Patho Exam 1 Flashcards
what closes once food goes into stomach to prevent acid from entering, culprit for GERD
lower esophageal sphincter
pyloric sphincter closes when ___________
food leaves stomach
what makes the mucus in our stomach? (mucosal blood flow)
prostaglandins
The mucosal barrier protects the gastric mucosa from
auto digestion
what causes GERD?
Decreased pressure in LES or increase in stomach pressures
4 symptoms of GERD
heartburn, epigastric pain, dry cough, laryngitis
3 places ulcer development can occur:
lower esophagus, stomach, duodenum
H. pylori is present in 100% of __________ ulcers and about 70% of patients with _______ ulcers
duodenal, gastric
t/f: H. pylori is the only bacteria known to be “oncogenic”
true
organ of nausea
duodenum
major site of nutrient absorption
small intestine
Bile from the liver and digestive enzymes from the pancreas empty into the __________ to aid in digestion
duodenum
normal potassium level
3.5-5
BIG FLUID and ELECTROLYTE ORGAN (diarrhea)
small intestine
which organ defends against bacteria–normal flora
large bowel
the large bowel produces vitamin ___
K
Peristalsis and movement of feces in the:
large bowel
in the large bowel, _______ triggers peristalsis
Acetylcholine (and serotonin)
if chyme passes through large bowel too rapidly=
diarrhea and potassium depletion
Primary organ of bowel elimination
large intestine
this Extends from the ileocecal valve to the anus
large intestine
functions of large intestine:
Absorption of water, Formation of feces, Expulsion of feces from the body
during peristalsis movements in intestine; Contractions occur every __ to ___ minutes
3 to 12
Peristalsis is under control of the _____________
autonomic nervous system
dark sticky feces (GI Bleed)
melena
fresh bright red blood
hematochezia
Not visible blood
occult blood
examples of Constipating foods:
cheese, lean meats, eggs, pasta
examples of Foods with laxative effect:
fruits and vegetables, bran, chocolate, alcohol, coffee
examples of Gas-producing foods:
onions, cabbage, beans, cauliflower
Delay or difficulty in defecation, present for two or more weeks, sufficient to cause significant distress to the patient
constipation
this Can be a protective response when irritants in the GI tract
diarrhea
normal stool passage
3 per day
Which food is a recommended for an older adult who is constipated?
fruit
Which of the following direct visualization tests uses a long, flexible, fiberoptic-lighted scope to visualize the rectum, colon, and distal small bowel?
colonscopy
Inserted to decompress or drain the stomach of fluid or unwanted stomach contents
nasogastric tube
Used to allow the gastrointestinal tract to rest before or after abdominal surgery to promote healing; Inserted to monitor gastrointestinal bleeding
nasogastric tube
an elderly client has constipation. what diet would be most therapeutic to aid this GI system disorder?
high fiber
increases bulk in the stool, (puts water in) makes stool more formed, safest OTC
bulk-forming laxative- psyllium (Metamucil)
lubricates stool & GI tract or softens stool by lowering surface tension, allows water and fat to be absorbed into stool
surfactant- emollient (colace)
stimulant intestinal mobility and increase about of water and electrolytes within the intestinal lumen
stimulant- bisacodyl (dulcolax)
Passage of loose watery stools or an abnormal increase in the frequency, fluidity and daily volume of stool that is acute or chronic.
diarrhea
Lasts up to one week; usually related to a bacterial, viral or parasitic infection
acute diarrhea
Lasts greater than two weeks; usually related to functional disorder, multiple disease or conditions, medications, food intolerances, intestinal surgery, genetic disorders, or inadequate management of acute diarrhea
chronic diarrhea
an elderly client with an acute onset of multiple episodes of diarrhea for the past 24 hours, is transferred from a long-term care facility to the ER. which nursing diagnoses would the nurse select as highest priority risk for patient?
