Download 1.1 `Geriatrics`

_________________________________________________Section 1.0
INTRODUCTION
1.1 ‘Geriatrics’ :It is a branch in medicine that is concerned with the elderly
patients and their problems. Infact, it is the study of human aging and the
care of the elderly.
Geriatrics prefer to focus the care of older adults on improving physical
and mental function rather than being solely concerned with disease
detection and cure.
The goal of geriatrics is however, not to promote senescence, but to
maximize the positive aspects of aging.
Patients who are considered as elderly are those with ages 60 and above.
As a person proceeds in age, his body starts reacting differently to various
situations. For example, the effect of stress on a child’s body differs from
that on the body of a person who is in the twenties. Similarly, the impact
of stress on the elderly is different and may cause severe deterioration of
health.
The elderly have multiple and often chronic diseases; thus they are the main
consumers of drugs. Infact, in most developed countries, the elderly now
account for 25% to 40% of drug expenditure.
1.2 ABNORMALITIES WITH AGING
The physiologic state for any organ in any individual, however, is determined by
the rate of change that organ has been experiencing multiplied by the number of
years that change has occurred.
Age related changes in one organ are not predictive of changes in other
organs. Also, the rate of change of function of any organ varies from
individual to individual.
1.2.1 Physiological changes
Cardiovascular changes do occur with aging, however some cardiovascular
functions do not decline due to age alone. There is no obligatory decline in
cardiovascular function at rest. There is no age-related change found in cardiac
output, end-diastolic or end-systolic volumes, or ejection fraction in the elderly at
rest. Cardiac tissue itself undergoes only small metabolic changes due to aging
itself .
Age related changes are seen, however, in the large arteries of the body
which lose their elasticity due to changes in elastin and collagen
composition. Thus, there will be an increased aortic stiffness, loss of
elasticity, and loss of diastolic recoil, resulting in increased peripheral
resistance. Systolic hypertension alone, or systolic and diastolic hypertension
may then become manifest and require treatment.
Left ventricular hypertrophy develops as an adaptive mechanism to the
untreated increased peripheral resistance. Increased ventricular wall thickness,
although not due to aging alone, does lead to increased ventricular wall
stiffness in early diastole with consequent potential cardiac compromise
when tachycardia occurs in the elderly.
The elderly respond to stress with less tachycardia
Changes in compliance of the chest wall with increased rigidity, lowered
diaphragms during tidal breathing, and loss of internal alveolar surface area
all combine for a slowly progressive loss of pulmonary function with aging.
The residual volume of the elderly is increased because the diaphragms
ascend less vigorously.
With aging, there is a progressive decrease in arterial oxygenation, which is
made worse when people are in the supine position.
Intrathoracic changes alter the lungs ability to clear infections. Chronic
obstructive pulmonary disease due to smoking, pneumonia, and pulmonary
emboli are disease processes which occur with frequency in the elderly.
When the additive limitations of smoking or pulmonary disease, however,
accumulate upon the age related decline in ventilitory function the sick
elderly have little reserve against hypoxia. Unfortunately, an age-related
diminished responsiveness to hypoxia and hypercapnia may further make
the older person more vulnerable to transient reductions in arterial oxygen
tension during pneumonia or exacerbation of COPD.
Gastrointestinal complaints are frequent in the elderly however, the
gastrointestinal tract basically retains physiologic function with aging
because of the large surface area and redundancy involved.
Swallowing in the elderly , for example is of great concern to geriatricians
and to caregivers. In patients who have had a stroke, coordination of the
cricopharyngeus muscle may be affected, resulting in an upper esophageal
sphincter which does not relax when food or liquid is ingested, and high
probability of aspiration of liquids especially.
1.2.2 Pharmacodynamic changes in the elderly
Molecular and cellular changes that occur with aging may alter the
response to drugs in the elderly.
Causes of pharmacodynamic changes in the elderly are :
1)
Reduction in hemostatic reseve.
2)
Changes in specific receptor and target sites.
Reduced hemostatic reserve
One)
Orthostatic circulatory responses
In normal elderly subjects, there is blunting of the reflex tachycardia that
occurs in young subjects on standing or in response to vasodilation and
this could be due to structural changes in the vascular tree.
Drugs that decrease the sympathetic outflow from the central nervous
system are more likely to produce hypotension in the elderly.
Two) Postural control
Postural stability is normally achieved by static reflexes, which involve
sustained contraction of the musculature, and phase reflexes, which are
dynamic, short term and involve transient corrective movements.
With aging, the frequency and amplitude of corrective movements increase
and an age- related reduction in dopamine receptors in the striatum takes
place.
Three) Thermoregulation
Accidental hypothermia can occur in the elderly with drugs that produce
sedation, impaired subjective awareness of temperature, decreased mobility
and muscular activity, and vasodilation. This is due to the impaired
thermoregulatory mechanisms in the elderly.
Four) Cognitive function
Aging is associated with marked structiral and neurochemical changes in
the central nervous system. Cholinergic transmission is linked with normal
cognitive function, and in the elderly the activity of choline acetyltransferase
is reduced in some areas in the cortex and limbic system.
Several drugs cause confusion in the elderly
Five) Visceral muscle function
Constipation is a common problem in the elderly as there is a
gastrointestinal motility with aging. Anti-cholinergics, opiates, and antihistamines are more likely to cause constipation or ileus in the elderly.
Anti-chlinergics may cause urinary retention in elderly men, especially those
who have prostatic hypertrophy.
Bladder instability is common in the elderly, and urethral dysfunction more
prevalent in elderly women. Loop diuretics may vause incontinence in such
patients.
1.3 Age-related changes in specific receptors and target sites
Response to drugs may be altered by the number of receptors, the affinity
of the receptor, post-receptor events within cells resulting in impaired
enzyme activation and signal amplification, or altered response of the target
tissue itself. Aging is associated with these changes.
Examples:.
Name of drug
Atropine
Benzodizepines
Propranolol
Digoxin
Warfarin
Response of the elderly
Produces less tachycardia in the elderly than in the
young
Elderly are more sensitive to them.
In the elderly it produces less beta blocking effect than
in the young due to the decrease in the beta receptors
that occur by age.
The elderly are more sensitive to the adverse effects of
digoxin.
The elderly are more sensitive to warfarin
1.4 Pharmacokinetic changes in the elderly
Aging results in many physiological changes that may effect absorption,
first-pass metabolism, protein binding, distribution and elimination of drugs.
Age related changes in the gastro-intestinal tract, liver and kidneys are :

