CPT CASE 10

Mayrong, Mario Alex Jr F

 OBJECTIVES
● Identify the common signs and symptoms of the
presented problems
● Discuss briefly the pathophysiology of the presented
diseases
● Discuss the pharmacologic and non-pharmacologic
management of the presented diseases (including follow-
up)
● Enumerate the desired therapeutic outcomes
 TABLE OF CONTENTS
1. Patient Presentation
2. Peptic Ulcer Disease
3. Osteoarthritis
4. Alzheimer's Disease
1.Patient Presentation
Chief Complaint:
● Epigastric Pain

General Data:
● PJ, 55 years old, male
History of Present Illness:
● Sought consult at the provincial hospital’s emergency section complaining of
feeling dizzy and nauseous, weak and with abdominal pain, localized at the
epigastric area, described as burning, on and off throughout the day, usually
occurring 1-2 hours after a meal which is not relieved even by food intake.
● Above symptoms were noted 3 weeks prior to consult. He denies any history
of passing out fresh blood in the stools nor dark stools. Because of the
nausea, he has not eaten or drank much in the last 3 days.
● He also complains of frequency of nocturnal urination with a feeling of
incomplete emptying of the bladder for the last 3 months. He also has
difficulty falling asleep during the past month due to problems at work and
abdominal pain.
● His family noticed also within the last 3 months that he had been having
difficulty remembering recent events and conversations and organizing things,
difficulty with problem solving and performing tasks
Past Medical History:
● Diagnosed with osteoarthritis of the left knee and is taking
Ibuprofen as needed. Diagnosed with benign prostatic
hypertrophy (BPH) 3 months ago and has been taking
Tamsulosin once daily

Family History:
● Father died of colon cancer at the age of 75.
● Mother is alive and well at the age of 76.
● No siblings.
Social History:
● Married and is working as a real estate agent. Although he
takes Ibuprofen whenever he suffers from an attack of arthritis,
he still feels that “natural” medicines are better than “artificial”
pills.
● Beer drinker (average of 2 bottles/day)
● No history of tobacco or illicit drug use

Medications:
● Ibuprofen 200 mg PO every 6 hours prn for pain
● Tamsulosin 0.4 mg 1 tab PO OD 30 min after dinner
ROS:
● Nausea and epigastric pain
● Dizziness, anorexia and body malaise X 3 days
● Left knee pain, especially when walking, seen 1st thing in the morning
 PHYSICAL EXAM FINDINGS
● Vital Signs:
○ Knee Pain 3/10
○ Epigastric Pain 5/10
● Abdomen:
○ non-tender/not distended
○ (+) epigastric pain
● Genitourinary:
○ Deferred
● Rectal:
○ Normal rectal tone; prostate is enlarged and non-tender with
rubbery consistency minimal stool in rectal vault that is occult
blood (-)
 LABORATORY TESTS
● (+) H.pylori serology
○ Normal is (-)
● PSA: 5 ng/mL
○ Normal values: < 2.5 ng/mL
Peptic Ulcer Disease
Basis
Age 55 y.o

Male

NSAID use- Ibuprofen

Epigastric pain - occurs 1-2 hours after meals, not relieved by food intake

Alcohol- 2 bottles/day

Serology: (+) H. pylori

Peptic Ulcer Disease
● Focal defects in the gastric or duodenal mucosa that extend into the
submucosa or deeper.
● Disruption of the mucosal integrity of the stomach and/or duodenum → leads
to local defect or excavation due to active inflammation
● May be acute or chronic
● Complicated or uncomplicated
● Complicated - GI complications (bleeding, obstruction, perforation)
● Uncomplicated - mild epigastric pain
● Epigastric gnawing or burning, often occurring nocturnally, promptly relieved
by food or antacids, exacerbated by fasting
Clinical Manifestation
● Majority are asymptomatic
● Later present with ulcer complications: hemorrhage, perforation
● Older adults - especially those taking NSAIDs
● Symptomatic

-Most prominent symptoms: upper abdominal pain (epigastric pain) or

discomfort

Radiation to back - not typical

DUODENAL ULCER GASTRIC ULCER

Worsening abdominal pain on an empty Nausea, vomiting, weight loss, postprandial

stomach abdominal pain

Occurs 2-5 hours after a meal and at night Early satiety Fatty food intolerance Pain at
(between 11pm - 2am least 1 hr after meal

