CASE

STUDIES ON
MAJOR
CONCEPTS
PERFUSION
 COMMUNITY ACQUIRED PNEUMONIA
By: ALCE
Case Scenario – The sister of C.K. brought her 71-year-old brother to the primary care clinic after he came down with a fever 2 days
ago. She said he has shaking chills, a productive cough, and he can't lie down to sleep because “he can't stop coughing.” After C.K.
is examined, he is diagnosed with community-acquired pneumonia (CAP) and admitted to your floor. The intern is busy and asks
you to complete your routine admission assessment and call her with your findings.
Your assessment findings are as follows: C.K.'s vital signs are 154/82, 105, 32, 103° F (39.4° C), SaO2 84% on room air. You
auscultate decreased breath sounds in the left lower lobe anteriorly and posteriorly and hear coarse crackles in the left upper lobe.
His nail beds are dusky on fingers and toes. He has cough productive of rust-colored sputum and complains of pain in the left side
of his chest when he coughs. C.K. seems to be well nourished and adequately hydrated. He is a lifetime nonsmoker. Past medical
history includes coronary artery disease and myocardial infarction (MI) with a stent; he is currently on metoprolol (Lopressor),
amlodipine (Norvasc), lisinopril (Zestril), and furosemide (Lasix); for his type 2 diabetes mellitus, he is also taking metformin
(Glucophage) and rosiglitazone (Avandia). He has never gotten the Pneumovax or flu shot. He does report getting “hives” when he
took “an antibiotic pill” a few years ago but doesn't remember the name of the antibiotic.
Physician's Orders 2100-Calorie ADA diet VS with temperature q2h IV of D5 ½ NS at 125 mL/hr Ceftriaxone (Rocephin) 1 g IV bid Metaproterenol
sulfate (Alupent) 0.4% nebulizer treatment q3h Titrate O2 to maintain SaO2 over 90% Obtain sputum for C&S Blood cultures for temperature over
102° F (38.9° C) CBC with differential and basic metabolic panel Urinalysis (UA) with C&S Chest x-ray (CXR) now and in the morning.
Pathophysiology

Any infectious organisms that reach the alveoli are likely to be highly virulent, as they have already evaded the host’s physical
defense mechanisms. Consequently, they may overwhelm the macrophages, resulting in production of a fibrin-rich exudate that fills
the infected and neighbouring alveolar spaces, causing them to stick together, rendering them airless (Driver, 2012). The
inflammatory response also results in a proliferation of neutrophils. This can damage lung tissue, leading to fibrosis and pulmonary
oedema, which also impairs lung expansion.
 
The inflammatory response can also lead to the development of a pleural effusion which is thought to complicate up to 40% of
cases of pneumonia (Koegelenberg et al, 2008 in Driver, 2012). These changes result in reduced gaseous exchange. As a result,
vital organs become oxygen deprived and the respiratory effort required with each breath will be increased as a result of the
disturbance in normal physiology. Respiratory and heart rate will increase in response to falling oxygen and rising carbon dioxide
levels.
Concept Map

Prevention
Prevention

••Get
Get vaccinated
vaccinated
••Practice
Practice good
good hygiene
hygiene
••Don't
Don't smoke
smoke
••Keep
Keep immune
immune system
system strong
strong

Risk
Risk factors
factors Signs
Signs and
and Symptoms
Symptoms

••Children
Children who
who are
are 22 years
years old
old or
or ••Chest
Chest pain
pain when
when you
you breathe
breathe or
or
younger
younger cough
cough
••People
People who
who are
are age
age 6565 or
or older
older ••Confusion
Confusion oror changes
changes inin mental
mental
awareness
awareness (in
(in adults
adults age
age 65
65 and
and
older)
older)
••Cough,
Cough, which
which may
may produce
produce phlegm
phlegm
••Fatigue
Fatigue
••Fever,
Fever, sweating
sweating and
and shaking
shaking chills
chills

Pneumonia
 PULMONARY HYPERTENSION
By: ADUNA

The patient is a 48-year-old woman with a history of pulmonary hypertension who presented to the outpatient pulmonary clinic for a
second opinion concerning her worsening dyspnea on exertion.
 Chief complain: Worsening dyspnea on exertion.
Past: Father is died from diabetes and her mother still alive but is hypertensive. She has two kids who are both alive and well. She had
been hospitalized two years prior with shortness of breath. She has smoked a pack of cigarettes a day from the age of 22 until she quit
smoking at age 43.
 Present: According to the client she was walking around her garden when she has developed palpitations and dizziness with exertion,
but did not endorse syncope or chest pain.
Pathophysiology

