ADAMSON UNIVERSITY 2ND SEM 2019-2020

COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

GROUP NO. _3_ Date: 04/19/20

GROUP MEMBERS: Score: ___________
1. Noe, Ma. Marella
2. Pagbilao, Meriel Maan A.
3. Quiao, Stephanie Grace G.

CASE NO. 1 - CARDIOVASCULAR DISEASE

I. PATIENT DEMOGRAPHICS

Name: Bo Gum
Age: 62 y/o
Gender: Male
Height: 6’2”
Weight: 95 kg
Race: African-American

II. SUBJECTIVE DATA (all in bullets)

A. CHIEF COMPLAINT
 Occasional mild headaches
 Dizziness after the patient takes his morning medications
 Usual chronic cough
 Shortness of Breath when walking moderate distances
 Patient is just getting over a cold
 Patient doesn’t like his low salt diet prescribed by his doctor
B. HISTORY OF PRESENT ILLNESS
 The patient presents to his new family medicine physician
 Patient has no general complains except for occasional mild headaches, and some
dizziness after he takes his morning medications
 Dissatisfied with being placed on a low sodium diet by his former primary care physician
 Patient reports a “usual” chronic cough and shortness of breath particularly when
walking moderate distances
 Patient states “I’m just out of shape” pertaining to his shortness of breath
C. PAST MEDICAL HISTORY
 Hypertension for 15 years
 Has Type 1 Diabetes Mellitus
 Chronic Obstructive Pulmonary Disease, Stage 2 (Moderate)
 Benign Prostatic Hyperplasia
 Chronic Kidney Disease
D. FAMILY HISTORY
 Patient’s Father died of Acute MI at the age of 71
 Patient’s Mother died of Lung Cancer at the age of 64
 Patient’s Mother had both HTN and DM
E. PERSONAL AND SOCIAL HISTORY
 Patient is a former smoker (quit 3 years ago; smoke 1 ppd x 28 years)
 Reports moderate amount of alcohol intake
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COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

 Patient admits he has been nonadherent to his low sodium diet

 Patient states “I can eat whatever I want”
 Patient does not exercise regularly
 Patient is limited somewhat functionally by his COPD
 Patient is retired and lives alone
F. MEDICATIONS

G. Triamterene/hydrochlorothiazide
37.5 mg/25 mg po Q AM
H. Insulin 70/30, 24 units Q AM, 12
units Q PM
I.Triamterene/hydrochlorothiazide
37.5 mg/25 mg po Q AM
J.Insulin 70/30, 24 units Q AM, 12
units Q PM
K. Doxazosin 2 mg po Q AM
L. Albuterol INH 2 puffs Q 4–6 h
PRN shortness of breath
M. Tiotropium DPI 18 mcg 1 capsule
INH daily
N. Salmeterol DPI 1 INH BID
O. Entex PSE 1 capsule Q 12 h PRN
cough and cold symptoms
P. Acetaminophen 325 mg po Q 6 h
PRN headache
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COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

 Triamterene/hydrochlorothiazide 37.5 mg/25 mg po Q AM

 Insulin 70/30, 24 units Q AM, 12 units Q PM
 Doxazosin 2 mg po Q AM
 Albuterol INH 2 puffs Q 4–6 h PRN shortness of breath
 Tiotropium DPI 18 mcg 1 capsule INH daily
 Salmeterol DPI 1 INH BID
 Entex PSE 1 capsule Q 12 h PRN cough and cold symptoms
 Acetaminophen 325 mg po Q 6 h PRN headache
Q. REVIEW OF SYSTEMS (ROS)
 Patient states that overall he is doing well and just getting over a cold
 Patient noticed no major weight changes over the past few years
 Complains of occasional headaches and is usually relieved by acetaminophen
 Denies blurred vision and chest pain
 Patient states that his shortness of breath is “usual” for him and that his albuterol helps
 Denies experiencing any hemoptysis or epistaxis
 Denies nausea, vomiting, abdominal pain, cramping, diarrhea, constipation or bloody
stool
 Denies urinary frequency
 Patient states difficulty urinating until physician prescribed him with Doxazosin a few
months ago