Reduced gastric acid secretion

Decreased gastro-intestinal motility

Reduced total surface area of absorption

Reduced splanchnic blood flow

Reduced liver size

Reduced liver blood flow

Reduced glomarular filtration

Reduced renal tubular filtration.
1.4.1Absorption
There is a delay in gastric emptying, reduction in gastric acid output and
splanchnic blood flow with aging.
These changes do not significantly affect the absorption of the majority of
drugs. Although the absorption of some drugs may be slower, the overall
absorption is similar to that in the young.
The absorption of D-Xylose decreases by age due to decreased intestinal
absorption of carbohydrates.
There is however, no evidence for decrease in absorption of either fat
soluble or water soluble vitamins, iron, or protein with age. A perceived agerelated decrease in calcium absorption may be related to vitamin D
deficiency, an altered responsiveness of calcium binding proteins in the
intestinal mucosa , or other factors.
1.4.2 First-pass metabolism
After absorption, drugs are transported via the portal circulation to the liver,
where many lipid soluble agents are metabolized extensively (more than 9095%).This results in marked reduction in systemic bioavailibility. Obviously,
even minor reductions in first pass metabolism can result in a significant
increase in the bioavailibility of such drugs.
Impaired first pass metabolism may alter the effects of certain drugs;
example : the hypotensive effect of Nifidipine which is a calcium channel
blocker is enhanced in the elderly.
Also, in frail hospitalized elderly patients, i.e. those with chronic debiliating
diseases, the reduction in presystemic elimination is even more significant.
1.4.3 Distribution
The age related physiological changes which may affect drug distribution
are :