deficient fluid volume (dehydration)
Alkaline compounds that neutralize stomach acid Indications:
PUD & GERD
Does not stop acid production; react with gastric acid to produce neutral salts
MOA (antacids)
Neutralization of gastric acid and decrease in associated pain with gastritis and healing of gastric ulcers; Promotes secretion of mucus (protective barrier) by stimulating production of Prostaglandins
therapeutic effect of antacides
wait an hour between other drugs and _________ (interactions-antacid can chelate onto another drug and make non effective)
antacids
Rapid acting High ANC (acid -neutralizing capacity) antacid of choice. Liquid form (milk of magnesia). ADVERSE EFFECT: diarrhea ( retention of water in the intestinal lumen)
magnesium hydroxide
buffer against HCL
sodium bicarbonate
patients with renal insufficiency should NOT get
magnesium products
Rapid acting High ANC and long lasting effect. Once considered the ideal antacid but due to concerns with acid rebound (stimulation of acid secretion)
calcium carbonate
Aluminum and calcium products=
constipation
Use with caution with Kidney stones-
calcium products
antacid adhesion to other medication surfaces that are in contact with the antacid - reducing ability for drug to be absorbed
adsorption
inactivation of drug and the formation of insoluble complexes
chelation
with increased absorption of basic drugs and decreased absorption of acidic drugs
increased stomach pH
every alveoli has a ____ ______
capillary membrane
where gas exchange occurs, terminal part of respiratory tract
alvioli
substance around alveoli that allows it to move freely
surfactant
if alveoli collapses, ______ occurs
Atelectasis
Process of obtaining O2 & making it available to
organs/tissues
oxygenation
ability to oxygenate depends on:
PaO2, SaO2
Amount of O2 bound to hemoglobin compared to amount of O2 hemoglobin CAN carry
SaO2
t/f: both SaO2 and SpO2 measure saturation in arterial blood
true
_______ measures O2 saturation of functional AND nonfunctional hgb, while _______ measures ONLY functioning hgb
SaO2, SpO2
Insufficient oxygen in the blood that CAN be measured
hypoxemia
Lack of oxygen available to tissue that CANNOT be measured
hypoxia
Inspiration or expiration; air moves in and out of the lungs
ventilation
Flow of blood to the alveolar capillaries
perfusion
Tendency of lungs to return to normal; elastin fibers; normal = passive
elastic recoil
Product of elastic recoil, Measure of the ease of expansion
compliance
Any obstacle to airflow
resistance
Mucin responsible for trapping & transporting inhaled foreign bodies, secretes mucins
goblet cells
Hair like projections that move microbes & debris out of airways
cilia
2 types of upper respiratory tract infections
rhinovirus or influenza
t/f:
treatment of URI’s treats symptoms but DOES NOT eliminate causative pathogen
true
Inflammatory mediator
histamine
2 Types of histamine receptors:
H1 and H2
smooth muscle contraction & dilation of capillaries
H1
acceleration of heart rate & gastric acid secretion
H2
H1 antagonists:
• Aka H1 blockers
• Known as ”antihistamines”
Prevent release & actions of histamine stored in cells, Do not push histamine already bound; compete for
unoccupied receptors
MOA (antihistamine)
this prevents: Vasodilation
-GI, respiratory, salivary, & lacrimal secretions
-Increased capillary permeability and edema
antihistamine (MOA)
things H1 antagonists work for:
- Nasal & seasonal allergies
• Symptoms of common
cold
• Allergic reactions
• Motion Sickness
• Vertigo
• Sleep aids
• Parkinson’s dx
adverse effects of H1 antagnoists
Drowsiness
• Dry mouth, vision
changes, difficulty
urinating & constipation
(anticholinergic)
nonsedating, Developed to eliminate unwanted
effects of older antihistamines, Work peripherally
2nd generation H1 antagonists
indications: insomnia to motion sickness, Work peripherally and centrally, sedative