III. OBJECTIVE DATA

A. VITAL SIGNS (all in bullets)
 BP - 168/92 mm
 Hg - (sitting; repeat 170/90)
 HR - 76 bpm (regular)
 RR - 16 per min
 T - 37°C
 Wt - 95 kg
 Ht - 6'2''
B. PHYSICAL EXAM (all in bullets)
 HEENT: TMs clear; mild sinus drainage; AV nicking noted; no hemorrhages,
exudates, or papilledema
 Neck: Supple without masses or bruits, no thyroid enlargement or
lymphadenopathy
 Lungs: Lung fields CTA bilaterally. Few basilar crackles, mild expiratory
wheezing
 Heart: RRR; normal S1 and S2. No S3 or S4
 Abd: Soft, NTND; no masses, bruits, or organomegaly. Normal BS.
 Genit/Rect: Enlarged prostate; benign
 Ext: No CCE
 Neuro: No gross motor-sensory deficits present. CN II–XII intact. A & O × 3.

C. LABORATORY EXAM
ADAMSON UNIVERSITY 2ND SEM 2019-2020
COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

Parameters Results Normal values Interpretation

ADAMSON UNIVERSITY 2ND SEM 2019-2020
COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

Na 142 mEq/L 135 - 145 Normal

K 4.8 mEq/L 3.5 -5.0 Normal
Cl 101 mEq/L 95 - 105 Normal
Co2 27 mEq/L 20 - 29 Normal
BUN 22 mg/dL 7 - 20 Abnormal
SCr 1.6 mg/dL 0.6 – 1.3 Abnormal
Glucose
136 Abnormal

mg/dL
136
mg/dL 70 - 110

136
mg/dL
136 mg/dL
Ca 9.7 mg/dL 8.5 - 10.5 Normal
Mg 2.3 mEq/L 1.5 - 2.5 Normal
HbA1c 6.2% 5.6 - 7.5 Normal
Alb 3.5 g/dL 3.5 -5.0 Normal
Hgb 13 g/dL 13 - 18 Normal
Hct 40% 36 - 44 Normal
WBC 9.0×103/mm3 5 -10 Normal
Plts 189×103/mm3 150 - 450 Normal
Total Chol
169 Normal

mg/dL
169 <200

mg/dL
169 mg/dL
LDL 99 mg/dL Below 130 Normal
HDL 40 mg/dL Above 50 Borderline
TG 151 mg/dL Below 150 Normal
FVC 54% pred 80% - 120% Severely Abnormal
FEV1 38% pred 80% - 120% Severely Abnormal
FEV1/FVC 51% Less than 70% Normal

IV. ASSESSMENT
A. BACKGROUND OF THE DISEASE
a. DEFINITION
Renovascular disease - is the term given to the impairment of renal perfusion caused by disease affecting
the arterial supply of the kidney(s). Renal hypoperfusion leads to hyperactivation of the renin-angiotensin-
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COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

aldosterone axis, causing hypertension. Renovascular disease is an important cause of secondary

hypertension and chronic kidney disease.

b. SIGNS AND SYMPTOMS

People with renovascular hypertension may have a history of very high blood pressure that is hard to bring
down with medicines. Symptoms of renovascular hypertension include:
 High blood pressure at a young age
 High blood pressure that suddenly gets worse or is hard to control
 Kidneys that are not working well (this can start suddenly)
 Narrowing of other arteries in the body, such as to the legs, the brain, the eyes and elsewhere
 Sudden buildup of fluid in the air sacs of the lungs (pulmonary edema)
If you have a dangerous form of high blood pressure called malignant hypertension, symptoms can include:
 Bad headache
 Nausea or vomiting
 Confusion
 Changes in vision
 Nosebleeds

c. RISK FACTORS
 Hypertension (but up to 35% of patients with renovascular disease may be normotensive).
 Advanced age (much more common in those aged 60-70 years, with prevalence increasing in
those aged >70 years; one unselected post-mortem series showed a prevalence of 42% in those
aged over 75 years).
 Evidence of renal impairment.
 Evidence of peripheral arterial or cerebrovascular/cardiovascular disease.
 Diabetes mellitus.
 Smoking.
 Family history of cardiovascular disease or renovascular disease.
 Hyperlipidemia.
 White racial background (approximately twice the prevalence in those with a white racial
background compared with African Americans in a group of patients with severe hypertension).