Reduced lean body mass

Reduced total body water

Increased total body fat

Lower serum albumin level

Alpha 1-acid glycoprotein level unchanged or slightly raised.
Increased body fat in the elderly results in an increased volume of
distribution for fat soluble compounds such as diazepam and thiopentone.
On the other hand, reductions in body water results in a decrease in the
distribution volume of water soluble drugs such as cimitidine, digoxin and
ethanol.
Acidic drugs tend to bind to plasma albumin, whilst basic drugs bind to
alpha 1-acid glycoprotein.
Plasma albumin levels decrease with age and, therefore, the free fraction of
acidic drugs such as cimitidine, frusemide and warfarin will increase.
Plasma alpha 1-acid glycoprotein levels may remain unchanged or may rise
slightly with aging, and this may result in minimal reductions in free
fractions of basic drugs such as lignocaine.
The age related changes in distribution and protein binding are of
significance only in the acute administration of drugs, because at steady
state the plasma concentration of a drug is determined by free drug
clearance by the liver and the kidneys rather than by distribution volume
or protein binding.
1.4.4 Renal clearance
By age, the glomarular filtration rate declines. Also, the effective renal
plasma flow and the renal tubular function declines with age. Thus, the
doses of predominantly renally excreted drugs should be individualized.
It is also necessary to reduce the dose of drugs that have a narrow
therapeutic index.
Although total serum renin concentration remains stable with age, there is
an age-dependent decline in active renin concentration.This is responsible
for a blunted renin response to postural changes, and is one of the
mechanisms postulated for the frequency of postural hypotension in the
elderly.
Because of the decreased GFR, blunted renin-aldosterone axis, and decreased
tubular mass, the elderly may have less ability to protect against
hyperkalemia in the face of increased potassium loads.
There is a water conservation defect in the elderly which predisposes them
to dehydration due to a decreased responsiveness to vasopressin and a
resting decrease in total body water with age that is more pronounced in
women than in men. This can result in dehydration when water loss is
significant, as during a fever,or when the t hirst mechanism is blunted.
1.4.5 Hepatic clearance
Drugs that depend on the liver for their clearance have a rapid rate of
metabolism and the rate of extraction by the liver is very high.
Hepatic extraction is dependent upon liver size, blood flow, uptake into
hepatocytes, and the affinity and activity of hepatic enzymes.
Liver size falls with age and this will hence result in a decreased hepatic
blood flow
However, standard liver function tests such as bilirubin, amino transferases,
and alkaline phosphatase do not change with age. Storage capacity of the
liver may be affected, however, as demonstrated by altered clearance of dyes
such as bromsulphalein from the bloodstream.
Clearance of antipyrine, a measurement of microsomal oxidation, is slowed
with aging, however no age-related changes in the activities of other
microsomal enzymes systems have been found in other studies.
Clearance of alcohol, which occurs through non-microsomal oxidation
mechanisms, moreover, is not affected by aging. Neither is there an age
related change in the clearance of isoniazid or oxazepam which are cleared
by hepatic conjugation. Because of the fact that demethylation by the liver
is decreased with aging, the half life of drugs such as benzodiazepines ,
chlordiazepoxide, diazepam, and aminopyrine may be doubled in older
individuals.
PHARMACO-ECONOMICS
As managed care for older adults becomes the tren, there are special opportunities
for positive developments from a primary care perspective. One is the possibility
of shifting the focus away from disease-oriented care. In geriatrics, function, not
disease, is the issue. What we need are function-management care plans, not
disease-management care plans. Diseases do not predict utilization and healthcare
costs, but function does.
It is clear that if we can prevent disability, that is much more cost-effective than
dealing with what occurs after the onset of a disability. From the perspective of
managed care, the emphasis on prevention of disability will necessarily assume
increasingly greater importance.
With managed care, we can align the incentives for improvement with all of the
parties involved, and we could not do that in a normal fee-for-service
environment.
It would seem that there are many advantages to managed care in providing care
for elders, but still many of us in geriatrics are distrustful of it. This is because we
still do not know how to take care of older people well.
Another major problem is that we still have unintegrated systems, and it is
difficult to provide good managed care within an unintegrated system. We are
also in the midst of a changing culture in the medical establishment, away from
the overarching authority of specialists and toward giving much more power to
primary care physicians and, though this is a positive change in my opinion, it
does create discord within the healthcare system.
Another major problem is that we still have unintegrated systems, and it is
difficult to provide good managed care within an unintegrated system. We are
also in the midst of a changing culture in the medical establishment, away from
the overarching authority of specialists and toward giving much more power to
primary care physicians and, though this is a positive change in my opinion, it
does create discord within the healthcare system
________________________________________________________Section 2.0
COMMON DISEASES AND CONDITIONS THAT
ARE ASSOCIATED WITH THE ELDERLY
2.1 Cardiology
Cardiac disease is common in late life. As a person proceeds in age, he
becomes more prone to cardiac diseases and this is due to weakened
cardiac muscles.
2.2 Delirium
Acute confusion is a common occurrence in the elderly. Its presence
suggests increased morbidity and mortality. It serves primarily as an
indicator of severity of illness, but can unmask unrecognized dementia.
Some preventive measures may be useful.
2.3 Dementia
Cognitive impairment is most often recognized when it results in
memory loss. However, changes in personality, loss of judgement,
difficulty with problem-solving, and language disorders are also common.
The cumulative effect can be devastating on an individual, and on their
loved ones. The correct diagnosis is essential, in order to detect and treat
any reversible component.
2.4 Rheumatological Diseases
Older adults can suffer from painful joints and muscles for a variety of
reasons.
2.5 Sleep disorders (insomnia)
2.6 Urinary incontinence
It is important to be aware that this condition, although more common as a
person gets older, is not a normal function of aging. Causes range from
problems with nerve function to the adverse effects of medications or
surgery. Treatment can involve exercises, biofeedback, medications, and
surgical repair.
2.7 Anemia
Anemia is a frequent finding among the elderly, although healthy elderly do
not demonstrate a change in hematocrit with aging. Therefore, anemia in the
elderly is always due to a pathologic condition or represents a response to
a pathologic condition.
Likewise, although the elderly are prone to atherosclerotic cardiovascular
disease which impairs cardiac functioning, aging alone is associated with no
obligatory decline in cardiac functioning. Advances in health care, diet, and
smoking cessation are associated with declines in the advent of
atherosclerotic disease and its morbidity.
2.8 Constipation
This is a major complaint of the elderly, and is usually associated with
impaired physical activity, altered diet, and medications. In older adults who
are constipated, slower transit times and decrease in fecal water content may
occur.
2.9 Hemorrhoids
This may be made worse by constipation.
_______________________________________________________Section 3.0
PRINCIPLES AND GOALS OF DRUG THERAPY
IN THE ELDERLY
The Mission of a Clinical Pharmacist is:
“To improve the physiological, psychological, and social well being of older
persons through state-of-the-art interdisciplinary research, education and clinical
services.”