1st Generation H1 antagonists
Antihistamines have _______ S/E
- Rest & digest (↑ salivation, lacrimation, urination, diarrhea)
anticholinergic
Anticholinergic Side Effects:
can’t pee, can’t spit, can’t see, can’t shit
what is not for use in asthma, lower respiratory tract dx, at risk for PNA
antihistamines
things to monitor for with antihistamines:
allergic reaction & drug interactions
reason for nasal congestion
Blood vessels that surround nasal sinuses dilate, swelling blocks nasal passageway
a good medication for nasal congestion is Anticholinergics because they
decrease salivation, dry you up
Stimulate the sympathetic nervous
system, aka sympathomimetics
ephedrine
constrict small blood vessels surrounding nasal sinuses, Shrink engorged nasal mucus membranes; relieve stuffiness
ephedrine
Adverse Effects of Adrenergic Nasal Decongestants
Nervousness
Insomnia
Palpitations
tremors
Intranasal Adverse Effects for Adrenergic Nasal Decongestants
Mucosal irritation
Dryness
systemic effects in excessive dosages (HTN, palpitations,
headache, etc)
used to prevent or relieve a cough, suppress cough reflex
antitussive
promotes secretion of sputum by air passages, used to treat coughs
expectorant
Same as opioids
MOA (Non-Opioid Antitussives: Dextromethorphan)
Most common chronic lung diseases with ↑ resistance to airflow d/t airway obstruction & narrowing (problem getting air in and out)
Obstructive Pulmonary Diseases
causes of Chronic Obstructive Pulmonary Disease
cigarette smoking, noxious particles & gases
episodes of recurrent but reversible shortness of breath, Airways of lung (bronchi &
bronchioles) become narrow bc of Bronchospasm, Inflammation, Edema, Production of mucus
asthma
symptoms of asthma attack
wheezing, difficulty breathing
asthma attack becomes medical emergency when they don’t respond to meds
status asthmaticus
pt exposed to known allergens, allergic asthma
extrinsic
2 meds for asthma
-Bronchodilators
-Inhaled corticosteroids
Relax bronchial smooth muscle, Causes dilation of bronchi & bronchioles, used during acute phase of attack
bronchodilators
Beta 1 i located mostly on the ____ and Beta 2 on the ____
heart, lungs
is Beta2 Adrenergic Agonist: Albuterol short or long acting?
short (SABA)
Prevention/relief of bronchospasm
albuterol
Covert drug solutions to mist, Inhaled through facemask or
mouthpiece
nebulizer
Similar to natural steroid hormones in body (glucocorticoids)
corticosteroids
Stabilize membranes of cells that release
bronchoconstriction substances
corticosteroid
obstructed airway, barrel chest, resp, muscles can’t function, Air trapping leads to damaged
alveolar walls
COPD
breakdown of alvioli, Air spaces enlarge d/t
destruction of alveolar wall (no gas exchange/loss of elasticity= air trapped)
Emphysema
excessive mucus production from goblet cells
chronic bronchitis
symptoms of chronic bronchitis
Productive cough, Wheezing, Dyspnea, Hypercapnia & hypoxemia, Pulmonary Hypertension (if
severe), Flat Diaphragm
force exerted by blood against walls of blood vessel
blood pressure
BP and tissue perfusion require ____ and _____ vascular effects
system, local
amount of pressure in arteries during systole, when heart contracts
systolic BP
amount of pressure in arteries during diastole, when heart relaxes
diastolic BP
total blood flow through systemic or pulmonary circulation in 1 minute
cardiac output
average CO
4-8 L/min
what is CO impacted by
HY, contractility, conductivity
amount of blood pumped out of left ventricle with each contraction
stroke volume
average stroke volume
70 ml
how many times heart beats/contracts in one minute
heart rate
less time for filling and perfusion of coronary arteries =
increase in heart rate
impacted by preload, contractility, afterload
Stroke volume
if SV and HR increase, what demand gets higher?