d. STANDARD TREATMENTS
If medical management—medications and lifestyle changes—are insufficient, interventional radiologists can
perform angioplasty and, if needed, stenting, to improve blood flow to the kidney. The goal of the
treatment in renovascular disease is normalization of the blood pressure or improvement of its control with
medications, and improvement or preservation of kidney function. Angioplasty of the renal artery is
relatively low risk and can improve blood pressure control and thus prevent further damage to the kidney.
Balloon angioplasty and stenting has generally replaced surgery as the first-line treatment for renal arterial
occlusions.

Antihypertensive drug therapy is indicated. Optimal blood pressure control plays an essential role in the
therapeutic management of renovascular hypertension (RVHT); however, aggressive control of other risk
factors for atherosclerosis is also crucial. Cessation of smoking is important for its positive impact on the
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COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

cardiovascular risk profile in patients with hypertension. Similarly, antidyslipidemic therapy for those
patients with hyperlipidemia likely provides benefit in atherosclerotic RVHT.

The invasive and surgical options for treatment of renovascular hypertension include the following:
 Percutaneous transluminal angioplasty (PTA)
 Surgical revascularization
 Nephrectomy

B. PATHOPHYSIOLOGY OF THE DISEASE

Evidence from animal studies demonstrates that the renin-angiotensin (ANG II) system and sodium
retention play major roles in experimental renovascular hypertension (RVH). Two basic models have been
described. In the first, one-clip two-kidney Goldblatt hypertension, the ischemic kidney secretes renin,
which leads to increased ANG II formation and hence elevation of blood pressure (BP). As BP rises, sodium
excretion by the intact contralateral kidney increases (pressure natriuresis); therefore, there is no sodium
retention. In the second, one-clip one-kidney Goldblatt hypertension, the contralateral kidney is removed.

In this case the pressure natriuresis can no longer occur, and sodium retention occurs. The ensuing
expansion of plasma volume inhibits renin secretion, so that in this model the renin level is normal or low.
Following the clipping of the renal artery, renal blood flow and pressure are maintained distal to the
stenosis by an ANG II-mediated vasoconstriction. This acts prefrrentially on the efferent glomerular
arterioles, so that the ratio of preglomerular to postglomerular resistance is reduced, which helps to
maintain glomerular filtration despite the reduced renal perfusion pressure. In the contralateral kidney the
afferent arteriolar resistance is increased, probably as a direct result of exposure to the higher intrarenal
arterial pressure. ANG II constricts the efferent arterioles in the same way as in the ischemic kidney, so that
the ratio of preglomerular to postglomerular resistance is unchanged.

When an angiotensin converting enzyme (ACE) inhibitor is given, the efferent arterioles vasodilate. In the
ischemic kidney this may produce a reduction of glomerular filtration rate (GFR), which is not seen in the
contralateral kidney. Unilateral RVH in humans corresponds closely to the animal model of one-clip two-
kidney hypertension. Plasma renin activity is usually high, and converting enzyme inhibitors lower BP
effectively. The increased renin is due exclusively to increased secretion of renin by the ischemic kidney,
and is completely suppressed in the contralateral kidney.

It is not clear whether bilateral RVH corresponds to the one-clip one-kidney model, but there is
circumstantial evidence to suggest that both renin and volume factors may be involved. The majority of
cases of human RVH are caused by atheroma, which is commonly bilateral, or by fibromuscular dysplasia.
The former tends to be associated with atheroma elsewhere in the arterial tree, and often progresses to
complete occlusion and renal failure. The latter occurs in younger patients, and almost never progresses to
complete occlusion.