3.1 Strategies that must be followed when choosing a drug
for the elderly :
1)
Avoid unnecessary drug therapy.
2)
Effect of treatment on quality of life.
It must be kept in mind that the aim of treatment in the elderly is not just
to prolong life but to improve the quality of life.
3)
Treat the cause rather than the symptom to avoid dangers.
4)
A lot of attention should be paid on the drug history to ensure that
the patients are not given drugs to which they are allergic to.
5)
Concomitant medical illness.
Many illness in the elderly may increase the risk of adverse effects of
drugs. Examples are cardiac failure , renal and hepatic diseases.
6)
Choosing the drug properly
7)
The dose should be very accurately specified. Infact, it is rational to
start with the smallest possible dose of a given drug in the least
number of doses and then gradually increase both, if necessary.
8)
The right dosage form must be chosen.
9)
The medicine prescribed must be packaged in such a way that it
can be opened easily.
10) Information about the patient’s current and previous therapy, alcohol
consumption, smoking and driving habits also help in choosing appropriate
drug therapy when the treatment needs to be altered.
Also, it will help to reduce costly duplications and will avoid dangerous
drug interactions.
11 ) The elderly are more susceptible to adverse effects of the drugs thus
care should be taken when initiating any drug therapy.
12) Compliance is usually a problem in most elderly patients as many
elderly patients tend to forget when the due dose was which may hence
result in various complications. Thus, it is necessary that someone
professional is kept in charge of the patient.
3.2 COMPONENTS OF A COMPREHENSIVE GERIATRIC
ASSESSMENT
A. Patient demographics:
a. Date of assessment , patient name, address, age, sex , ehnic origin, marital
status, lifestyle, occupation and his social life.
ii. Reason for assessment which could be :
1.
initial comprehensive exam
2.
hospital/clinic admission reassessment
3.
home assessment
4.
discharge assessment
5.
episodic encounter assessment
6.
significant change in status
B. Activities of Daily Living
a. Ability for self-care, hygiene, housekeeping
One)
Bathing
Two)
self-feeding
Three)
dressing
Four)
transfer
Five)
toileting
Six)
continence (bowel/bladder)
Seven)
ambulation
b. Problems with Mobility
One)
Falls within the last 12 months?
Two)
Injuries within the last 12 months?
c. Abilities and Opportunities for telephone communication
d. Access to community
e. Emergency plan, phone, contacts
f. Transportation
g. Financial management
C. Nutritional
a. Weight changes
b. Appetite patterns, consumption patterns
c. Food preparation, means of obtaining food (shopping, etc.)
d. Digestion
e. Chewing, swallowing problems
f. Evaluation of diet adequacy
d. Sleep
a. Sleeping patterns (night time and naps)
b. Sleeping problems
E. Psychosocial History
a. Feelings about self
b. Social interactions, family, friends, Community involvement
c. Living alone or with others
d. Adequacy of home environment
e. Occupational/volunteer history, retirement plans
f.
Stressors, coping
F. Past Medical History
a. Chronic diseases
b. Major illnesses or surgery
c. Hospitalizations
d. Transfusions
e. Smoking (pack/years)
f. Alcohol intake (amount/type)
g. Did you fall within the past 12 months?
G. Medication Use
a. Prescription medications taken
b. Nonprescription medications taken
c. Allergies/adverse drug reactions
d. Recreational medications
e. How do you obtain your medications
f. How do you pay for your medications
g. Do you have problems taking your medications
h. How often do you not take any of your prescription medications
i. Knowledge of purpose of medications
H. Mental health assessment
a. During the past month, how have you been feeling in general?
b. If you had severe emotional problems, did you seek professional help?
c. List any major personal losses or major changes that have occurred in the
past 12 months.
d. Is anything really bothering you now?
e. Have you ever felt like hurting yourself?
f. When you get upset, how do you generally handle it?
I. Family History
a. Major diseases in family
b. Family genogram showing health status/age cause of death
J. Review of Systems
Query patient regarding major symptoms for each major body system. Emphasize
symptoms common to aging clients. Ask regarding pain in every system.
This may be an appropriate time to obtain a sexual history, if you have already
spent sufficient time with the patient to establish trust and rapport.
K. Physical Exam (Changes with normal aging)
a. Eyes-- decreased lubrication
1st)
Presbyopia-- thickening of lenses, causing blurring,
especially close objects
2nd)
Senile cataracts - cloudiness or opacity in lens
3rd)
Color vision changes - yellowing of lens, filtering
out violet, blue and green
b. Ears
One)
Conductive loss - loss of sensitivity at all
frequencies
Two)
Presbycusis - loss at higher frequency first, high
pitched, and consonant sounds
c. Other Senses
One)
Smell - decreased, fruit odor persists
Two)
Taste- decreased
Three)
Touch- decreased pain sensation
d. Heart
One)
Decreased efficiency
Two)
Decreased cardiac output
e. Lungs
One)
Increased rigidity
Two)
Limited expansion due to thoracic changes
Three)
Diminished cough reflex
f. Musculoskeletal
1st)
Bones become more porous and brittle
2nd)
Kyphosis, which may be accompanied by a
compensatory hyperflexed neck
3rd)
Decreased height from narrowing of intervertebral
spaces (1-4")
4th)
Loss of muscle mass-peripheral loss
5th)
Increased fat deposition on hips, ankles
6th)
Arthritic changes in joints
g. Skin
One)
Decreased moisture and elasticity
Two)
Wrinkling-reflects life patterns of muscle activity
Three)
Loss of subcutaneous fat- decreased insulation
Four)
Graying of hair, thinning, and loss
Five)
Nails - brittleness, changes in texture, thickening of
toe nails
h. Digestive system
One)
Decreased peristalsis and intestinal secretions
Two)
Teeth become worn.
_______________________________________________________Section 4.0
CLINICAL CASES ON GERIATRICS
4.1 CASE STUDY 1 :
Mrs. N is a 72-year-old widowed, black female living alone in a two-story
home. Her medical problems include hypertension, hyperlipidemia, diabetes,
chronic obstructive pulmonary disease, congestive heart failure, non-ulcer
dyspepsia, insomnia, glaucoma, and osteoarthritis. She is followed by two
different physicians at a University Health Center. She has a 20 pack-year
smoking history and continues to smoke a pack of cigarettes daily. She
drinks 4 to 5 cans of beer a day. She denies illicit drug use.
Mrs. N has been hospitalized four times in the past year for exacerbation of her
chronic disease states.
Her medication history reveals she is prescribed the following medications:
1.
Hydrochlorothiazide 25 mg qam
2.
Nifedipine 10 mg qid
3.
Cholestyramine 5 g tid
4.
NPH insulin 38 units qam
5.
Theophylline SR 400 mg bid
6.
Albuterol metered dose inhaler 2 puffs qid as needed for shortness
of breath
7.
Prednisone 10 mg qd
8.
Cimetidine 400 mg bid
9.
Pilocarpine HCl eye drops 4% 1 gtt ou qid
10.
Timolol eye drops 0.5% 1 drop twice daily.
11.
Mylanta 1 tablespoonful before meals as needed for heartburn
12.
Temazepam 15 mg hs as needed for sleep
Discussion and comment of the case and the medications
given :
HYPERTENSION:
The lady is hypertensive and this is due to many factors present in the
patient that gives rise to this problem.
The first factor is her age and race and both of these factors are
uncontrollable. The blood pressure rises as the person proceeds in age. The
second factor contributing to this condition is the fact that she is a heavy
smoker and a heavy alcoholic drinker.
The fact that the lady has many underlying diseases such as hyperlipidemia
and diabetes mellitus also contributes to hypertension. Thus, it is very
important to control these underlying diseases so as to control hypertension.
Hypertension must be treated to avoid complications. Nifidipine is the best
choice in this case and is given as sustained release to allow patient
compliance. Hydrochlorthiazide is not the best choice as the patient has
hyperlipidemia also and these diuretics may have an adverse effect on the
lipid profile. The use of diuretics in this case is necessary because the lady
has congestive heart failure and edema may be associated with it.
HYPERLIPIDEMIA
