UE: POWERPOINT
PURPLE= Notes from Patho Book
Black: Notes from Tutoring
Study Guide - NRS 306 Midterm Examination
1. Structure and Function of the Cardiovascular System – Patient Education regarding Principles of Cardiac
Function
Patient Education:
o Take diuretics in the early morning and early afternoon
o Restrict fluid and sodium as instructed
o Regulate potassium intake as instructed to prevent high or low
potassium levels
o A dietician can help with menu planning
o Check daily weight at the same time and notify the provider for a
weight gain of 2 lbs. in 24 hr. or 5 lb. in 1 week.
o Schedule regular follow up visits with the provider
o Obtain the pneumococcal and yearly influenza vaccines.
2. Structure and Function of the Cardiovascular System – Principles of
Blood Flow & Evaluation of Postural Hypotension, Heart Valves, Venous
Valves
Orthostatic Hypertension (Postural Hypotension)
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Abnormal drop in blood pressure on assumption of the standing
position
“Sustained reduction in systolic pressure of at least 20 mmHg or
more or diastolic blood pressure of 10 mm Hg within 3 minutes of standing or head-up tilt on a tilt
table to at least 60 degrees”
Etiology
 Age related
Pathogenesis
Diagnosis and treatment: BNP Beta Natriuretic
Peptide
Causative Factors of Orthostatic
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Hypotension
Fluid deficit
Medications
Aging
Defective function of ANS
Effects of immobility
The heart has 4 chambers, 2 upper chambers (atria) and 2 lower
chambers (ventricles). Blood passes through a valve before leaving each
chamber of the heart. The valves prevent the backward flow of blood.
Valves are actually flaps (leaflets) that act as one-way inlets for blood
coming into a ventricle and one-way outlets for blood leaving a
ventricle. Normal valves have 3 flaps (leaflets), except the mitral valve. It
only has 2 flaps.
The 4 heart valves are:
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Tricuspid valve. This valve is located between the right atrium and the
right ventricle.
Pulmonary valve. The pulmonary valve is located between the right
ventricle and the pulmonary artery.
Mitral valve. This valve is located between the left atrium and the left
ventricle. It has only 2 leaflets.
Aortic valve. The aortic valve is located between the left ventricle and the aorta.
How do the heart valves work?

As the heart muscle contracts and relaxes, the valves open and shut. This lets blood flow into the
ventricles and atria at alternate times. Here is a step-by-step description of how the valves work
normally in the left ventricle:

When the left ventricle relaxes, the aortic valve closes, and the mitral valve opens. This lets blood flow
from the left atrium into the left ventricle.

The left atrium contracts. This lets even more blood to flow into the left ventricle.

When the left ventricle contracts, the mitral valve closes, and the aortic valve opens. This is so blood
flows into the aorta and out to the rest of the body.

While the left ventricle is relaxing, the right ventricle also relaxes. This causes the pulmonary valve to
close and the tricuspid valve to open. This lets blood flow into the right ventricle that was returned to the
right atrium from the body.

When the left ventricle contracts, the right ventricle also contracts. This causes the pulmonary valve to
open and the tricuspid valve to close. Blood flows out from the right ventricle to the lungs before it is
returned to the left atrium as fresh, oxygenated blood.
Venous valves (one way, blood return, prevent clots)

Valves in the veins of extremities prevent retrograde flow. With the help of skeletal muscles that
surround and compress leg veins, blood is moved to the heart through one-way valves. This
action is known as the venous or muscle pump. There are no valves in abdominal or thoracic
veins, so pressure changes in these cavities cause venous blood flow in these veins.
3. Structure and Function of the Cardiovascular System – Echocardiogram Interpretation of Result
Echocardiogram:


The echocardiogram is a widely used method of evaluating pericardial effusion. The ECG
often reveals nonspecific T-wave changes and low QRS voltage
Useful for determining ventricular dimensions and valve movements, obtaining data on
the movement of the LV wall and septum, estimating diastolic and systolic volumes, and
viewing motions during systole and diastole.
Ejection Fraction
During diastole, ventricular volume increases to 120 mL (end-diastolic volume). At
the end of systole, 40 to 50 mL of blood (end-systolic volume) remains in the
ventricles (see Fig. 25-8). The difference between end-diastolic and end-systolic
volumes is the stroke volume (SV). The ejection fraction (SV divided by enddiastolic volume) is the percentage of end-diastolic volume ejected during systole.
Left ventricular ejection fraction (normally about 55% to 75% when determined by
echocardiography or angiocardiography) may be used to evaluate the prognosis of
people with various heart diseases
Normal ejection fraction: 55-70%
4. Disorders of Blood Flow – Arterial Occlusion vs. Venous Occlusion vs Aneurysm
Aneurysms
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Abnormal localized dilation of a blood vessel
Can occur in veins or arteries
o Types of Aneurysms #1
 Berry aneurysm
 Most often found in the circle of Willis in the brain circulation
 Consist of a small, spherical vessel dilation
 Fusiform and saccular aneurysms
 Most found in the thoracic and abdominal aorta
 Characterized by gradual and progressive enlargement of the aorta
 Types of Aneurysm # 2
 Acute, life threatening
 Involves hemorrhage into the vessel wall with longitudinal tearing
(dissection) of the vessel wall to form a blood-filled channel.
Aortic Dissection (Dissecting Aneurysm)
o Acute, life-threatening condition.
o Hemorrhage into the vessel wall with longitudinal tearing of the vessel wall to form a
blood-filled channel (see Figure 26-16)
o Etiology and pathogenesis
o Clinical manifestations
o Diagnosis and treatment
Venous Occlusion

Veins are blood vessels that return blood to the heart. Venous occlusion describes a condition in which a
vein becomes narrowed, blocked, or compressed by nearby structures such as clots, muscles, arteries, or
other veins. This can result in blood pooling and flowing backward, causing swelling and pain in the area.
5. Disorders of Blood Flow – HTN Lifestyle Modifications ***WINK***
 Modifiable Risks ***WINK***WINK
o Diet: restrict sodium intake, fats, and cholesterol
o levels of blood lipids
o tobacco and alcohol consumption
o
o
o
 Excess ETOH= ↑ BP; Moderate levels ETOH= effective against heart disease
fitness and activity level (20-30 min a day)
 ↓ lowers BP and more favorable blood lipid levels
overweight/obesity (BMI: 18.5-24.9%) (BMI: 30% is OBESE)
 ↓ weight reduction can decrease blood pressure
blood glucose control
6. Disorders of Cardiac Function, and Heart Failure and Circulatory Shock – Atherosclerosis
Mechanisms of Development of Atherosclerosis