O2
volume of blood stretching the ventricles at the end of diastole,
(end diastolic volume)
THE STRETCH
preload
preload is increased in patients with:
HTN and hypervolemia
preload is decreased in patients with
higher HR and hypovolemia
resistance left ventricle needs to overcome to circulate blood
(occurs during systole)
THE RESISTANCE
afterload
afterload depends on:
size of ventricle, wall tension, arterial BP
afterload is increase in patients with:
hypertension, vasoconstriction
The force of contraction during systole
(impacts CO)
THE SQUEEZE
contractility
inotropic=
contractility
contractility increases because of
epinephrine & norepinephrine from SNS
↑ contractility raises SV by increasing what?
ventricular emptying
Force opposing the movement of blood within the blood vessels
vascular resistance (SVR)
Vascular resistance depends on
diameter of arteries/arterioles
change in diameter =
change in SVR
Arteries narrowed =
resistance to blood flow increased
Arteries dilated =
resistance to blood flow decreased
BP=
(formula)
CO x SVR
is sympathetic nervous a system short or long term mechanism?
short term (seconds)
SNS activation =
(wide vasoconstriction)
↑ BP, HR, contractility
Increases CO & SVR =
increase in BP
epinephrine and norepinephrine =
neurotransmitters
epinephrine and norepinephrine =
neurotransmitters
epinephrine and norepinephrine are released from
SNS
what Activate receptors located throughout body
SNS (neurotransmittors)
(response depends on receptor)
When baroreceptors are stimulated (↑ in BP) =
send inhibitory impulses
baroreceptors are sensitive to
stretching
SNS inhibited=
↓HR, ↓ force of contraction, & vasodilation in peripheral arterioles
If sense a fall in BP, ____ is activated
SNS
baroreceptors become adjusted & recognize BP as the “new normal” =
extended hypertension
Mimic effects of SNS neurotransmitters, stimulate SNS
(alpha and beta receptor sites throughout)
adrenergic
Vascular smooth muscle; heart
Stimulation by NE = constriction
alpha 1 receptor
Vascular smooth muscle; heart
Stimulated by NE & epi = ↑ HR, force of contraction & speed of conduction
Beta 1 receptor
Smooth muscle of coronary blood vessels & lungs
Activated by epi = vasodilation
Beta 2 receptor
Beta1 stimulation will increase:
-Force of contraction (inotropic)
-Heart rate (chronotropic)
-Conduction of cardiac electrical
impulses (dromotropic)
Force of contraction
inotropic
heart rate
chronotropic
Conduction of cardiac electrical impulses
dromotropic
B1 on juxtaglomerular cells of kidney=
Increased renin secretion
alpha 1 ____ arteries
constricts
alpha 2 ____ arteries
dilates
beta 1 ____ heart vessels
constricts
beta 2 _____ lungs
dilates
Released in times of stress, relaxes bronchioles, increase HR and force of contraction
-Contracts blood vessels (keeping BP up)
neurotransmitters and beta receptors
Maintain BP under conditions (pain, stress, & exercise)
SNS
Causes ↑ CO & BP to adjust to O2 demands
SNS
Postural changes =
↓ in BP
vasoconstriction to increase venous return to the heart =
SNS response
If no reaction –> blood flow inadequate =
syncope or dizziness
Short term BP regulation mechanism
cell layer that lines blood vessels
Regulation of vasodilation & vasoconstriction
VASCULAR ENDOTHELIUM
Releases vasoactive substances that dilate or constrict
VASCULAR ENDOTHELIUM
Smoking & diabetes reduce function of _____ cells
endothelial
Kidneys contribute to __ regulation
BP
Control sodium (Na) excretion & extracellular fluid (ECF) volume
renal system
is renal system short or long term mechanism
long term
Na retention =
water retention –> EFC volume ↑
More volume =
↑ venous return to heart & SV
is renin angiotensin aldosterone system (RAAS) short or long term mechanism?
long term
Juxtaglomerular apparatus in kidneys secrete ____
renin
enzyme that converts angiotensinogen to angiotensin 1
renin
renin is secreted if:
↓ BF through kidneys
↓ serum Na concentration
Baroreceptors tell kidneys to release _____
renin
Renin reacts with ______
angiotensinogen (liver enzyme)
Conversion of angiotensinogen to
angiotensin I
Angiotensin I converted to angiotensin II (in the lungs) by ________
angiotensin converting enzyme (ACE)
Angiotensin II =
increases BP
angiotensin II Directly stimulates adrenal cortex to secrete ______
aldosterone
stimulates kidneys to retain sodium & water
aldosterone
Increase in blood volume & osmolarity stimulates release of ____ ______
antidiuretic hormone (ADH)
ADH Increases ECF by reabsorption of water in ______
tubules of kidney
increase of blood volume =
increase of CO and BP
high blood pressure
hypertension
46% of adult/ 75 million in the US have ____
htn
heart disease = ____% of deaths
23.7% of deaths
what can htn cause?