Pain at least 2 hrs after meal Abdominal pain
relieve after food intake
Occurs more commonly I individuals aged 20 –
45 years Nocturnal pain
Abdominal pain aggravated by food intake
Occurs more commonly in the sixth decade of
life (ages 51 - 60)
Risk of malignancy
Risk Factors
Smoking

Alcohol - high concentrations

damage the asterisk mucosal barrier

Family history

NSAID use

Other factors:

o Blood groups O and A

o Diet

o Psychological factors
Diagnostic Test
Esophagogastroduodenoscopy (EGD) or upper endoscopy

o Most sensitive (90%) and accurate

o Allows for biopsy, histology, culture, rapid urease test, detection of H. pylori,

differentiating between a malignant and benign lesion

Barium swallow - when endoscopy is contraindicated

Non-invasive, less costly tests:

o Serology

o Urea breath testing

o Stool test
Therapeutics
Alleviate the patient of PUD symptoms

Facilitate healing of ulcers

Reduce acid secretion

Prevent development of complications of PUD

Prevent recurrence of PUD

Eradicate H.pylori infection

NON-PHARMACOLOGIC MANAGEMENT
Avoid smoking and alcohol intake

Diet

o High fiber, vegetables, fruits and whole grains

o Proteins

o Micronutrients - zinc

Reduce NSAID use - if not possible, decrease the dose

PHARMACOLOGIC MANAGEMENT
Drug of choice: Omeprazole
PHARMACODYNAMICS

o Irreversibly blocks the H/K ATPase in the active parietal cell which is involved in the final step of acid production, thus inhibiting
gastric acid secretion

o Antisecretory effect is dose-related o Inhibition of both basal and stimulated acid secretion

PHARMACOKINETICS

Onset: 1 hour o Duration: 72 hours

o Bioavailability: 40-65% o T ½: 0.5 - 1 hour

o Distribution: plasma protein binding is 95% o Absorption: Rapidly absorbed

o Metabolism: in the liver primarily by the cytochrome P450 system

o Excretion: Mainly in the urine as an unchanged drug and its metabolites

DRUG INTERACTIONS: o Decrease plasma concentrations of nelfinavir and atazanavir

o Increase plasma concentration of methotrexate o Decrease absorption of itraconazole and ketoconazole

CONTRAINDICATION: History of hypersensitivity

Drug of choice: Clarithromycin
PHARMACODYNAMICS: A macrolide that selectively binds to the 50s ribosomal subunit of susceptible bacteria that prevents the activated
amino acid translocation resulting in inhibition of protein synthesis.

PHARMACOKINETICS:

o Peak plasma concentration achieved 2-3 hours

o Bioavailability: 50% o T ½: 6 hours

o Distribution: Widely distributed into most body tissues. Plasma protein binding approx. 80%

o Absorption: Rapidly and well absorbed from the gastrointestinal tract

o Metabolism: Partially metabolised in the liver and undergoes extensive firstpass metabolism into 14-hydroxyclarithromycin

o Excretion: Urine and some in the feces as unchanged drug

SIDE EFFECTS: headache, nausea, vomiting, diarrhea, bloating and indigestion

CONTRAINDICATION: Hypersensitivity to clarithromycin or any macrolide antibiotics.

DRUG INTERACTIONS:

o May increase plasma concentration and exposure with fluconazole o

Metabolism significantly inhibited by ritonavir

Drug of choice: Amoxicillin
PHARMACODYNAMICS: Binds to penicillin-binding proteins that inhibit transpeptidation, leading to activation of autolytic enzymes
in the bacterial cell wall leading to cell wall lysis, thus destroying the bacterial cells.

PHARMACOKINETICS:

o Peak plasma concentration is 1-2 hours (oral)

o Bioavailability: 70% (oral)

o T ½: Approximately 1 hour

o Distribution: Plasma protein binding approx. 20% o

Absorption: Rapidly and well absorbed from the gastrointestinal tract.