Types of lesions associated with atherosclerosis
o Fatty streaks
 Thin, flat yellow intimal discolorations that progressively enlarge
o Fibrous atheromatous plaque
 The accumulation of intracellular and extracellular lipids, proliferation of vascular
smooth muscle cells, and formation of scar tissue.
o Complicated lesion
 Contains hemorrhage, ulceration, and scar tissue deposits.
Major Risk Factors for Atherosclerosis
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Hypercholesterolemia
Cigarette smoking
Hypertension
Family history of premature CHD in a first-degree relative
Age (men ≥45 years; women ≥55 years)
HDL cholesterol <40 mg/dL
CRP levels
Homocysteine levels
Major Complications of Atherosclerosis
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Ischemic heart disease
Stroke
Peripheral vascular
disease
Clinical manifestations of atherosclerosis
o Narrowing of the vessel and resulting ischemia
o Vessel obstruction due to plaque hemorrhage or rupture
o Thrombosis and formation of emboli
o Aneurysm formation
Specific Arterial Involvement in Atherosclerosis
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In larger vessels, the important complications are those of thrombus formation and weakening of
the vessel wall.
In medium-sized arteries, ischemia and infarction due to vessel occlusion are more common.
Arteries supplying the heart, brain, kidneys, lower extremities, and small intestine are most
frequently involved.
Clinical Manifestations of Atherosclerosis
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Narrowing of the vessel and production of ischemia
Sudden vessel obstruction due to plaque hemorrhage or rupture
Thrombosis and formation of emboli resulting from damage to the vessel endothelium
Aneurysm formation due to weakening of the vessel wall
***What types of fats are bad: LDL***
7. Disorders of Cardiac Function, and Heart Failure and Circulatory Shock ST-segment myocardial infarction (STEMI), Pulmonary Edema, Heart Failure
Assessment Findings and Diagnostic Testing
STEMI
ST-Elevation Myocardial Infarction (STEMI) is a very serious type of heart attack during which one of the heart’s
major arteries (one of the arteries that supplies oxygen and nutrient-rich blood to the heart muscle) is blocked. STsegment elevation is an abnormality detected on the 12-lead ECG.
Patients experiencing acute STEMI are at risk for developing life-threatening arrhythmias like ventricular fibrillation
which causes sudden cardiac arrest, sometimes referred to as a “massive heart attack”. These patients require
cardiopulmonary resuscitation (CPR) and defibrillation — a “shock” to restore a normal heart rhythm.
Signs and symptoms of a STEMI include:
 Chest pain or discomfort
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Shortness of breath
Dizziness or light-headedness
Nausea or vomiting
Diaphoresis (sweatiness) unexplained by ambient temperature
Palpitations (uncomfortable awareness of the heartbeat)
Anxiety or a feeling of impending doom
Some patients experience denial and dismiss their symptoms as heartburn or indigestion. When this happens, they
may delay seeking care for hours.
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STEMI can be treated with “clot-busting” drugs called thrombolytics (also called fibrinolytics) or with a
primary percutaneous coronary intervention (PCI) in a cardiac catheterization lab. This procedure is
also referred to as angioplasty or stenting.
There is a direct relationship between the amount of time a heart artery is blocked and the severity of
the heart attack and odds of survival. Cardiologists have a mantra that “time is muscle” to express the
importance of early treatment.
Pulmonary Edema
Pulmonary edema, also known as pulmonary congestion, is excessive liquid accumulation in the tissue and air
spaces (usually alveoli) of the lungs. It leads to impaired gas exchange and may cause hypoxemia and respiratory
failure. It is due to either failure of the left ventricle of the heart to remove oxygenated blood adequately from
the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung tissue directly or blood vessels of
the lung (non-cardiogenic pulmonary edema).

Causes:
o Opiate toxicity, inhalation of gases rapid administration of IV fluids

Symptoms:
o Anxiety, tachycardia, acute respiratory distress, dyspnea at rest, change in level of
consciousness, ascending fluid level within lungs, Crackles, cough, productive of frothy,
blood tinged sputum.
CHF diagnostic findings
Blood

sodium and potassium (sometimes called electrolytes), albumin (a type of protein), creatinine (which is
connected with kidney function) and certain biomarkers, which can help diagnose heart failure and predict
outcomes.
o What blood tests show: abnormal results may indicate a strain on the heart or on other organs such
as the kidneys and liver, which often results from heart failure.
X-ray
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X-rays reveal:
Whether the heart is enlarged
Whether there is congestion in the lungs
EKG
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Whether you've had a heart attack
If the left ventricle is thickened (enlarged heart muscle wall)
If the heart rhythm is abnormal (noting any arrhythmias such as atrial fibrillation, or AFib)
Echocardiography reveals:
 The images produced by the echocardiogram can show how thick the heart muscle is, and how well the
heart pumps. This is the most common test used to assess your heart's ejection fraction.
 If the left ventricle is thickened (enlarged heart muscle wall)
 If the heart rhythm is abnormal (noting any arrhythmias such as atrial fibrillation, or AFib)
Exercise Stress Test

Shows whether your heart responds normally to the stress of exercise.
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Reveals whether the blood supply is reduced in the arteries that supply your heart.