Increased pulmonary vascular resistance is caused by obliteration of the pulmonary vascular bed and/or by pathologic vasoconstriction.
Pulmonary hypertension is characterized by variable and sometimes pathologic vasoconstriction and by endothelial and smooth muscle
proliferation, hypertrophy, and chronic inflammation, resulting in vascular wall remodeling. Vasoconstriction is thought to be due in part.
The increased pulmonary vascular pressure that results from vascular obstruction further injures the endothelium. Injury activates
coagulation at the intimal surface, which may worsen the hypertension. Thrombotic coagulopathy due to platelet dysfunction. Platelets,
when stimulated, may also play a key role by secreting substances that increase proliferation of fibroblasts and smooth muscle
cells. Meanwhile, Increased pulmonary venous pressure is typically caused by disorders that affect the left side of the heart and raise left
chamber pressures, which ultimately lead to elevated pressure in the pulmonary veins. Elevated pulmonary venous pressures can cause
acute damage to the alveolar-capillary wall and subsequent edema. Persistently high pressures may eventually lead to irreversible
thickening of the walls of the alveolar-capillary membrane, decreasing lung diffusion capacity. The most common setting for pulmonary
venous hypertension is in left heart failure with preserved ejection fraction typically in older women who have hypertension and metabolic
syndrome. (Reference: Relevant issues in the pathology and pathobiology of pulmonary hypertension. J. Am. Coll. Cardiol. 2013)
Concept Map
 PULMONARY EMBOLISM
By: BAYAUA

Case Scenario: A 61 year old male complains of new onset shortness of breath for 4 days. He also noticed a cough, with blood-
tinged sputum. He has no chest pain, no orthopnea or paroxysmal nocturnal dyspnea, or fever. He used albuterol inhaler
several times with no improvement in his shortness of breath.
History Of Present Illness
-hypertension
-asthma
-remote history of left lower limb swelling that subsided after treatment for 6 years.
Pathophysiology

An embolism is the lodging of an embolus, a blockage-causing

piece of material, inside a blood vessel. The embolus may be a
blood clot (thrombus), a fat globule (fat embolism), a bubble of air
or other gas (gas embolism), amniotic fluid (amniotic fluid
embolism), or foreign material.
Concept Map
A 61 year old male complains
of new onset shortness of
breath for 4 days.
He has no chest
pain, no
noticed a orthopnea or
cough, with PULMONARY EMBOLISM paroxysmal
blood-tinged nocturnal
sputum. dyspnea, or fever

He used albuterol inhaler

History:
several times with no
Hypertension and asthma improvement in his
shortness of breath.
remote history of left lower limb
 
swelling that subsided after
treatment for 6 years.
 
 BUDD-CHIARI SYNDROME
By: BERNABEO

Case Scenario: Mr. K is a 37-year-old Indian dental clerk who was admitted to the University Hospital after
having been found unconscious in bed by his mother. Earlier, the patient had felt drowsy and went to bed early.
He could not be awakened by his mother the next day. Three days before admission, he had had watery
diarrhea. His illness dated back 18 years before when he noticed sudden swelling of his abdomen. He was
admitted to a hospital for treatment and was later discharged from hospital with diuretic.

History of Present Illness: The client complaint of watery diarrhea and swelling of the abdominal

Family History: His father died of liver cirrhosis and was heavy drinker.
Pathophysiology

 
Once the hepatic veins occlude, the liver venous outflow is compromised, the sinusoidal and portal pressures
increase, and the portal flow decreases; if this process continues, it leads to hepatic congestion; formation of
ascites; and, in certain cases, portal vein thrombosis. Hepatocytes undergo hypoxic damage that eventually
evolves into noninflammatory centrilobular cell necrosis. If this hepatocellular damage is massive, the patient will
present with a fulminant form of BCS, which is a potentially fatal condition. Otherwise, the process evolves
slowly and allows the patient to develop portal hypertension and ascites; histologically, the liver develops
fibrosis and, in later stages, cirrhosis. If BCS is not treated, the natural course is that of a progressive and fatal
condition. Previous reports, when no specific therapy was available, showed that 90% of patients with BCS had
died by 3 years. The most common causes of death are intractable ascites, gastrointestinal bleeding, and liver
failure.
Concept Map:

SIGNS &
RISK FACTORS
SYMPTOMS

Liver failure Hematologic Tumors

Hepatomegaly
disorders

Congenital
Hepatic Pregnancy &
Jaundice membranous
encephalopathy postpartum
obstruction

