
345
bronchodilating medications
short acting beta 2 agonist, long acting beta 2 agonist, and anticholinergics
346
immune suppressant medications
leukotriene receptor antagonist and corticosteroids
347
short acting beta 2 agonist example
albuterol
348
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
349
short acting beta 2 agonist indication
exercise-induced asthma, acute bronchospasm, bronchitis, emphysema, and other airway obstructions
350
if albuterol is used too much can
lose beta 2 affinity and stimulate beta 1
351
side effects of short acting beta 2 agonist
tremors, anxiety, restlessness, hypo/hypertension, dizziness
352
Long acting beta 2 agonist example
Advair (Fluticasone)
353
anticholinergic bronchodilator example
Ipratropium (atrovent)
354
anticholinergic bronchodilator MOA
Block acetylcholine receptors to prevent bronchoconstriction which indirectly causes airway relaxation and dilation.
355
anticholinergic bronchodilator indication
prevents bronchospasms in chronic bronchitis or emphysema
356
Leukotriene Receptor Antagonist (LTRAs) example
Montelukast (Singulair)
357
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
358
most important guardians of the lung
alveolar macrophages
359
what do alveolar macrophages do?
activate t and B cells, plasma protein systems (inflammation), and pattern recognition receptors (PRRs)
360
widespread inflammation during pneumonia
damage to bronchial mucosa and capillary membranes which cause neutrophil infiltration which causes lung consolidation
361
during pneumonia accumulation of exudate (consolidation) leads to
V/Q mismatch, hypoxemia, and hypercapnia
362
treatment for anaphylactic shock
diphenhydramine, famotidine (Pepsid), epinephrine
363
emphysema
loss of elastic recoil, decrease expiration, enlargement of acini, alveolar destruction without fibrosis, changes in lung tissue cause obstruction, air trapping
364
air trapping leads to
V/Q mismatch, hypoxemia, hypercapnia
365
bull and blebs
air blisters from alveolar destruction without fibrosis in emphysema patients - decreases ventilation
366
treatment for emphysema patients
inhaled anticholinergics, beta 2 agonist, and avoid steroids until late/severe