Can help determine the kind and level of exercise that's appropriate for you.
8. Disorders of Cardiac Function, and Heart Failure and Circulatory Shock - Hypovolemic shock vs Septic
shock vs Neurogenic shock vs Obstructive shock
***Know the difference between Obstructive, Neurogenic, Septic, Hypovolemic*** Wink
Shock:
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Shock is a rapidly
progressing, lifethreatening condition
that results from
inadequate tissue
perfusion
Inadequate blood flow to
the cells->causes
impaired delivery of
oxygen and nutrients,
cellular hypoxia, and cell
death-> can lead to
organ failure and
eventually death
Can be caused by any
condition that
compromises oxygen
delivery to organs and
tissues, types are
classified by cause
o Cardiogenic:
altered cardiac
function
o Hypovolemic:
decreased
blood volume
o Distributive:
excessive
vasodilation
with
maldistribution
of blood flow
o
 Neurogenic, anaphylactic, sepsis and septic shock
Obstructive: obstruction of blood flow through circulatory system

Hypovolemic Shock: ***Know the difference*** Wink
o occurs when there is diminished intravascular blood volume due to fluid/blood loss (15-30% loss of
circulating blood volume)
 Most common type of shock
 Pathophysiology:
 decrease in intravascular fluid volume→ decreased venous return to heart and
decreased ventricular filling→ low CO and decreased tissue perfusion→ alters
cell function and causes cell damage/death
 Compensatory mechanisms: sympathetic nervous system activation, RAAS
system, ADH secretion
 Causes:
 diuresis
 Vomiting and diarrhea
 blood loss
 burns
 Severe dehydration
 severe edema or ascites
 S/sx: (Symptoms)
 Increase HR (compensatory)
 Decrease BP
 Weak and thready pulse
 Rapid and deep respirations
 thirst
 Cool and clammy skin
 Decreased urine output
 Altered LOC
 Decreased Hgb and Hct
 Tx: (Treatment)
 goal is to restore blood volume and improving tissue perfusion
 Correct underlying cause
 Fluid and blood replacement
 Trendelenburg position
 Oxygen administration

Sepsis and Septic Shock: (UTI→complication→Kidneys→back pain→) ***Know the difference*** Wink
o occurs with severe infection and systemic response to infection
 Sepsis: presence of infection with systemic inflammatory response syndrome (SIRS) that
can lead to septic shock.
 S/sx: fever, tachycardia, tachypnea, elevated WBC, altered LOC)
 Septic Shock: severe sepsis with persistent hypotension (despite fluid resuscitation) and
elevated lactate
 Pathophysiology: infection-> immune response activated-> SIRS-> injured cells release
potent vasodilators and chemicals that increase capillary permeability, also increased
coagulation factors-> reduced perfusion, oxygen, and nutrients to body cells->severe
sepsis with organ dysfunction-> hypotension, hypoxemia, oliguria, acidosis
 S/sx: (Symptoms)
 Early stages: decreased BP, elevated HR, hyperthermia and fever, warm and
flushed skin, bounding pulse, elevated RR, n/v/d, altered mental status
 Late stages: severe persistent hypotension that does not respond to fluid
resuscitation, elevated HR, signs of organ damage, skin is cool, and pale,
elevated HR, oliguria, multiple organ dysfunction
 Labs: elevated WBC, CRP, serum lactate
 Tx: (Treatment)
 control cause and support circulation
 Antibiotics
o Culture and sensitivity
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Fluid replacement
Vasopressors
Airway management/ mechanical ventilation
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Neurogenic Shock: (Traumatic Injury) ***Know the difference*** Wink
o results from loss of sympathetic tone that causes massive vasodilation
o Causes: head trauma, spinal cord injury, epidural anesthesia, some meds
o S/sx: (Symptoms)
 skin is dry and warm
 Decrease BP
 Decrease HR
o Tx: (Treatment)
 restore vasomotor tone, treat cause
 Stabilize spinal cord injury
 Reposition patient if caused by spinal anesthesia
o Complications of Shock: serious and often fatal
 Pulmonary injury
 Acute renal failure
 GI complications
 Disseminated intravascular coagulation
 Multiple organ dysfunction syndrome

Obstructive Shock: (Pulmonary embolism causes obstructive shock) ***Know the difference*** Wink
o Occurs when there is mechanical obstruction of blood flow through central circulation (great veins,
heart, lungs)
o Causes:
 Pulmonary Embolism (PE), cardiac tamponade, pneumothorax collapsed lung, aortic
dissection, dissecting aortic aneurysm, cardiac tamponade, pneumothorax, atrial myxoma,
and evisceration of abdominal contents into the thoracic cavity
o S/sx: (Symptoms)
 symptoms of R sided HF (JVD, increased central venous pressure)
o Tx: (Treatment)
 treat underlying cause chest tube (out of pleural space), fibrinolytic drugs)
9. Organization and Control of Neural Function = Cranial Nerves (CN), CSF, Multiple Sclerosis, CVA
Assessment
Cranial Nerves***WINK**
Multiple Sclerosis Assessment

MS diagnosis is based on established
clinical and laboratory criteria. There is no
one definitive diagnostic test.

definite diagnosis of MS requires evidence
of one of the following patterns:
o Two or more episodes of
exacerbation separated by 1
month or more and lasting more
than 24 hours, with subsequent
recovery.
o A clinical history of clearly defined exacerbations and remissions, with or without complete
recovery, followed by progression of symptoms over a period of at least 6 months
o Slow and stepwise progression of signs and symptoms over a period of at least 6 months
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Primary progressive MS may be suggested by a progressive course that lasts over 6 months. A
person who has not had a relapse or progression of symptoms is described as having stable MS.
MRI studies can detect lesions and measure size when CT scans appear normal.
Many new areas of myelin abnormality are asymptomatic.
o Serial MRI studies can be done to detect asymptomatic lesions, monitor existing lesions,
and evaluate the effectiveness of treatment. Although MRI can provide evidence of
disseminated lesions, normal findings do not exclude the diagnosis.
o
Electrophysiologic evaluations and CT scans may assist in identifying and documenting
lesions.
o A large percentage of people with MS have
elevated immunoglobulin G (IgG) levels in
the cerebrospinal fluid (CSF), and some
have oligoclonal patterns even with normal
IgG levels.
Cardiovascular Assessment →
10. Organization and Control of Neural Function – ALOC Assessment of Reflexes
Altered Level of Consciousness (ALOC)
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Brain injury and disease can lead to altered levels of consciousness.
Consciousness is the state of awareness of self and environment and of being able to orient to new
stimuli. It is divided into
o (1) arousal and wakefulness
 Require function of both cerebral hemispheres and an intact reticular activating
system (RAS).
o (2) content and cognition.
 Determined by a functioning cerebral cortex.
11. Somatosensory Function, Pain, and Temperature -Sensory History & Examination – Graphesthesia vs
Stereognosis vs Somesthesia vs Astereognosis
Graphesthesia: is the ability to recognize symbols when they’re traced on the skin.