Vomiting & Chronic Oral

Ascites
Fatigue infections contraceptives

Inherited or
Pain in the upper Chronic
Edema in the acquired
right part of the inflammatory
legs thrombotic
abdomen disease
diathesis
 BROWN SEQUARD SYNDROME
By: COCUSA

34-year-old man was brought to the emergency department with minor wounds on the face and a single screwdriver stab
wound on the back. The patient was admitted with normal and stable vital signs, a motor deficit on the left leg and a retained
right paravertebral foreign metallic body. The neurological examination revealed a Brown Sequard syndrome, with grade IV
motor deficit on the left leg below T9 level. The joint position and vibration modalities were preserved, with no sphincter
disturbances.Radiological evaluation with thoracic Computed tomography (CT) and CT angiography revealed a retained 9 cm
linear metallic element in the mid thoracic region. The screwdriver entered and trespassed the spinal canal at T6 level from the
right to the left, reaching the vertebral body and the T5-T6 discal space. The object tip reached the posterior mediastinum with
close relation to the thoracic aorta There was no radiological evidence of pneumothorax or pneumo/ hemomediastinum,
however we could not exclude a vascular injury. Esophagoscopy showed no perforation. the joint decision between the
neurosurgery and the vascular surgery teams was the surgical removal of the screwdriver under direct visualization, after
considering the possibility of a fatal bleeding in case of vascular injury
Pathophysiology

Brown Sequard syndrome results from damage to or loss of ascending and descending spinal
cord tracts on 1 side of the spinal cord. Scattered petechial hemorrhages develop in the gray
matter and enlarge and coalesce by 1 hour postinjury. Subsequent development of hemorrhagic
necrosis occurs within 24-36 hours. White matter shows petechial hemorrhage at 3-4 hours.
Myelinated fibers and long tracts show extensive structural damage.
Concept Map

B
R
O
W Sign and Symptoms of angina:
N •Loss of the sensations of pain and temperature
S •Loss of bladder and bowel control
E •Weakness and degeneration (atrophy)of muscles in the affected area
Q •Paralysis
U Complications
A •Untreated BSS may bring complications like hypotension or spinal shock,
R depression, pulmonary embolism and infections most commonly in the lungs and
D urinary tract. Respiratory support is critical for patients with high thoracic and cervical
S lesions.
Y
N
D
R
O
M
E
 CORONARY ARTERY DISEASE
By: DELA CRUZ

Case Scenario: A male patient of age 65 years was admitted in the hospital with chief complaint of SOB,
palpitations, urinary frequency. His appetite and sleep are normal.
History of Past Illness: type-2 DM
History of Present Illness: A male patient of age 65 years was admitted in the hospital with the c/o shortness of
breath –grade II, palpitations, urinary frequency and is having a past history of type 2 DM and he is diagnosed that
he is having mild CAD with triple vessel disease.
Pathophysiology

Coronary artery disease is usually caused by a build-up cholesterol rich deposits or plaques on the lining inside the artery. These plaques are
also called atheromatous plaques or simply atheromas and they cause a thickening of the arterial wall and a narrowing of the arterial space
through which blood flows to reach the heart. The amount of blood reaching and supplying the heart muscles with oxygen and nutrients can
therefore be reduced in the presence of atheromas. An atheroma usually starts to develop as a result of damage or injury to the inner lining of
the artery called the endothelium. Once the endothelium is damaged, cholesterol, fats, lipoproteins and other debris start to accumulate at the
site of injury in the wall or intima of the artery.High concentrations of low density lipoprotein (LDL) penetrate the damaged endothelium and
undergo a chemical process called oxidation. This altered LDL acts as a beacon that attracts white blood cells or leukocytes to migrate towards
the vessel wall. As macrophages appear, they engulf the lipoproteins and become foam cells. These foam cells give rise to the earliest visible
form of an atheromatous lesion called the fatty streak. Once the fatty streak is formed, it then attracts the smooth muscle cells to the site, where
they multiply and start to produce extracellular matrix comprising of collagen and proteoglycan. It is this extracellular matrix that forms a large
portion of the atherosclerotic plaque. This turns the fatty streak into a fibrous plaque. The lesion then starts to bulge into the inner wall of the
blood vessel causing a significant narrowing of the luminal space. Next, the fibrous plaque starts to support itself. It develops its own small
vessels to provide it with a supply of blood in a process called angiogenesis. Thereafter, the plaques begin to calcify as calcium starts to
deposit. The final plaque is made up of a cap of fibrous tissue covering a core that is rich in lipids as well as necrotic or dead cells. The edge of
this cap is key in acute coronary disease. This region is prone to rupture, which exposes the underlying core of lipids and necrotic material to
thrombogenic factors in the blood. This can cause the aggregation of platelets that form a clot across the plaque and further narrow the artery.
Arteries that have become narrowed due to the presence of plaques may lead to angina or chest pain as the muscles of the heart are deprived
of oxygen. As the deposits on the plaques grow in size and dimension, the blood vessels become further narrowed and there may be
obstruction leading to a heart attack or a myocardial infarction.
Concept Map