The total serum cholesterol level increases with age in males and females
above the age of 20 years. High alcohol intake and Diabetes mellitus
contribute to hyperlipidemia. Cholestyramine is hence given.
There are certain drugs that have to be avoided in any patient with
hyperlipidemia as it has an adverse effect on the lipid profile. Examples of
such drugs :
Diuretics, Oral contraceptives, Corticosteroids, Cyclosporins, Hepatic
microsomal enzyme inducers. And beta adrenergic blockers.
DIABETES MELLITUS
The sugar level in the blood must be controlled. The lady is hence on
insulin. Any underlying hypertension and hyperlipidemia must be controlled.
CONGESTIVE HEART FAILURE
To relieve edema hydrochlorothiazide was hence give since it will increase
the excretion of sodium and water thereby relieving edema.
INSOMNIA
This could be due to the high nicotine intake since she is a heavy smoker
and nicotine is a CNS stimulant. Also, it is related to age.
GLUCOMA
Timelol and Pilocarpine were given to control this condition.
The patient has osteoarthritis and there was no medication given to relieve
the pain. The problem however arises from the fact that this patient has
dyspepsia and is prone to ulcers. Thus, there is a hesitation in giving a
non-steroidal anti-infalmmatory drug.
One of the main strategies in the clinical management of an elderly is to
simplify the medicaments given since too much of medicines may lead to
patient compliance problems.
Looking at the above drug plan we can easily point out the unnecessary
drugs.
To implement the plan :
1.
Cimetadine is probably unnecessary as the patient has nonulcer dyspepsia. The condition of dyspepsia can be easily
controlled by Mylanta which is given before food.
2.
Temazepam which is a hypnotic, might be contributing
to cognitive impairment. Also, Temazepam may cause confusion,
ataxia especially in the elderly. Perhaps non-pharmacologic
treatment of insomnia could be tried instead of Temazepam.
3.
Maybe the patient could be weaned off of the prednisone,
which might be interfering with control of the diabetes as it can
cause antagonism of the hypoglycemic effect of anti-diabetics.
Also, since the patient is hypertensive, prednisone will only
make it worse. Also, the intake of of Prednisone with
Theophyllin will lead to an increased risk of hypokalemia.
4.
Sustained release Nifedipine might be preferable to the four
times a day dosing currently being prescribed to allow patient
compliance. Nifidipine is a good choice since it has no effect
on the lipid profile.
PATIENT COUNSELLING.
The patient should be encouraged to stop smoking and alcohol as these are
always precipitating factors of ulcers and since the patient has got
dyspepsia, it means that she is prone to ulcers.
The patient should also be advised to avoid stress as it may contribute to
insomnia, ulcers, hypertension and hyperlipidemia.
Daily monitoring of the blood sugar level and blood pressure is mandatory.
Diet should contain less sugar and salt.
The patient must abide by the medications given and instantly report any
new emerging symptoms.
__________________________________________________________________
4.2 CASE - STUDY 2
CLINICAL HISTORY:
The patient is a 77-year-old white male who presented to the Emergency
Department with persistent nose bleeding. According to the patient, he woke
up in the morning with a nose bleed which continued on and off during
the day. He also reported multiple episodes of epistaxis in the past. The
patient had a medical history of prostate cancer with bony metastasis, status
post prostatectomy and hormonal therapy. Other medical problems included
coronary artery disease, hypertension, stroke, and atrial fibrillation. His past
medications included:
Atenolol,
Prinivil,
Ecotrin,
Lasix (Frusemide)
Zocor (Simvustatin) and
Duragesic patch (Fentanyl _ opioid analgesic)
Physical examination of this patient was unremarkable except for some
blood oozing from the nostrils and blood stains in the posterior oropharynx.
LABOARTORY FINDINGS:
The complete blood count and coagulation profile of this patient is shown
in the following table :
Test
HGB
HCT
WBC
Platelet
PT
PTT
INR
Fibrinogen
Factor II
Factor V
Factor VII
Factor VIII
Factor IX
Factor X
Factor XI
Factor XII
FDP
D-Dimer
Antithrombin III
Plasminogen
Antiplasmin
Value
10.4 g/dl
30.2 %
6.8 x 103/µl
157 x 103/µl
13.7 sec
31.6 sec
1.2
68 mg/dl
0.85 U/ml
0.65 U/ml
1.13 U/ml
0.65 U/ml
1.40 U/ml
0.74 U/ml
1.20 U/ml
0.70 U/ml
320.0 µg/ml
64.0 µg/ml
91 %
62 %
50 %
Reference Range
13.5-17.0 g/dl
40.5-50.0 %
4.0-10.0 x 103/µl
140-440 x 103/µl
10.5-13.0 sec
25-33 sec
150-350 mg/dl
0.60-1.40Uml
0.50-1.50 U/ml
0.60-1.60 U/ml
0.50-1.50 U/ml
0.60-1.35 U/ml
0.60-1.40 U/ml
0.60-1.40 U/ml
0.50-1.70 U/ml
0.0-2.5 µg/ml
0.0-0.4 µg/ml
80-120 %
80-150 %
80-120 %
TREATMENT:
The patient was treated with Amicar (epsilon aminocaproic acid) in the
Emergency Department with resolution of his bleeding. He was later
discharged and scheduled for further chemotherapy to control his metastatic
prostatic carcinoma.
DIAGNOSIS:
Hyperfibrino(geno)lysis, secondary to metatstaic prostatic carcinoma.
DISCUSSION:
Hypertension could be a cause of epistaxis.
Fibrin formation (coagulation) and dissolution (fibrinolysis) are carefully
coordinated physiologically. Hyperfibrino(geno)lysis occurs when there is
greater fibrinolytic activity than fibrin formation, thus leading to
hemorrhage. The central event of Hyperfibrino(geno)lysis is the generation
of plasmin within the general circulation (plasminemia). Plasmin, which is a
protease converted from plasminogen, degrades fibrin, fibrinogen, coagulation
factors V and VIII, complement components and other plasma proteins. The
fibrinolytic activity of plasmin is initiated by the plasminogen activators
(tissue plasminogen activator (t-PA) and urokinase (u-PA)) and down-regulated
by plasminogen a ctivator inhibitors (PAI-1 and 2) and plasmin inhibitors (α2antiplasmin).
Hyperfibrino(geno)lysis has been reported in various pathologic conditions.
Examples include hypotension, trauma, heatstroke, cardiac bypass surgery and
severe liver diseases. In these cases, excessive amounts of plasminogen
activators may be released into the blood from body stores (mainly
endothelial cells) and exceed the capacity of inhibitors. Occasionally, patients
with disseminated neoplasms, such as acute promyelocytic leukemia or
metastatic prostate cancer, also exhibit enhanced fibrinolytic activities with
symptoms of GI or GU bleeding, epistaxis or other forms of hemorrhage. It
has been demonstrated that the tumor tissue or cells contain plasminogen
activators, especially u-PA. The secretion of these activators into the
circulation may rapidly lead to plasminogen activation and, occasionally, to
hyperfibrino(geno)lysis. The coagulation profiles in these patients usually
show:
(1) normal or slightly prolonged PT and PTT due to the anticoagulation
effects of FDP (fibrinogen degradation product);
(2) normal platelet count;
(3) normal plasma levels of clotting factors, except for factors V and VIII
which are more sensitive to the proteolytic action of plasmin;
(4) hypofibrinogenemia;
(5) depletion of plasminogen or a 2-antiplasmin and the presence of a2antiplasmin-plasmin complexes in the plasma;
(6) normal plasma level of antithrombin III;
(7) increased plasma level of FDP with normal level of D-dimer;
(8) normal erythrocyte morphology shown by peripheral blood smear. The
laboratory findings in hyperfibrino(geno)lysis are summarized the table
below.
It should however be noted that the fibrinolytic activation seen in DIC is a
secondary response to microvascular thrombosis. It has been indicated that
there is an acute release of large quantities of t-PA into the circulation in
patients with DIC. The abnormal hemostasis, therefore, is due to a
combination of activation of coagulation and accelerated fibrinolysis.
However, in cases of DIC,
(1)
the platelet count is usually low;
(2)
there is depletion of clotting factors, and thus prolonged PT
(prothrombin time) and PTT;
(3)
there is decreased plasma level of antithrombin III and increased
level of D-Dimer;
(4)
schistocytes and microspherocytes are present in the peripheral blood
Lab. findings in hyperfibrinogenolysis and DIC
Test
Platelet count
PT
PTT
Thrombin time
Fibrinogen
Factor II
Factor V
Factor VII
Factor VIII