Graphesthesia test is done during a neurological exam. It’s usually performed by a neurologist.
o Doctor will have you close your eyes.
o With the back of a pen or applicator stick, they’ll trace a letter or number on the palm of your
hand.
o Your doctor will ask you to identify the character.
o They’ll repeat the procedure on your other hand with a different symbol.
Stereognosis: is the ability to identify objects that are placed in the hand when the eyes are closed.
The patient is given common objects and asked to identify them without looking at them.
The inability to do this called astereognosis and indicates parietal lobe dysfunction. (Indicates a
problem with somatosensory cortex)
Somesthesia: is the perception of bodily sensations that include the skin, muscles, joints, and
tendons. Such sensations would encompass the perception of pain, temperature, light touch, deep
touch, vibration, proprioception (recognition of the relative position of a body part), and kinesthesia (awareness of
movement of a limb or joint).
12. Somatosensory Function, Pain, and Temperature – Pediatric Pain Assessment
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Self-report is usually the most reliable estimate of pain.
Children of 8 years of age or older: numeric scales and word graphic scales can be used.
Children 3 to 8 years of age, scales with faces of children or cartoon faces can be used to obtain a
report of pain.
Another supplementary strategy for assessing a child’s pain
o
is to use a body outline and ask the child to indicate where the pain is located.
Care must be taken in assessing children’s reports of pain as they may be influenced by factors
including age, anxiety and fear levels, and parental presence.
Physiologic measures, such as heart rate, are convenient to measure and respond rapidly to brief
nociceptive stimuli, but they are nonspecific.
Relying on indicators of sympathetic nervous system activity and behaviors can also be problematic
because they can be caused by things other than pain and they do not always accompany pain,
particularly chronic pain.
13. Somatosensory Function, Pain, and Temperature – Chronic Pain vs Acute Pain
Acute Pain

is elicited by injury and activation of
nociceptive stimuli at the site of local
tissue damage.

Generally, of short duration and resolves
with resolution of the pathology.

Alerts a person of actual or impending
tissue damage.
o The location, radiation,
intensity, duration, and factors
that aggravate or relieve pain
provide essential diagnostic
clues.

Interventions that alleviate pain usually
relieve concomitant problems such as
anxiety and musculoskeletal spasms.

Inadequately treated pain can provoke
responses that alter circulation and
tissue metabolism and increase
sympathetic activity.

Inadequately treated acute pain tends to
decrease mobility and respiratory movements and may complicate or delay recovery.
Chronic Pain

Chronic pain persists longer than might be reasonably expected after an inciting event.

Sustained by both pathologically and physically remote factors from the originating cause.

Chronic pain can continue for years. It may be unrelenting and severe, as with metastatic bone pain, or
continuous with or without periods of escalation, as with some forms of back pain.
o Recurring episodes of acute pain are particularly problematic because they have characteristics of
both acute and chronic pain (as in sickle cell crisis or migraine headaches).

Chronic pain is a leading cause of disability and usually serves no useful function.
o
It imposes physiologic, psychological, familial, and economic stresses.

Psychological and environmental influences may play an important role in the
development of behaviors associated with chronic pain.
o The biologic factors that influence chronic pain include peripheral, peripheral–central, and central
mechanisms.
o Peripheral mechanisms result from persistent stimulation of nociceptors and are mostly involved
with chronic musculoskeletal, visceral, and vascular disorders. Peripheral–central mechanisms are
related to abnormal function of the peripheral and central portions of the somatosensory system,

such as those resulting from partial or complete loss of descending inhibitory pathways or
spontaneous firing of regenerated nerve fibers (as with causalgia and phantom limb pain).
o Central pain mechanisms are associated with CNS disease or injury and characterized by burning,
aching, and other abnormal sensations (as with thalamic lesions, spinal cord injury, surgical
interruption of pain pathways, and multiple sclerosis).
People with chronic pain may not exhibit behaviors often associated with acute pain.
o As pain becomes prolonged and continuous, autonomic nervous system responses decrease.
o
Loss of appetite, sleep disturbances, and depression often are associated with chronic pain.
o Depression commonly is relieved once the pain is removed.

The link between depression and decreased pain tolerance may be due to how both
respond to changes in serotonergic and noradrenergic systems.

Tricyclic antidepressants and other medications with serotonergic and
noradrenergic effects have been shown to relieve a variety of chronic pain
syndromes.1
14. Disorders of Motor Function – Neuro Testing - Segmental reflex vs Posture vs Proprioception vs
Crossed-extensor reflex
Romberg test: is a test of proprioception. This test is performed by asking the patient to stand, feet
together with eyes open, then with eyes closed. The patient with significant proprioceptive loss will
be able to stand still with eyes open because vision will compensate for the loss of position sense
but will sway or fall with their eyes closed because they are unable to keep their balance.
15. Disorders of Motor Function - Guillain-Barré syndrome, Parkinson’s disease
Parkinson Disease
 Degenerative disorder that results in combinations of tremors, rigidity,
akinesia, bradykinesia, and postural changes
 Patho: dopaminergic neurons die in the basal ganglia → depletion of
dopamine stores → imbalance of dopamine and ACh
o Role of dopamine: provides accuracy with movement, dopamine
(inhibitory) and ACh (excitatory) balance to control complex body
movements
o How do we see this in Parkinson disease? (tremors and rigidity)
 S/sx: (Symptoms)
o tremors/shocking
o Slow shuffling gait
o Bradykinesia → swallowing issues, expressionless face
o Muscle rigidity
o Constipation
 Nursing interventions:
o Assess for assistive devices (walker for balance)
o Teach move slowly
o Provide special cookware and utensils
o Provide soft and easy foods to chew with high fiber
o Administer dopamine agonists (carbidopa and levodopa) and/or anticholinergic
16. Respiratory Tract Infections and Neoplasms – Pneumonia
Pneumonia
 Lower respiratory tract infection causing inflammation of the alveoli and the bronchioles
 Causes more than 1.25 million hospitalizations annually
o 8th leading cause of death in the United States
o Most common cause of death from an infection
 Patho:
o

Pathogen enters the lung through inhalation, aspiration, or blood → alveolar sacs become
inflamed → fill with fluid, RBCs/WBCs, and pathogen → lose ability to inflate and deflate →
impaired gas exchange→ hypoxemia
Causes
o