o Metabolism: Hydrolysis to inactive penicilloic acid

o Excretion: Urine as unchanged drug

SIDE EFFECTS: Headache, dizziness, agitation, nausea, diarrhea and vomiting

CONTRAINDICATION: Hypersensitivity or history of severe allergic reactions to amoxicillin or other B-lactams Drug interactions: o
May reduce the excretion and increase toxicity of me
Osteoarthritis
Basis
● Left knee pain: 3/10 (Especially when walking, seen 1st thing in the morning)
● Age: 55 years old
● BMI: 23.7 (Normal)
● Current medication for OA: Ibuprofen 200 mg PO Q6 PRN for pain
Osteoarthritis
● Most common type of arthritis
● Commonly affects the joints of the hip, knee, and first metatarsal phalangeal
joint (MTP) and cervical and lumbosacral spine
● Can be diagnosed based on structural abnormalities or on the symptoms
these abnormalities evoke
● PROCESS: MMPs and pro-inflammatory cytokines (e.g., IL-1)

o Mediators of cartilage destruction

o Increase concentrations in OA cartilage

o Catalyze both collagen and proteoglycan degradation

Risk Factors
Diagnosis (ACR)
Clinical and Laboratory Diagnostic
Criteria
Knee pain plus at least 5 / 9:
o Age >50 years
o Stiffness <30 minutes
Clinical and Radiographic Diagnostic
Criteria
● Knee pain plus
● Osteophytes plus
● At least 1 / 3 :

o Crepitus o age >50 years

o Bony tenderness o stiffness <30 minutes

o Bony enlargement o crepitus
o No palpable warmth

o ESR <40 mm/hour

o RF <1.40

o Synovial fluid signs of OA

Laboratory
● Clinical history
● Physical examination
● Imaging studies (Radiographic findings)
● Routine laboratory tests (Synovial fluid analysis)
Complications
● Chondrolysis
● Osteonecrosis
● Stress fractures
● Bleeding inside the joint
● Infection
Therapeutic Goals:
● To alleviate pain
● To minimize loss of physical function
Recommended therapies for the management of osteoarthritis (OA) (2019 American College of Rheumatology/Arthritis
Foundation Guideline for the Management of Osteoarthritis of the Hand, Hip, and Knee)
Treatment of osteoarthritis (DiPiro)
Recommended stepped-care approach for the treatment of osteoarthritis
Management of Knee Osteoarthritis In Europe And Internationally: A Report From A Task Force Of The European Society
For Clinical And Economic Aspects Of Osteoporosis And Osteoarthritis (ESCEO)
Management of Knee Osteoarthritis In Europe And Internationally: A Report From A Task Force Of The European Society
For Clinical And Economic Aspects Of Osteoporosis And Osteoarthritis (ESCEO)
NON-PHARMACOLOGIC MANAGEMENT
● Avoiding painful activities
● Improving the strength and conditioning of muscles that bridge the joint
● Unloading the joint
PHARMACOLOGIC MANAGEMENT
NON-PHARMACOLOGIC MANAGEMENT
● Avoiding painful activities
● Improving the strength and conditioning of muscles that bridge the joint
● Unloading the joint
DRUG OF CHOICE: PARACETAMOL
Mechanism of action: An active metabolite of phenacetin and is responsible for its analgesic effect

o A weak COX-1 and COX-2 inhibitor in peripheral tissues

o Inhibits prostaglandin synthesis in the CNS

o Does not affect platelet function or increase bleeding time

Pharmacokinetics:

Absorption: Acetaminophen is administered orally. Peak blood concentrations are usually reached in 30–60 minutes

Distribution: Distributed into most body tissues. Crosses placenta and enters breast milk. Plasma protein binding: Approx 10-
25%

Metabolism: Mainly metabolised in the liver via glucuronic and sulfuric acid conjugation. N-acetyl-p-benzoquinone imine
(NAPQI), a minor metabolite produced by CYP2E1 and CYP3A4, is further metabolized via conjugation with glutathione in
the liver and kidneys
DRUG OF CHOICE: PARACETAMOL
Excretion: Mainly via urine (<5% as unchanged drug; 60-80% as glucuronide metabolites and 20-30% as sulphate metabolites). Elimination half-life: Approx 1-3 hours

PHARMACODYNAMICS: o It has been suggested that it may act predominantly by inhibiting prostaglandin synthesis in the CNS and to a lesser extent through a
peripheral action by blocking pain-impulse generation. The peripheral action may also be due to inhibition of prostaglandin synthesis or to inhibition of the synthesis or
actions of other substances that sensitize pain receptors to mechanical or chemical stimulation. The drug has no effect on the cardiovascular and respiratory systems,
and unlike salicylates it does not cause gastric irritation or bleeding.