myocardial infarction, stroke, heart failure, renal disease, retinopathy
t/f: SBP increases with age
true
DBP rises until age __; then decreases
55
idiopathic, ↑ BP without a cause
primary hypertension
↑ BP with specific cause that can be identified
secondary hypertension
“silent killer”- “normal” htn symptoms
• Asymptomatic until severe HTN
• Fatigue, dizziness, palpitations, angina,
dyspnea
cardiovascular complications of htn:
-Heart disease
• Coronary artery disease (CAD)
• Left ventricular hypertrophy
• Heart failure
Pharmacological treatment of htn
Decrease volume of circulating blood, Reduce SVR
non-pharmacological treatment of htn
lifestyle changes;
DASh diet, weight loss, avoid tobacco products, sodium reduction, physical activity
for htn, start with
diuretic, sodium channel blockers, ACE or ARB
If NO calcium =
muscles of blood vessels CANNOT contract
Crosses the cell membrane, excitation of heart
calcium/ heart
Cause smooth muscle relaxation, Promotes muscle relaxation -> dilation of coronary arteries
• Decreased BP, SVR & afterload
MOA (calcium channel blocker)
Prevent Ca+ from binding =
muscle relaxation
contradictions of calcium channel blockers:
drug allergy
heart attacks
drug interactions with CCB
grapefruit juice
(CCB wont be metabolized)
Calcium channel blocker pneumonic for its side effects
SHRED
S- slower HR
H-hypotension/headaches
R-reflex tachycardia
E-edema
D-dizziness
CCB: Dihydropyridines “dipines”
amlodipine
CCB: Nondihydropyridines “Non dipines”
diltiazem
Treat HTN because vaso-selective
Dihydropyridines ”dipines”
Used more to treat tachyarrhythmias & vasospasm
Nondihydropyridines
More effect on vasodilation; less effect on heart
dipines
Less effect on vasodilation; MORE effect on heart
non-dipines
1st line drugs for HTN
ACE inhibitor
Reduce vasoconstriction & sodium/H2O retention
Reduce BP by reducing SVR
Prevent breakdown on bradykinin & substance P
MOA (ACE inhibitors)
brings blood to the glomerulus
(Constrict in response to adrenergic stimulation, decreased GFR)
Afferent arteriole
carries blood away from the glomerulus
(Angiotensin 2 constricts arteriole to maintain pressure)
efferent arteriole
Decrease in angiotensin 2 =
vasodilation of kidneys efferent arteriole
vessel carrying blood AWAY from glomerulus is more ____
dilated
ACE inhibitors =
decreased pressure in glomerulus
t/f: ACE inhibitors are good for people with good kidneys, but not for bad kidneys
true
contraindications of ACE inhibitors:
drug allergies, angioedema, baseline potassium > 5, renal artery stenosis
adverse effects of ACE
1st dose hypotensive, hyperkalemia, angioedema, renal impairment
ACE inhibitor drug interacts with
NSAIDS (reduces effect of ACE, renal failure)
Drug that is inactive in its administered form, Must be metabolized to its active form in the body
prodrug
prodrugs are ideal for
liver dysfunction
is catopril a prodrug
no, doesnt need anything to help metabolize it (doesn’t need liver, good for someone with liver failure)
Use ACE inhibitor cautiously in older adults and patients with
renal dysfunction
Block SNS stimulation of beta receptors by competing with norepinephrine & epinephrine
Beta blockers (MOA)
ARB adverse effects:
hypoglycemia (masks symptoms)
will stimulate all beta receptors
if non-selective
decreased contractility & worsening heart failure with BB
heart failure
beta 1 blockers =
cardiac only effects
Relaxes arterial & venous smooth muscle, dilates vessels, Result is decreased preload & SVR
nitroglycerin