Infectious agents: such as bacteria and viruses

most common is bacteria (streptococcus pneumoniae),
viral, fungal
o Noninfectious agents: such as gastric secretions aspirated into the
lungs
Classifications:
o Typical or atypical
 Typical: bacterial, more severe symptoms, infection
multiplies in the alveoli
 Atypical: non-bacterial, milder symptoms, infection
occurs between the alveoli
o Lobar or bronchopneumonia
 Lobar: single or multiple lobes
 Bronchopneumonia: patches throughout both lungs
o Setting
 Community-acquired: before 48 hours of admission
 Nosocomial (hospital) acquired:
after 48 hours of admission
Diagnosis: **Where is this infection; what does it sound like?*** Wink***
o Abnormal/absent lung sounds (crackles) **** Wink***
o Chest X-ray → cloudy, white spots
o Sputum culture → cough deeply into a sterile cup
S/sx: (Symptoms)
o productive cough, elevated labs (↑ WBC, ↑ CO2, ↑ HCO3 (bicarb=respiratory acidosis), unusual
lung sounds, dyspnea, fever, fatigue, low O2 stat, SOB w/ activity, and mental status changes
Tx: (Treatments)
o Prevention of spreading: handwashing, encouraging face masks to pts w/ cough
o Prevention education: elevate HOB, oral care, encourage walks, coughing, deep breathing,
incentive spirometry
 What does incentive spirometry do? (expands, strengthens muscles, clears mucus/breath
in= expands lungs)
o Monitor: O2 stats, lung sounds, RR
o Encourage fluids
o RT treatments → bronchodilators
o Antibiotics if bacterial
17. Respiratory Tract Infections and Neoplasms – Upper Respiratory Tract Infection (URI), Croup, Cystic
Fibrosis


Respiratory Disorders in Children
Upper Airway infections
o Viral croup
o Spasmodic croup
Cystic Fibrosis
 Autosomal recessive disorder involving the exocrine glands in the epithelial lining of the respiratory, GI, and
reproductive tracts.
o Cause: Mutations in a single gene on the long arm of chromosome 7 that encodes for the cystic
fibrosis transmembrane regulator (CFTR), which functions as a chloride (Cl−) channel in epithelial
cell
o More than 10 million persons are asymptomatic carriers of the defective gene.
 The defective gene (cystic fibrosis transmembrane regulator) causes excessive thick mucus that obstruct
the lung & Pancreas .
 s/sx: (Symptoms)
o Symptoms related to:
 Thick mucus in the bronchi



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
Impaired mucociliary clearance
Lung infections
o Pancreatic exocrine deficiency
 Damaging of the pancreatic cells can lead to improper secretion of insulin , putting
patients at risk of developing diabetes . (comorbidity)
o Malabsorption and malnutrition
o Elevation of NaCl in sweat
Other manifestations:
o Pancreatic exocrine deficiency
o Pancreatitis
o Elevation of sodium chloride in the sweat
o Excessive loss of sodium in the sweat
o Nasal polyps
o Sinus infections
o Cholelithiasis
Dx: (diagnosis)
o Early diagnosis and treatment are important in delaying onset and severity in children.
o Testing:
 Sweat chloride test
 CFTR functional testing
 CFTR genetic analysis
Tx: (Treatment)
o No approved treatments for correcting the genetic defects in CF
o Treatment is directed toward slowing the progression of
secondary organ dysfunction
o Medications:
 Oral & inhaled antibiotics (increase risk for lung
infections)
 Bronchodilators (increase airway circumference)
 Anti-inflammatory meds
o Chest physical therapy (chest percussion & postural drainage) (clears airways, treatment can
include nebulizers and chest treatment)
18. Disorders of Ventilation and Gas Exchange – Pulmonary Embolism, COPD
Pulmonary Embolism (PE) **Ventilation/Perfusion concept->slide
 Obstruction of pulmonary artery or one of its branches by:
o Thrombus, air, fat, amniotic fluid
o Most likely thrombus from venous system (system returns blood to heart)
 Causes/ Risk factors:
o DVT is most common cause; air embolism is possible too
o Virchow’s Triad:
 venous stasis:
 prolonged bed rest, HF, MI
 hypercoagulability:(increased coagulation or clotting)
 cancers, birth control_, hormone therapy
 endothelial injury:
 trauma, surgery, MI, hip/femur fractures
 Pathophysiology:
o obstruction of one of pulmonary arteries →impaired alveolar perfusion → impaired/absent gas
exchange V/Q mismatch, perfusion is the problem here →vasoconstriction and
bronchoconstriction →increased pulmonary vascular resistance → increased work on R ventricle
→R heart failure →decreased CO and BP →shock
 S/sx: (Symptoms)
o Chest pain, dyspnea, tachypnea
o Productive cough with hemoptysis (coughing up blood)
o Pleuritic pain (sharp chest pain when breathing deeply)
o Tachycardia
o Moderate hypoxemia
o Severe s/sx:



shock, loss of consciousness, crushing chest pain, rapid and weak pulse, low BP, JVD,
cyanosis, diaphoresis
Dx: (Diagnosis)
o EKG, chest Xray, troponin
o Ultrasonography
o Labs:
 D-dimer
 Troponin why? (cardiac injury, released by heart tissue), (show heart
failure)
 ABG hypoxemia and hypocapnia (from tachypnea) (caused by fast breathing)
o Pulmonary angiography
Tx: (Treatment)
o PREVENTION:
 anticoagulants, lifestyle, compression stockings, early ambulation-after surgery
why?(preventing venous stasis)
o Thrombolytic therapy: tPA (tissue plasminogen activator)
COPD (Chronic Obstructive Pulmonary Disease)
 Respiratory disease characterized by chronic obstruction (blockage) of airflow in pulmonary airways,
causing breathing difficulties
o Usually progressive disease that is not fully reversible, but preventable
 Causes/Risk Factors:
o smoking
o Environmental pollutant exposure
o Occupational hazards
 2 types depending on location of obstruction:
o Emphysema: destruction of alveolar walls
 Pathophysiology: destruction of alveoli → leads to decreased lung
elasticity and decreased surface area for gas exchange → can
cause:
 Dead space: ventilated space in respiratory system that
cannot participate in gas exchange
 Hyperinflation of lungs
 Impaired O2 diffusion → what manifestation will we see? hypoxemia
 Increased CO2 retention → what acid/base imbalance? Respiratory acidosis
 S/sx: (Symptoms)
 pink puffers) hyperventilation and pink complexion (accumulation of CO2 is
the issue)
 Pursed lip breathing
 Use of accessory muscles. What does this look like? (External intercostals
muscles)
 Barrel chest
 Tripoding (bent over, hunched over easier to activate accessory muscles)
 Hyperventilation
 Fatigue, exercise intolerance, shortness of breath, dyspnea, low O2 sat
o Chronic Bronchitis: inflammation of airways and hypersecretion of mucus
 Pathophysiology:
 smoke or other environmental pollutants irritate the
airways causing inflammation and hypersecretion of
mucus (due to increased goblet cells), causing:
o Narrowing of bronchial lumen and reduced
ciliary function
o Recurrent respiratory infections
o Impaired O2 diffusion→ hypoxemia
o Increased CO2 retention → respiratory
acidosis
 Dx: (Diagnosis)
 chronic productive cough for at least 3 consecutive
months, in at least 2 consecutive years