V. PLANNING
A. PHARMACOLOGIC INTERVENTION
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COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

Dosage &
Intervention Indication Frequenc Route MOA
y
Triamterene/HCT Diuretic/ 37.5 PO Triamterene: inhibit Na+ reabsorption;
Z Antihypertensiv mg/25 inhibits Na/K-ATPase, decreases Ca++ , Mg++
e mg Q AM and hydrogen excretion
Hydrochlorothiazide: Inhibits sodium
reabsorption in distal renal tubules, resulting
in increased excretion of water and of
sodium, potassium, and hydrogen ions

Insulin Type 1 DM 70/30, 24 IM Lowers blood glucose by stimulating

Type 2 DM units Q peripheral glucose uptake primarily by
AM, 12 skeletal muscle cells and fat, and by inhibiting
units Q glucose production and release by the liver.
PM
Doxazosin BPH 2mg Q PO Selectively inhibits the postsynaptic alpha-1
AM receptors on vascular smooth muscle by
nonselectively blocking the alpha-1a, alpha-
1b, and alpha-1d subtypes. This action on
blood vessels decreases systemic peripheral
vascular resistance, reducing blood pressure,
exerting minimal effects on the heart rate
due to its receptor selectivity.
Albuterol Bronchospasm INH 2 Inhalatio Relaxing the smooth muscles of the airways.
puffs Q 4- n It activates the beta2-adrenergic receptors in
6h PRN the lungs, which begins a cascade of actions
that result in bronchodilation
Tiotropium COPD DPI 18 Inhalatio Antagonist of muscarinic receptors M1 to M5.
mcg 1 n Inhibition of the M3 receptor in the smooth
capsule muscle of the lungs leads to relaxation of
INH daily smooth muscle and bronchodilation.
Salmeterol Anti-asthma DPI 1 INH Inhalatio Bind to 2 sites on the beta-2 adrenoceptor.
BID n The saligenin moiety binds to the active site
of the beta-2 adrenoceptor. The hydrophilic
tail of salmeterol binds to leucine residues in
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COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

the exo-site of the beta-2 adrenoceptor

almost irreversibly, allowing salmeterol to
persist in the active site, which is responsible
for it's long duration of action.
Entex PSE Decongestant, 1 capsule PO Pseudoephedrine hydrochloride is an (alpha)
Expectorant Q 12h adrenergic receptor agonist (sympathomimeti
PRN c) which produces vasoconstriction by
stimulating (alpha)-receptors within
the mucosa of the respiratory tract

Guaifenesin promotes lower respiratory tract

drainage by thinning bronchial secretions,
lubricates irritated respiratory tract
membranes through increased mucous flow,
and facilitates removal of viscous,
inspissated mucus.
Type of Mechanism of
Drug Combination
Acetaminophen Analgesic Interaction
325 mg PO Intervention
InteractionReduce the production of prostaglandins in
Q6 h PRN the brain
pseudoephedrine + Drug-Drug pseudoephedrine Use
doxazosin decreases effects of Caution/Monitor.
doxazosin by
sympathetic B. ADVERSE
(adrenergic) effects, DRUG
Drug ADR including increased
Regimen REACTION
blood pressure and MONITORING
(if N/A N/A N/A heart rate. applicable)
albuterol + salmeterol Drug-drug albuterol and Use
salmeterol both Caution/Monitor.
decrease sedation,
both increase
sympathetic
(adrenergic) effects,
including increased
blood pressure and C. DRUG
heart rate. INTERACTION
albuterol + Drug-drug albuterol and Use MONITORING
(if pseudoephedrine pseudoephedrine both Caution/Monitor. applicable)
increase sympathetic
(adrenergic) effects,
including increased
blood pressure and
heart rate.
salmeterol + Drug-drug salmeterol and Use
pseudoephedrine pseudoephedrine both Caution/Monitor.
increase sympathetic
(adrenergic) effects,
including increased
blood pressure and
heart rate. 
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C. NON-PHARMACOLOGIC INTERVENTION

Lifestyle changes are important:

 Eat a heart-healthy diet.
 Exercise regularly, at least 30 minutes a day (check with your doctor before starting).
 If you smoke, quit. Find a program that will help you stop.
 Limit how much alcohol you drink: 1 drink a day for women, 2 a day for men.
 Limit the amount of sodium (salt) you eat. Aim for less than 1,500 mg per day. Check with your
doctor about how much potassium you should be eating.
 Reduce stress. Try to avoid things that cause stress for you. You can also try meditation or yoga.
 Stay at a healthy body weight. Find a weight-loss program to help you, if you need it.