INDICATIONS: o For mild analgesia, acetaminophen is the preferred drug in patients allergic to aspirin, when salicylates are poorly tolerated. It is preferable to aspirin
in patients with hemophilia, in those with a history of peptic ulcer, and in those in whom bronchospasm is precipitated by aspirin. Unlike aspirin, acetaminophen does
not antagonize the effects of uricosuric agents.

CONTRAINDICATIONS: o Severe hepatic impairment or active liver disease (IV)

DRUG INTERACTION: o Reduced rate of absorption with colestyramine. Increased absorption with metoclopramide and domperidone. Prolonged use of paracetamol
may enhance the anticoagulant effect of warfarin and other coumarins, thus increasing the risk of bleeding. Concomitant use of other potentially hepatotoxic drugs or
drugs that induce liver microsomal enzymes (e.g. barbiturates) may increase the risk of paracetamol toxicity. Reduced clearance with probenecid and isoniazid.
Elimination half-life may be prolonged with salicylamide. Reduced bioavailability and efficacy of lamotrigine. May increase the plasma concentration of chloramphenicol
and busulfan. Increased risk of high anion gap metabolic acidosis with flucloxacillin.

ADVERSE EFFECTS: o In therapeutic doses, a mild reversible increase in hepatic enzymes may occasionally occur. With larger doses, dizziness, excitement, and
disorientation may occur. Ingestion of 15g of acetaminophen may be fatal, death being caused by severe hepatotoxicity with centrilobular necrosis, sometimes
associated with acute renal tubular necrosis
 Benign Prostatic Hyperplasia
● common condition encountered in aging men and a
common cause of lower urinary tract symptoms.
Histological prevalence of BPH is common, and
disease progression is associated with bladder
outflow obstruction, this may present clinically in both
the emergency surgical and outpatient clinical
settings.
Ng M, Baradhi KM. Benign Prostatic Hyperplasia. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK558920/

Mayrong
Benign Prostatic Hyperplasia
Basis:
● Age
● Frequent nocturnal urination
● Incomplete emptying of the bladder
● Abdominal pain
● (+) history of BPH 3 months ago thus taking
tamsulosin once daily
● DRE(+); enlarged and non tender prostate witn
rubbery consistency
● Lab: PSA 5ng/mL

Mayrong
 PATHOPHYSIOLOGY
● Aging
● Decrease testosterone level
● Testosterone converted to dihydrotestosterone
● Dihydrotestosterone accumulated in the stromal
cell
● Prostate enlargement
● Urine obstruction

Mayrong
RISK FACTORS

● Metabolic syndrome
● Age
● Obesity
● Genetic predisposition

Mayrong
Diagnostic tests
 Complications
● Sudden inability to urinate
● Urinary Tract Infections
● Bladder Stones
● Bladder Damage
● Kidney Damage

Mayrong
 Therapeutic goals
● Symptomatic relief
● Improved urinary flow rate
● Improve quality of life

Mayrong
Non pharmacologic management
● Fluid reduction at night
● Healthy lifestyle and diet maintenance
● Bladder training
● Active surveillance
● Avoidance of irritants such as smoking, alcohol,
tea, fizzy drinks, dairy products such as milk and
yogurt, spicy foods

Mayrong
Pharmacologic management
Drug of choice
Dutasteride

● Mechanism of Action: Dutasteride, a 4-azo

analog of testosterone, is a competitive, selective
inhibitor of both type 1 (skin and liver) and type 2
(reproductive tissues) 5α-reductase, resulting in
the inhibition of the conversion of testosterone to
dihydrotestosterone thus reducing levels of
circulating dihydrotestosterone.
Mayrong
● Pharmacokinetics:
○ Absorption: Absorbed from the gastrointestinal tract.
Bioavailability: Approx 60%. Time to peak plasma
concentration: 1-3 hours.
○ Distribution: Volume of distribution: 300-500 L. Plasma
protein binding: 99% to albumin.
○ Metabolism: Extensively metabolised in the liver by
CYP3A4 and CYP3A5 isoenzymes into 6-
hydroxydutasteride (same activity with dutasteride); 4′-
hydroxydutasteride and 1,2-dihydrodutasteride (less
potent than dutasteride).
○ Excretion: Via faeces (40% as metabolites, approx 5% as
unchanged drug); urine (<1% as unchanged drug).
Mayrong
Elimination half-life: Approx 3-5 weeks.
Tamsulosin
● Mechanism of Action: Tamsulosin is an antagonist
of α1-adrenoceptors, which mediate smooth
muscle tone in the prostate. This leads to the
relaxation of smooth muscle in the bladder neck
and prostate thereby improving urine flow and
reducing the symptoms of benign prostatic
hyperplasia (BPH).