Hyperfibrino(geno)lys DIC
is
Normal
Decreased
Normal or prolonged Prolonged
Normal or prolonged Prolonged
Prolonged
Prolonged
Decreased
Decreased
Normal
Decreased
Normal or decreased Decreased
Normal
Decreased
Normal or decreased Decreased
Factor IX
Factor X
Factor XI
Factor XII
Euglobulin clot lysis time
FDP
D-Dimer
Antithrombin III
Plasminogen
α2-Antiplasmin
Normal
Normal
Normal
Normal
Shortened
Increased
Normal
Normal
Decreased
Decreased
Decreased
Decreased
Decreased
Decreased
Shortened
Increased
Increased
Decreased
Decreased
Decreased
α2-antiplasmin-plasmin complexes Increased
Increased
Erythrocyte morphology
Schistocytes
Normal
.
The patient's coagulation profile showed normal platelet count, borderline
PT and PTT, levels of clotting factors within normal ranges,
hypofibrinogenemia, significant increase of FDP, decreased activities of
plasminogen and antiplasmin, and normal level of antithrombin III. These
results are consistent with the diagnosis of hyperfibrino(geno)lysis, which is
most likely secondary to the patient's underlying malignant neoplasm that
may secret plasminogen activators into the blood.
The elevated plasma level of D-Dimer in this patient may be explained by
the degradation of fibrin generated from the tissue damage related to his
metastatic carcinoma.
The treatment of choice for hyperfibrino(geno)lysis is antifibrinolytic agents.
EACA (epsilon aminocaproic acid) and related agents are specific and potent
inhibitors of plasminogen activation and action of plasmin. However, such
antifibrinolytic agents are potentially dangerous in the presence of DIC.
Therefore, the diagnosis of DIC should be ruled out before administering
these agents to the patients.
__________________________________________________________________
4.3 CASE STUDY # 3
PATIENT HISTORY:
Sixty-seven year old female with longstanding hypertension and peripheral
vascular disease.
The following Plasma Renin assay results are from samples taken during
the catheterization described above.
Location
ng/ml
Right renal vein
112.5
left renal vein
21.4
Inferior vena cava
20.7
FINAL DIAGNOSIS:
RIGHT RENAL ARTERY STENOSIS
Over 90% of patients with high blood pressure have primary or "essential"
hypertension. Secondary causes may be renal (glomerulonephritis, reninproducing tumors), vascular (polyarteritis nodosa), endocrine (Cushing's disease,
thyrotoxicosis, pheochromocytoma, oral contraception use) or neurogenic
(increased intracranial pressure) in origin. Renovascular hypertension accounts
for approximately 2% of total cases.
In the current case, this patient's hypertension appears to be related to her
right renal artery stenosis, and hence, involves the renin-angiotensinaldosterone system. The pathophysiology is as follows:
Renal artery stenosis causes decreased blood flow into one of the kidneys:
This results in a lowered blood pressure within the cortex of that kidney.
The cells of the juxta-glomerular apparatus which line the afferent arteriole
leading into the glomerulus, react to the decreased blood pressure by
secreting renin. Renin is a protease that splits the plasma protein
angiotensinogen into angiotensin I. On the surface of endothelial cells is
angiotensin converting enzyme which converts angiotensin I to angiotensin II.
It is angiotensin II which is the active factor that raises blood pressure. It
does this directly by inducing smooth muscle contraction, and also
stimulates the adrenal cortex to secrete aldosterone. Aldosterone
(mineralocorticoid) acts on the kidney by promoting the reabsorption of
sodium, and the secretion of potassium. Sodium retention leads to
hypervolemia.
In the current case, the finding of significantly increased plasma renin levels
unilaterally, as well as the ultrasound finding of right renal atrophy is
diagnostic. Causes of renal artery stenosis include atherosclerosis, arteritis and
fibromuscular dysplasia.
TREATMENT
Renovascular hypertension typically responds well to treatment with ACE
inhibitors for obvious reasons. Surgery, in the form of angioplasty or
nephrectomy, may be curative
The ACEI have three drugs belonging to them :
Captopril
Enalapril
Lisinopril
Drug interactions, Patient Counseling, and Comment:
If the patient was on diuretics then it is necessary to advice the patient to
stop the diuretics one week before the initiation of the ACEI. This is so
because together they may cause hypovolemia hence leading to shocks.
Also, it must be noted that by using ACEI, there is a tendency of
hyperkalemia. This in the elderly is dangerous as there might hence be
adverse effects on the heart of the patient as it may cause bradycardia and
may lead to heart failure. It is hence advisable that the patient should avoid
OTC and other medications containing potassium in it.
ACEI do not have any interaction with Zocor.
0The patient should also avoid any precipitating factor of hypertension.
The intake of diuretics with Atenilol (looking at her prescription of drugs)
leads to an enhanced hypotensive effects which may hence lead to
ventricular arrhythemias.
Daily monitoring of blood pressure is essential.
_______________________________________________________________________________
4.4 CASE STUDY # 4
HISTORY OF PRESENT ILLNESS:
A 67 year-old Hispanic female, born and raised in McAllen, Texas, was
referred to a pulmonologist because of severe asthma.
Her asthma symptoms began during childhood and were controlled with
Marex, an over-the-counter combination of a bronchodilator and
antihistamine used to treat asthma. She never had to be hospitalized, but
required frequent visits to the ER for asthma exacerbations. During youth her
symptoms became quiescent and she was able to practice sports while in
college.
Five years prior to this visit her asthma relapsed, with symptoms including
chest pressure, cough, shortness of breath and wheezing. She is unable to
identify any triggers for her asthma exacerbations. However, her symptoms
are worse at the end of the week. Before the asthma exacerbations she
frequently develops itching and increased secretions in her eyes and nose.
Her asthma symptoms have become progressively worse. She now has
symptoms every day and night, and over the past year she has received
several courses of oral prednisone to control asthma exacerbations. She is
afraid of cortisone side effects, and would rather not use that medication.
She was also prescribed inhaled beclomethasone (Beclovent), albuterol
(Ventolin), and theophylline (Slobid).
She has not used Beclovent since December 1993, and prior to that she used
it very irregularly. She believes Beclovent is a steroid, does not work, and is
too expensive.
During the past six months she has had seven ER visits for asthma
exacerbations, and has missed 21 days at work. She uses two to three
canisters of Ventolin per month. She describes no medicine allergies and has
never been allergy tested.
She works in a textile factory, does not smoke, but is exposed to
environmental tobacco smoke because her grand sons , with whom she lives,
smoke. There are a cat and two dogs where she lives. One of the dogs is a
Chihuahua recently acquired because of the belief that this type of dog can
ameliorate asthma symptoms.
She has a sister with asthma and hay fever. Both parents are dead and her
mother suffered from diabetes.
As part of her evaluation, she showed poor technique in the use of MDIs,
and lack of knowledge about environmental control and asthma triggers. She
feels she could lose her job if she continues missing work due to her
asthma. She does not want to use steroids, she prefers to have the interview
in English, and she expresses a desire to be trained in asthma management.
Physical Exam:
The physical examination revealed a slightly obese Latin American female
in mild respiratory distress. She is normocephalic, pupils are symmetrical
and reactive, conjunctiva are hyperemic. Nasal mucosa are edematous, pink,
with increased clear secretions. No polyps. Pharynx is slightly hyperemic
without exudates. Neck is unremarkable. Chest is symmetrical. Auscultation
shows diffuse expiratory wheezes in both lung fields without crackles or
ronchi. Heart rate is 100 and regular. No murmurs. Rest of physical exam is
within normal limits.
Laboratory:
Differential blood count :
Hb 13.2,
WBCs 10500
Neutrophils 64%, Lymphocytes 20%,
Eosinophils 6%
URINE AND BLOOD ANALYSIS