S/sx: (Symptoms)
 (blue bloaters) cyanosis; edema
 Chronic, productive cough
 Recurrent pulmonary infections
 Cyanosis
 V/Q mismatch
 Edema (late) (why?)
o Cor Pulmonale: low oxygen → vasoconstriction of pulmonary vessels &
RBC production stimulated (being stimulated by the low oxygen) why?
attempting to increase O2) → further impairment of gas
o Exchange → severe hypertension in pulmonary vessels → increased
work on the heart →R sided HF over time (build up in left side)
 Fatigue, exercise intolerance, shortness of breath, dyspnea, low O2 sat
o

o
Most patients have overlapping s/sx of both conditions
Tx: (Treatment)
o Stop smoking **only thing that slows progression of disease
o Avoid exposure to others with respiratory infxn
 Immunizations for Influenza and pneumonia
o Bronchodilators
o O2 therapy for severe hypoxemia (< 55)
 Goal O2 sat 88-92% why? (if you over saturate, become oxygen dependent)
19. Acute Kidney Injury vs. Chronic Kidney Disease
Acute Renal Failure





Abrupt in onset
Often is reversible if recognized early and treated appropriately
Most commonly occurs in critically ill,
hospitalized patients
Risk factors: advanced age, autoimmune disorders, and liver disease
Causes of Acute Renal Failure



Prerenal conditions
o Extremely low blood pressure or blood volume
o Heart dysfunction
Intrarenal conditions
o Reduced blood supply within the kidneys
o Hemolytic uremic syndrome
o Renal inflammation
o Toxic injury
Postrenal conditions
o Ureter obstruction
o Bladder obstruction and dysfunction
Phases of Acute Renal Failure




1. Asymptomatic phase.
2. Oliguric phase: daily urine output decreases to approximately 400 mL or less, such that waste
products begin to accumulate.
3. Diuretic phase: daily urine output increases to as much as 5 L.
4. Recovery phase: glomerular function gradually returns to normal.
Manifestations of Acute Renal Failure



Oliguric phase: decreasing urine output, electrolyte disturbances, fluid volume excess, azotemia,
and metabolic acidosis
Diuretic phase: increased urine output, electrolyte disturbances, dehydration, and hypotension
Recovery phase: symptoms begin resolving
Diagnosis:

history, physical examination, blood chemistry, arterial blood gasses, urinalysis, complete blood
count, renal ultrasound, and biopsy
Treatment






Correct fluid and electrolyte imbalances
Dialysis
A diet high in calories and restricted in protein, sodium, potassium, and phosphates
Hypertension management
Anemia treatment with synthetic erythropoietin
Infection prevention strategies
Chronic Renal Failure



The end result of irreparable damage to the kidneys
It develops slowly, usually over the course of a number of years.
Causes: diabetes mellitus, hypertension, urine obstructions, renal diseases, renal artery stenosis,
ongoing exposure to toxins and nephrotoxic medications, sickle cell disease, systemic lupus
erythematosus, smoking, advancing age
Stages





Stage I: kidney damage present but GFR is > 90
Stage II: kidney damage worsens as the GFR falls (60–89)
Stage III: kidney function is significantly impaired as GFR is between 30 and 59
Stage IV: kidney function is barely present with GFR dropping between 15 and 29
Stage V: kidney failure as the GFR drops to less than 15 or the patient begins dialysis
Manifestations

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Hypertension
Polyuria with pale urine (early)
Oliguria or anuria with dark-colored urine (late)
Anemia
Bruising and bleeding tendencies
Muscle twitches and cramps
Electrolyte imbalances
Pericarditis, pericardial effusion, pleuritis, and pleural effusion
Congestive heart failure
Respiratory distress and abnormal breath sounds
Sudden weight change
Edema of the feet and ankles
Azotemia
Manifestations con’t…

Peripheral neuropathy, restless leg syndrome, and seizures

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Nausea and vomiting
Anorexia
Malaise
Fatigue and weakness
Headaches that seem unrelated to any other cause
Sleep disturbances
Decreased mental alertness
Flank pain
Jaundice
Persistent pruritus
Recurrent infections
Diagnosis:


history, physical examination, urinalysis, blood chemistry, computed
tomography, magnetic resonance imaging, renal ultrasound, biopsy, complete blood count, and
arterial blood gasses
Treatment:

manage and prevent complications and alternative medication dosing
20. Structure and Function of the Kidney – Renal Function Testing
Tests of Renal Function
 Urine Tests:

Glomerular Filtration Rate
o Test that measures how well the kidneys are filtering waste.
o The GFR can be measured clinically by collecting timed samples of blood and urine.
o Measures levels of creatinine in the blood, or albumin in the urine.
 Special Note:
 Estimated glomerular filtration rate (eGFR) is one of the primary diagnostic
methods for detecting and managing kidney diseases, and identifying treatments
like dialysis. The eGFR equation includes serum creatinine, age, sex, race
and/or body weight to approximate directly measured kidney function. However,
race is a social, not a biological, construct.
 The inclusion of race in this equation is inaccurate, unrepresentative, biased, and
non-standardized, but has become the norm.
o https://www.kidney.org/news/removing-race-estimates-kidney-function
 Early clinical studies concluded that people who identify as african americans
tend to have higher levels of creatinine, (creatinine not functioning )so results

are modified depending on this notion. The race modifier is only used with black
people.
o Since then, studies have concluded that this connection to race was an
overgeneralization, but the cause is still unknown.
According to the National Kidney Foundation, Black people are 3 to 4 times more
likely than white people to develop kidney failure.
o https://www.healthline.com/health/kidney-disease/egfr-africanamerican#effects

Blood Tests
o Serum Creatinine
 Creatinine is produced by muscles as a product of the metabolism of a molecule called
creatine.
 If the creatinine level is above normal, we can assume that the kidneys function has
decreased.
 ***Creatinine over 1.3 = bad kidney***
o Blood Urea Nitrogen BUN
 Urea is an end product of protein metabolism.
 High BUN indicates an impaired kidney function.