Signs and Symptoms Risk Factors

Chest pain Family history of heart disease

Overweight
Weakness, light-headedness,
nausea, or a cold sweat CORONARY
Physical inactivity
ARTERY
Pain or discomfort in the DISEASE
arms or shoulder Smoking

Shortness of breath Unhealthy eating

 TETRALOGY OF FALLOT
By: MUNGCAL

Case Scenario: The authors report a case of a 72-year-old Caucasian woman with a history of controlled
hypertension, followed in the cardiology consultation for uncorrected TOF. In the past, she had a pregnancy that
elapsed without complications and gave birth to a healthy daughter. Currently, she usually complains of
dyspnea.
 
History of Present Illness: The patient sought medical assistance several times and was medicated with four
antibiotics for the proposed diagnosis of respiratory and urinary infections. Given the persistence of fever and
progressive worsening of heart failure, she was brought to a hospital. At admission, she was in class III of the
NYHA and presented with fever, slight peripheral cyanosis, finger clubbing despite oxygen saturation of 91%, a
regular pulse of 95 beats per minute and a blood pressure of 149/70mmHg. Cardiac examination revealed a
single second heart sound, a systolic thrill and loud systolic ejection murmur (grade IV) at the base of her heart.
An electrocardiogram showed normal sinus rhythm with first degree atrioventricular block and incomplete right
bundle branch block.
Pathophysiology
 
 Physiologically the pulmonic stenosis causes concentric right ventricular
hypertrophy without cardiac enlargement and an increase in right ventricular
pressure.
 When the right ventricular pressure is as high as the left ventricular or the
aortic pressure , a right to left shunt appears to decompress the right ventricle
 Once the left and right ventricular become identical, increasing severity of
pulmonic stenosis reduces the flow of blood into the pulmonary artery and
increases the right to left shunt
 As the systolic pressure between two ventricle are identical there is little or no
left to right shunt and the VSD is silent
 The flow from the right ventricle into the pulmonary artery occurs across the
pulmonic stenosis producing as ejection systolic murmur
 More severe the pulmonic stenosis, the less the flow into the pulmonary artery
and the bigger the right to left shunt more the cyanosis
 Thus the severity of cyanosis is directly proportional to the severity of pulmonic
stenosis.
 The VSD of TOF is always large enough to allow free exit to the right to left
shunt.
 Concept Map

DEFINITION SIGNS AND

  RISK
Tetralogy of Fallot is made up of the following four defects of the SYMPTOM
FACTORS
heart and its blood vessels:
1. A hole in the wall between the two lower chambers―or
S
ventricles―of the heart. This condition also is called a These risk factors include:
a bluish skin color.
ventricular septal defect. clubbed fingers, or growths of
A viral illness during pregnancy,
such as rubella (German
2. A narrowing of the pulmonary valve and main pulmonary skin and bone around the
fingernails.
measles)
Alcoholism during pregnancy.
artery. This condition also is called pulmonary stenosis. problems with eating.
Poor nutrition during pregnancy.
3. The aortic valve, which opens to the aorta, is enlarged and
seems to open from both ventricles, rather than from the left
ventricle only, as in a normal heart. In this defect, the aortic failure to gain weight.
A mother older than age 40.
valve sits directly on top of the ventricular septal defect. developmental delays or
problems. A parent who has tetralogy of
4. The muscular wall of the lower right chamber of the heart episodes of passing out.
Fallot.

(right ventricle) is thicker than normal. This also is called

ventricular hypertrophy.
 CROUP
By: OMLANG

The patient is a 3-year-old female with no history of chronic illness who presents to the primary care clinic for evaluation of a
4-day history of cough and fever. She is accompanied by her mother who is a nurse at Baylor University Medical Center.
Chief Complaint: The child has had a “barky, croupy, cough” for 4 days. The cough began on Sunday but worsened on
Monday and Tuesdays (Day 1 and 2 of symptoms). On Tuesday (Day 2) evening the child spiked a temperature of 104 that
has come down to 101-102 between doses of Tylenol and Motrin. Today, the child’s mother noticed that her upper lip is mildly
swollen and the child refused to allow her mother to wipe her nose.
History of Present Illness: As stated above, the patient presented with a 4-day history of cough with onset of fever on day 2 of
symptoms. The cough has a barky quality and is worse when the patient lies down. She has a decreased appetite and is
taken less fluids by mouth. She has had clear nasal drainage for several days and significant nasal congestion. She was
seen by her primary care physician on Day 3 of symptoms (Wednesday) and was diagnosed with croup. No medications
were given or prescribed.
Past Medical History Birth History: The patient was a 36-week infant born to G1 P0→1 female. She weighed 5 lbs. 15 oz. at
birth and had no complications. She was breast fed as an infant.
Pathophysiology