BUN 18

Creatinine 0.7

Glucose 103

Uric Acid 3.1

Cholesterol 234

Triglycerides 106

Calcium 9.3

Phosphorus 2.8

Total Protein 6.7

Albumin 4.1

Glob 2.5

Total Bilirrubin 0.9

Alk Phos. 69

ALT 21

AST 33

LDH 256
Ig E Level: 790
CXR: Normal
Spirometry: FVC is 85% or predicted
FEV1 is 65% of predicted.
FEV1/FVC ratio is 67%.
Improvement in FEV1 after inhaled albuterol: 22%.
Allergy testing revealed allergies to dust mites, cats, dogs, and grass.
Assessment
A diagnosis of asthma is indicated based on the patient's history of
recurrent cough, wheezing and shortness of breath since childhood. The
presence of wheezing during physical examination and the reversible airway
obstruction documented on spirometry confirm the diagnosis. The high
eosinophil count, high Ig E level and positive results of her allergy testing
point toward an allergic origin for her asthma.
Management
The management plan is directed at improving asthma control through more
effective use of medications and removal of environmental allergens. At
present she is using high doses of inhaled bronchodilators, but is not using inhaled
corticosteroids adequately. Several possible aggravating factors are present in the
environment: a work place where she may be exposed to textile byproducts
known to trigger asthma problems, and could explain why her asthma is worse at
the end of the week; tobacco smoke at ho me; pets at home (dogs and cats).
Her medication regimen should include an inhaled corticosteroid
(Beclomethasone), initially 4 puffs 4 times per day until symptoms are
stabilized. Later she may lower her dose to a 3 times/day regimen. She will
continue to use Ventolin (albuterol) on a ‘when needed basis’, keeping a
record of how much medicine she is using. The medication regimen should
be kept as simple as possible to reduce the cost of medications and to
increase patient compliance.
The patient is at high risk of diabetes in view of her Mexican-American
origin, family history of diabetes in her mother, obesity and a borderline
high blood glucose value.
Patient Counselling and Education
A session will be scheduled with her husband present in order to review the
following:

1) The concept of asthma as a chronic inflammatory problem
which requires continuous anti-inflammatory medication, even
during symptom-free periods.
Need for anti-inflammatory medication. The anti-inflammatory medication
in her case will be an inhaled corticosteroid (Beclomethasone). Because of
her fear of "steroids," the following points will be emphasized: the need
for regular use of anti-inflammatory medications, the advantage of using
inhaled vs. systemic steroids, and the difference between corticosteroids
and anabolic steroids, the different actions of inhaled corticosteroids and
inhaled bronchodilators and the need to use beclomethasone regu larly in
order for it to be effective.

2) The use of metered dose inhalers (MDIs). She should be
trained in the correct use of inhalers.

3) Identification of environmental triggers. The patient should
be trained to keep a diary and measure her peak flow rates
twice a day in order to establish a pattern between her
symptoms, flow rates and environmental circumstances.

4) The environmental changes that may be required to
control her asthma. In the session with her grandsons, who
smoke, the adverse effect of tobacco smoke on the patient,
should also be emphasized.
The pets situation should be addressed, particularly the fact that
asthma is not improved by owning a chihuahua dog. The results of
her allergy testing will be stressed to support the need to remove the pets
from the home environment.
She should hence be advised to wear a mask in her work
environment to avoid the inhalation of allergens that may worsen
asthama.