Cystoscopy and Ureteroscopy:
o Cystoscopy is the visualization of the bladder by the insertion of an instrument called a cystoscope
through the urethra into the bladder.
o Cystoscopy provides a means for direct visualization of the urethra, bladder, and ureteral insertion
sites.
 Biopsy specimens, lesions, small stones, and foreign bodies can be removed from the
bladder via the cystoscope.
o Ureteroscopy involves the use of a smaller, thinner scope that may be used to remove stones from
the ureter and aid in the treatment of ureteral disorders, such as ureteral strictures (restrictions).
Ultrasonography:
o Ultrasonography is used to visualize the structures of the kidneys and has proved useful in the
diagnosis of many urinary tract disorders, including congenital anomalies, renal abscesses,
hydronephrosis, and kidney stones.
o Bladder scanning

o
21. Disorders of Renal Function – UTI vs Pyelonephritis vs Glomerulonephritis vs Hydronephrosis vs. Kidney
Stones
UTI’s


A frequent type of bacteria infection
Most UTIs are caused by bacteria that enter through the urethra

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

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Lower (bladder) or upper (kidney) urinary tract infection
o Kidney UTI is called pyelonephritis
Washout phenomenon: sterile urine formed in the kidneys and found in the bladder washes bacteria and
pathogens out of the urethra
Risk factors/ causes:
o Having a prior UTI
o Sexual activity with a new partner
o Changes in vaginal flora via pH changes
o Neurogenic disorders that impair bladder emptying
o Postmenopausal women
o Men with diseases of the prostate
o Older adults
o Urinary obstruction or reflux (goes down and then goes back up)
o
o
Female anatomy
Indwelling urinary catheters
S/sx: *can be asymptomatic*
o High frequency of urination
o Lower abdominal or back discomfort
o Burning and pain during urination (dysuria)
o Cloudy or foul-smelling urine
o Older adults: confusion
Diagnosis: based on symptoms or urinalysis discovery of bacteria
Nursing interventions
o Based on the pathogen causing the infection → usually treated with a short course of antimicrobial
therapy
o Increasing fluids
o Teach/do: ALWAYS wipe front to back, sterile method for catheter insertion
o Recurrent infections (urinary catheter or infected bladder stones) → remove
Pyelonephritis
 Infection of the kidneys parenchyma and renal pelvis
 Usually caused by untreated lower urinary tract (bladder) infections can travel up the ureters to one or both
kidneys
 Classifications
o Acute
 Upper UTI, specifically the renal parenchyma and renal pelvis
 Factors that contribute are catheterization and urinary instrumentation, vesicoureteral
reflux, pregnancy, and neurogenic bladder
o Chronic
 progressive process → scarring and deformation
of the renal calyces and pelvis, usually related to
anatomic abnormalities → leads to scarring
and atrophy of both kidneys → chronic renal
insufficiency
 S/sx

o
o
o
o
o
Abrupt onset of chills and high fever
Ache or tenderness in the flank area of the back that is unilateral or bilateral
Dysuria, frequency, and urgency
Nausea and vomiting
Chronic: may be more gradual
Nursing interventions/ Tx
o Appropriate antimicrobial drugs
o Adequate hydration
Characteristics of Glomerulonephritis*** fill in the blank***


Immune mechanisms
o Glomerular antibodies
o Circulating antigen–antibody complexes
Characteristics
o Hematuria with red cell casts
o A diminished glomerular filtration rate (GFR)
o Azotemia (presence of nitrogenous wastes in the blood)
o Oliguria
o Hypertension
Causes of Glomerulonephritis (Systemic)-> renal failure


Diseases that provoke a proliferative inflammatory response of the endothelial, mesangial, or
epithelial cells of the glomeruli
The inflammatory process:
o Damages the capillary wall
o Permits red blood cells to escape into the urine
o Produces hemodynamic changes that decrease the GFR
Cellular Changes in Glomerular Disease

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Proliferative
o Endothelial
o Mesangial
o Leukocyte
o Crescent formation
Basement membrane thickening
o Sclerosis
o Fibrosis
Diffuse glomerular changes
Focal glomerular changes
Segmental glomerular changes
Mesangial changes
Urinary Changes in Glomerulonephritis
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Proteinuria
Hematuria
Pyuria
Oliguria
Edema
Hypertension
Azotemia
22. Disorders of Renal Function – Nephrotoxic Agents ****
 Nephrotoxic ATN or acute tubular injury
o





complicates the administration of or exposure to many structurally diverse drugs and other
nephrotoxic agents.
How do these Nephrotoxic Agents Cause Injury?
o These agents cause tubular injury by inducing varying combinations of renal
vasoconstriction, direct tubular damage, or intratubular obstruction.
Why are Kidneys vulnerable?
The kidney is particularly vulnerable to nephrotoxic injury because of its rich blood supply and
ability to concentrate toxins to high levels in the medullary portion of the kidney.
o The toxic effects, which cause some minor necrosis, are generally limited to the proximal
tubule.
o In addition, the kidney is an important site for metabolic processes that transform
relatively harmless agents into toxic metabolites.
What agents are toxic? And where? → *** Wink Wink***
o Directly toxic to the Renal Tubule
 Antimicrobials such as aminoglycosides (vancomycin, gentamicin)
 Cancer chemotherapeutic agents: cisplatin, radiocontrast agents
 Ibuprofen
Nephrotoxicity Causes
o Decrease in GFR
o Pre-Existing renal disease
o Hypovolemia
o Concurrent administration of other drugs that have nephrotoxic effects.
 Radiocontrast media-induced nephrotoxicity
 Results from direct tubular toxicity and renal ischemia
o highest in older adults
o those with preexisting kidney disease
o volume depletion,
o diabetes mellitus, and
o recent exposure to other nephrotoxic agents.
23. Disorders of the Bladder and Lower Urinary Tract – Urinary Incontinence, Bladder Cancer
Types of Incontinence #1 ***WINK***WINK***