VI. DISCUSSION
VII. CONCLUSION

VIII. REFERENCES (APA Format, in bullets)

 Abimbola Farinde. (2019). Lab Values, Normal Adult. Retrieved at:
https://emedicine.medscape.com/article/2172316-overview
 American College of Physicians 190 N. Independence Mall West, Philadelphia, PA 19106-1572.
Retrieved at: http://idgateway.wustl.edu/Normal%20lab%20values.pdf
 Erica Cirino. (2017). Spirometry: What to Expect and How to Interpret Your Results. Retrieved
at: https://www.healthline.com/health/spirometry
 TIMOTHY J. BARREIRO, D.O., and IRENE PERILLO, M.D., University of Rochester School of Medicine
and Dentistry, Rochester, New York Am Fam Physician. 2004 Mar 1;69(5):1107-1115. Retrieved at:
https://www.aafp.org/afp/2004/0301/p1107.html
 Colin Tidy. (2016). Renovascular Disease. Retrieved at: https://patient.info/doctor/renovascular-
disease
 Deepak Sudheendra. (2018). Renovascular hypertension. Retrieved at:
https://medlineplus.gov/ency/article/000204.htm
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COLLEGE OF PHARMACY PHARMACOLOGY and THERAPEUTICS 2

 Siu AL, US Preventive Services Task Force. Screening for high blood pressure in adults: US Preventive
Services Task Force recommendation statement. Ann Intern Med. 2015;163(10):778-786. PMID:
26458123 www.ncbi.nlm.nih.gov/pubmed/26458123.
 Rebecca J Schmidt. (2018). Renovascular Hypertension Treatment & Management. Retrieved at:
https://emedicine.medscape.com/article/245140-treatment#showall
 Standford Health Care. Treatment of Renovascular Hypertension. Retrieved at:
https://stanfordhealthcare.org/medical-conditions/blood-heart-circulation/renal-
hypertension/treatments.html
 Thomas G.Pickering. (2006). Renovascular hypertension: Etiology and pathophysiology.
Cardiovascular Center, The New York Hospital-Cornell University Medical Center, New York, USA.
Retrieved at: https://www.sciencedirect.com/science/article/abs/pii/S0001299889800030
 Cerner Multum (2019). Triamterene and Hydrochlorothiazide. Retrieved at:
https://www.drugs.com/pro/triamterene-and-hydrochlorothiazide.html
 Triamterene/hydrochlorothiazide (Rx). Retrieved at:
https://reference.medscape.com/drug/dyazide-triamterene-hydrochlorothiazide-342342#0
 Omudhome Ogbru. (2019). Insulin for Diabetes Treatment (Types, Side Effects, and Preparations).
Retrieved at:
https://www.medicinenet.com/insulin_for_diabetes_treatment_types_side_effects/article.htm#
what_is_diabetes
 Michel MC, Grubbel B, Taguchi K, Verfurth F, Otto T, Kropfl D: Drugs for treatment of benign
prostatic hyperplasia: affinity comparison at cloned alpha 1-adrenoceptor subtypes and in human
prostate. J Auton Pharmacol. 1996 Feb;16(1):21-8. [PubMed:8736427]
 Justine Fritzel. Albuterol: Pharmacokinetics & Mechanism of Action. Retrieved at:
https://study.com/academy/lesson/albuterol-pharmacokinetics-mechanism-of-action.html
 Hansel TT, Barnes PJ: Tiotropium bromide: a novel once-daily anticholinergic bronchodilator for the
treatment of COPD. Drugs Today (Barc). 2002 Sep;38(9):585-600. [PubMed:12582447]
 Brogden RN, Faulds D: Salmeterol xinafoate: a review of its pharmacological properties and
therapeutic potential in reversible obstructive airways disease. Allergol Immunopathol (Madr). 1992
Mar-Apr;20(2):72-84. [PubMed:1359777]
 RxList. Entex PSE. Retrieved at https://www.rxlist.com/entex-pse-drug.htm#description

IX. RUBRICS
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