Mayrong
● Pharmacokinetics:
○ Absorption: Absorbed from the gastrointestinal tract.
○ Bioavailability: 30% increase in fasting state. Food
reduces rate and extent of absorption. Time to peak
plasma concentration: 4-5 hours (fasting state); 6-7 hours
(fed state).
○ Distribution: Volume of distribution: 16 L (immediate-
release); approx 0.2 L/kg (prolonged-release). Plasma
protein binding: 94-99%, mainly to α1-acid glycoprotein.
○ Metabolism: Extensively and slowly metabolised in the
liver by CYP3A4 and CYP2D6 to metabolites; undergoes
further extensive conjugation to glucuronide or sulfate.
○ Excretion: Via urine (76%, <10% as unchanged drug);
faeces (21%). Elimination half-life: 9-13 hours (healthy
Contraindications:
● Dutasteride: drug hypersensitivity and to other alpha
reductase inhibitor
● Tamsulosin: women lactating and children

Interactions:
● Dutasteride: possible inc. in blood conc and decrease in clearance with
CYP3A4 inhibitors
● Tamsulosin: hypotensive effects with anes agents, PDE5 inhibitors and other
a1 adrenergic blockers. Inc cmax in ketoconazole and paroxetine, reduce
with furosemide. Significant increase in exposure with CYP3A4 n CYP2D6
inhibitors. Increased AUC and decrease clearance with cimetidine, warfarin.
PRESCRIPTION:
 Follow up advice
● A minimum of 6 months of treatment may be necessary to
determine if an individual will respond to treatment.
● Compare the PSA level before and after the administration of
the drugs to know if there is reduction of prostate volume.
● Lifestyle changes
● If less invasive treatment fails or symptoms worsen and
complications arise, surgical intervention should be indicated
– Transurethral resection of the prostate (TURP) (gold standard)
ALZHEIMER'S DISEASE

● brain disorder that slowly destroys memory and thinking skills, and eventually,
the ability to carry out the simplest tasks.
 ALZHIEMERS DISEASE
BASIS
● Difficulty of remembering recent events
● Difficulty of remembering conversations
● Difficulty in organizing things
● Difficulty with problem solving and performing tasks
PATHOPHYSIOLOGY
 Types:
EARLY ONSET:
● Appearance at 3rd to 5th decade of life
● s/s: similar to late onset but it is active
● Passed down from parent to child

LATE ONSET:
● Mid 60s
● Sporadic
● Increasing risk as increasing age
● Has a predilection of ApoE inheritance
● Most common type
 CLINICAL MANIFESTATION
● Cognitive: memory loss, problems with language,
disorientation to time, place, decreased judgement,
learning problems - abstract thinking and misplaces
things
● Non cognitive: changes in mood or behavior,
personality or loss of iniative
● Functional: difficulty of performing familiar tasks
 ETIOLOGY
● Unknown
○ Beta amyloid plaques
○ Neurofibrillary tangles
 Risk Factors
● AGE
○ Uncommon at <40 year olds, prevalent at >60 years old
○ Increasing age; < chondrocytes response
○ Cartilage thinner with age (more risk damage)
● Lifestyle
● Occupation
● More common in women
● Genetics
A Armstrong R. (2019). Risk factors for Alzheimer's disease. Folia neuropathologica, 57(2), 87–105.
https://doi.org/10.5114/fn.2019.85929
 COMPLICATIONS
● Restlessness and Agitation
● Bladder and bowel problem
● Depression
● Falls
● Infections
● Wandering
● Malnutrition and dehydration
 Non Pharmacologic Management
● Using a gentle calm approach to the patient
● Maintenance of daily routines
● Providing day time activities
● Providing safe environment
 Therapeutic goals
● Maximize function in daily activities
● Maintain QoL
● Enhance cognition, mood and behavior
● Foster a safe environment
Pharmacologic Management
PRESCRIPTION
END OF PRESENTATION