Stress Incontinence
o Involuntary loss of urine during coughing, laughing, sneezing, or lifting
o Increases intra-abdominal pressure
Urge Incontinence
o Involuntary loss of urine associated with a strong desire to void (urgency)
Types of Incontinence #2


Overflow Incontinence
o Involuntary loss of urine that occurs when intravesicular pressure exceeds the maximal
urethral pressure because of bladder distention in the absence of detrusor activity
Mixed Incontinence
o Combination of stress and urge incontinence
Treatment Options for Incontinence







Management depends on the type of incontinence, accompanying health problems, and the
person’s age.
Behavioral and pharmacological measures
Exercises to strengthen the pelvic muscles (Kegel exercises)
Surgical correction
Non-catheter devices to obstruct urine flow or collect urine
Indwelling catheters
Self-catheterization
Elderly Incontinence

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Overall capacity of the bladder is reduced.
Urethral closing pressure is reduced.
Detrusor muscle function declines with aging.
o To larger PVR volumes
Advancing age
Restricted mobility
Increased medication
Comorbid illness
Infection
Stool impaction
Bladder Cancer


Signs
o
o
o
o
Increased frequency
Urgency
Dysuria
Hematuria
Cancerous Lesion Types
o Superficial
o Invasive
Diagnostic Measures for Cancer of the Bladder

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Cytologic studies
Excretory urography
Cystoscopy
Biopsy
Ultrasonography
CT scans
MRI
Treatment Methods for Bladder Cancer


Treatment methods depend on
o The cytologic grade of the tumor
o The lesion’s degree of invasiveness
Methods include
o Surgical removal of the tumor
o Radiation therapy
o Chemotherapy
24. Disorders of the Bladder and Lower Urinary Tract – Urinary Retention Assessment & Diagnostic Testing
Urine Tests and Studies

Laboratory and Radiographic Studies
o Urine tests and x-rays
 Urinalysis
 Evaluates wastes products detects neurologic disorders
 Identifies: concentration/dilution; specific gravity; acidity/alkalinity,
presence of drug metabolites, glucose, ketone bodies, protein.
o Glucose; ketone bodies; protein; leukocyte esterase, nitrates
→ not usually present urine → indicates DM; fat metabolism;
infection; or cancer
 Identifies bacteria→ determines antibiotic

o
o
o
o
o
o
o
Types of Tests
 Blood Creatinine
 Kidney disease only condition that increases creatinine levels
o Kidney disease of 50%→causes ↑ elevation of blood creatinine
o ↓ Muscle mass + creatinine decreases with age, remains
constant in older adults who do not have lung disease
 Blood urea nitrogen “BUN” ***WINK***WINK***
 Results from breakdown of protein in the liver, creating the byproducts
urea nitrogen excreted by the kidneys
o Factors affecting
 Dehydration, infection, chemotherapy, steroid
therapy, reabsorption of blood in the liver from
damaged tissue
 Elevated BUN→ kidney disease
 Because liver failure limits urea production, BUN is
decreased when liver/kidney failure occur
Urodynamic Studies
Uroflowmetry
Cystometry
Urethral pressure profile
Sphincter electromyography
Ultrasound bladder

First-voided morning specimens are useful for qualitative protein and specific gravity testing. A freshly
voided specimen is the most reliable. Urine specimens that have been left standing may contain lysed red
blood cells, disintegrating casts, and rapidly multiplying bacteria

How do you obtain: Urine Sample
o
Clean Front→ to back→ not initial first stream→ clean catch specimen midstream→
o
What is in urine if abnormal?

WBC’s, blood if bladder, leukocytes, RBC’s, presence of bacteria, Nitrite → nitrates
(metabolites bacteria turn nitrate to nitrite→ (Not on period**** wink***)
25. Organization and Control of Neural Function –Neurons Structure, Function, Metabolic Requirements.
Metabolic Requirements
o Receives 15% to 20% (750 mL/minute) of the total resting cardiac output
o Consumes 20% of its oxygen
o Brain cannot store oxygen or engage in anaerobic metabolism
 Interruption in blood or oxygen supply leads to clinical signs and symptoms

o
Unconsciousness
o Occurs simultaneously with
cardiac arrest
 Brain Cell death
o Begins within 4-6 minutes
 Leads to accumulation of metabolic by
products that are toxic to neural tissue.
Major fuel source
 Glucose
 Neurons cannot store it, must rely on blood
glucose or glycogen stores of supporting
neuroglial cells.
 TEMPORARY energy requirements
o Ketones can be fulfilled, but
rapidly depleted.
26. Organization and Control of Neural Function - afferent, efferent, ganglia, synapse, neurotransmitters
Peripheral neurons can be classified as afferent and efferent neurons according to function




Afferent (sensory)
o carry information toward the CNS
o reception of sensory information from the external environment and from within the body.
Efferent (motor)
carry information away from the CNS
needed for control of muscle fibers and endocrine and exocrine glands.
.
Ganglia

Ganglia are clusters of nerve cell bodies found throughout the body. They are part of the
peripheral nervous system and carry nerve signals to and from the central nervous system.
Synapses



Are structures that permit communication between neurons or muscle cells.
Two types of synapses
Electrical and chemical.
o Electrical synapses: consist of gap junctions between adjacent cells that allow action potentials
to move rapidly from one cell to another.
o Chemical synapses: involve special presynaptic and postsynaptic structures, separated by a
synaptic cleft. They rely on chemical messengers, released from the presynaptic neuron, that cross
the synaptic cleft and then interact with receptors on the postsynaptic neuron.

A chemical synapse contains
o (1) the axon terminal of one neuron
o (2) the area of the cell membrane that contains receptors on the target cell, and (3)
the space between these two cells.
 At the chemical synapse, neurotransmitters bind
to receptors on target cells such as another
neuron or muscle cell.
o In addition, electrical synapses exist where neurons are
linked through gap junctions that allow ions to pass from
one cell to another.
Neurotransmitters


Neurotransmitters are chemical messengers that control neural function.
They selectively cause excitation or inhibition of action potentials.

Three major types of neurotransmitters are known—amino acids, neuropeptides, and monoamines.
Neurotransmitters interact with cell membrane receptors to produce either excitatory or inhibitory actions.