The infection causes inflammation of the larynx, trachea, bronchi, bronchioles, and lung parenchyma. Obstruction caused
by swelling and inflammatory exudates develops and becomes pronounced in the subglottic region. Obstruction increases
the work of breathing; rarely, tiring results in hypercapnia. Atelectasis may occur concurrently if the bronchioles become
obstructed.
Croup is usually preceded by upper respiratory infection symptoms. A barking, often spasmodic, cough and hoarseness
then occur, commonly at night; inspiratory stridor may be present as well. The child may awaken at night with respiratory
distress, tachypnea, and retractions. In severe cases, cyanosis with increasingly shallow respirations may develop as the
child tires.
 
The obvious respiratory distress and harsh inspiratory stridor are the most dramatic physical findings. Auscultation reveals
prolonged inspiration and stridor. Crackles also may be present, indicating lower airway involvement. Breath sounds may
be diminished with atelectasis. Fever is present in about half of children. The child’s condition may seem to have improved
in the morning but worsens again at night.
Recurrent episodes are often called spasmodic croup. Allergy or airway reactivity may play a role in spasmodic croup, but
the clinical manifestations cannot be differentiated from those of viral croup. Also, spasmodic croup usually is initiated by a
viral infection; however, fever is typically absent.
Concept Map
 ATELECTASIS
By: ONIA
A 33 year old female client was brought to Emergency Department with a chief complaint of shortness of breath on exertion.
History of Present Illness: She reports that she was seen for similar symptoms previously at her primary care physician’s office six months
ago. At that time, she was diagnosed with acute bronchitis and treated with bronchodilators, empiric antibiotics, and a short course oral
steroid taper. This management did not improve her symptoms, and she has gradually worsened over six months. She reports a 20-pound
intentional weight loss over the past year. She denies camping, spelunking, or hunting activities. She denies any sick contacts. A brief
review of systems is negative for fever, night sweats, palpitations, chest pain, nausea, vomiting, diarrhea, constipation, abdominal pain,
neural sensation changes, muscular changes, and increased bruising or bleeding.

One hour prior admission, she experienced cough, shortness of breath, and shortness of breath on exertion.

Vital Signs: BP: 100/60 HR:102 bpm RR: 32cpm TEMP: 37C O2 Sat: 80%

ABG: pH 7.47, PaCO2 29.9 mmHg, PaO2 32.5 mmHg, HCO3 21.3 mmol/L, saturation 67.7%, hemoglobin 7.4 g/dL, white blood cell count
100/µL, absolute neutrophil count 0/µL, and platelet count 25,000/µL (TC: severe hypoxia and pancytopenia)

Family History: Lung CA Maternal, DM 2 Paternal

Pathophysiology

Lung injury> alveolar type ll cells damage> lack of surfactant

production> there will be increased surface tension of the alveoli>
resulting to decreased alveolar compliance and recoil> affected portion
of alveoli becomes airless> Alveolar collapse
Concept Map:
ATELECTASIS
SIGNS AND SYMPTOMS
- Respiratory Distress
- Low grade fever
- Dyspnea, Tachycardia
- Tachypnea, pleural pain and
central cyanosis
- Orthopnea
- Anxious
TREATED WITH
- Chest physical therapy (percussion
and postural drainage
- Nebulizer with bronchodilator
- Sodium Bicarbonate for expectoration
of secretions
- ET tube and Mech Vent if necessary
- Incentive spirometry
- Early Ambulation
- Surgery: Lobectomy/ wedge
resection/ bronchoscopy
RISK FACTORS
- Immobility- shallow respirations
- Pain: fear of deep breathing/ coughing
following surgery or trauma
- Elderly Patients
- Retained Secretions
- Immunocompromised pt
- Depressed cough reflex
- Smoking
- COPD and Bronchial Asthma
- Pneumothorax
- Pleural Effusion
- Pneumonia
- Chest Trauma
 A
By: PANOPIO
 A
By: PERENA
 A
By: SANTOS