5) Her risk of diabetes. The importance of weight control
through proper dietary habits and simple exercise must be
emphasized on.
4.5 CASE STUDY #5
CASE HISTORY
Mr. H.C is 70 years old and weighs 75kg. He presents with symmetrical
polyarticular arthritis and fever. He has very painful red and swollen
metacarpophalangeal joints, wrists, elbows and knees. On admission, he was
taking Digoxin 125ug/day, Frusemide 40mg/day, Warfarin 3mg/day and
Isosorbid mononitrate 20mg twice daily.
He is a non-smoker, who enjoys a glass of wine. The house officer has
commenced Azapropazone 600mg twice daily.
Diagnosis : Gout
Acute management of the case and Drug-Drug interactions.
The treatment options in this case are NSAIDs, Colchicine, or intra-articular
steroids.
Azapropazone, which is a non-steroidal anti-inflammatory drug has
tendency to cause rashes and is associated with an increased risk of gastrointestinal toxicity. It is however not a good choice to use Azapropazone
because the patient is on Warfarin. Azopropazone usually interacts with
Warfarin by displacement of Warfarin from protein binding sites and
inhibits its hepatic metabolism, hence prolonging its action.
In addition, all NSAIDs will aggravate heart failure by sodium and water
retention and may cause gastro-intestinal side-effects in the elderly.
Thus Azopropazone must hence be stopped and treatment should start with
Colchicine.
Colchicine is effective for acute gout, with treatment commencing with 1mg
initially followed by 500ug/ every 3 hours until pain is reduced or sideeffects occur or until a maximum dose of 10mg is reached. It is effective
especially in patients with hypertension or those receiving diuretics in
cardiac failure, those with gastro-intestinal toxicity, bleeding diathesis or
renal impairment.
Intra-articular steroids are effective and work within 12-24 hours, but the
differential diagnosis of joint infection must be carefully made. Intraarticular steroids are unlikely to effect this patient’s heart failure. It wont be
effective if the patient started prophylactic therapy.
These intra-articular steroids can provide quick relief when only one or two
joints are involved.
It is advisable that the patients stops Frusemide to avoid further acute
attacks. Only patients who have more than 2
acute attacks are usually
considered for long term therapy. Starting uricosuric therapy or allopurinol
will prevent the acute attack from setting and may hence precipitate
another attack.
Allopurinol should be considered for patients who suffer from recurrent
gouty attacks. It reduces uric acid production by inhibiting the enzyme
xanthine oxidase. Allopurinol is not active but undergoes hepatic conversion
to its active metabolite oxipurinol.
Oxipurinol may accumulate in patients with renal failure, those with gout
and those receiving thiazide diuretics in whom volume contraction and
hypovolemia may occur.
Allopurinol may prolong an attack or it may precipitate another, and thus it
should not be commenced until an attack has subsided
Relationship between Gout and Diuretic therapy
The main side-effect in all diuretics is hyperuricemia which hence leads to
gout. They decrease the excretion of uric acid hence depositing it in the
bones and joints. This will hence result in gout which may present as acute
synovitis but sometimes takes the form of a generalized arthritis that may
be misdiagnosed as osteoarthritis or rheumatoid arthritis.
Drug-drug interactions
It is wrong for the patient to take digoxin and Frusemide (diuretics) at the
same time as Frusemide can cause hypokalemia hence increasing the
toxicity of digoxin. It is however best if Amiloride which is a potassium
sparing diuretic is taken instead. Potassium supplements should be added to
the regimen if the doctor insists on Frusemide.
It is however not a good choice to use Azapropazone because the
patient is on Warfarin. Azopropazone usually interacts with Warfarin by
displacement of Warfarin from protein binding sites and inhibits its hepatic
metabolism, hence prolonging its action
Patient counseling and advice
The patient should be advised to reduce his alcohol intake, lose weight,
commence a low saturated fat diet and avoid vigorous exercise. He should
reduce his dietary salt intake and avoid low dose aspirin.
He should be however advised to continue his anti-hypertensive medication.
Alcohol and Gout
Heavy drinkers are always known to suffer gout despite treatment with
Allopurinol and NSAIDs. This poor response to treatment may be due to
antagonism of the effect of allopurinol, as ethanol contributes to
hyperuricemia by increasing the production of uric acid and impairing its
excretion in the urine.
__________________________________________________________________
4.6 CASE STUDY # 6
History
A 70-year-old man presents with enlargement of left anterior neck. He has
noted increased appetite over past month with no weight gain, and more
frequent bowel movements over the same period.
Physical Exam
He is 5'8" tall and weighs 150 lb. The heart rate is 82 and the blood
pressure is 110/76. There is an ocular stare with a slight lid lag. The
thyroid gland is asymmetric to palpation, weighing an estimated 40g (normal
= 15-20g). There is a 3 x 2.5 cm firm nodule in left lobe of the thyroid.
PREDICTION:
Probable hyperthyroidism
REASON
The history of increased appetite (without weight gain) and increased bowel
motility is classic for hyperthyroidism. The resting heart rate is mildly
elevated, which is consistent but is a common finding in physician's offices.
The findings of an ocular stare, lid lag, and an enlarged thryoid are also
consistent with hyperthyroidism.
The orbital symptoms noted in this case are most typically associated with
Grave's disease and result from inflammation and swelling of retro-orbital
tissues (this effect is separate from the elevation in thryoid hormone).
However, in this case the thyroid is asymmetrical and contains a nodule,
whereas the thyroid gland in Grave's disease is symmetrically enlarged and
homogeneous.
LABORATORY TESTS
Initial evaluation of a patient's thyroid status is most commonly done by
measuring thryoid stimulating hormone (TSH) concentration in the serum, which
is a sensitive indicator of the body's perception of its own thryoid status. In
hyperthyroidism, TSH concentration is markedly decreased (the converse is true
in hypothyroidism). Usually, serum free T4 will be measured as well and can
serve as a confirmatory test for the TSH findings. In some labs, free T4 assay is
not routinely available; similar data can be derived from measuring total T4 and
T3 resin uptake, and calculating the Free Thyroxine Index (FTI) which is
proportional to free T4.
In this patient, there is a nodule associated with the thyroid gland. This finding
might result from thyroid pathology but might also indicate a parathyroid
adenoma (which would appear in the same area). Thus it is prudent to check the
patient's calcium status. Active parathyroid adenomas produce hypercalcemia
and may also be associated with marked elevations in circulating alkaline
phosphatase (due to active bone resorption).
The test results for this patient were as follows (S = measured in serum):
Patient's value
Calcium, total (S)
10.6 mg/dl
Phosphorus
4.8 mg/dl
Alkaline phosphatase (S)
160 U/L
T4, Total (S)
12.2 ug/dl
T3 resin uptake (S)
35%
T3, Total (S)
311 ng/dl
TSH (S)
<0.1 uU/ml
Free thyroxine index (FTI)
14.6
Reference range
8.4 - 10.2
2.7 - 4.5
49 - 120
5 - 11.5
25 - 35
100 - 215
0.7 -7.0
6 - 11.5
Interpretation of the above results:
The most important result is the strongly suppressed TSH. The remainder of
the thyroid tests are also consistent with hyperthyroidism (elevated FTI and
T3). The tests for parathyroid problems do not rule out a parathyroid
process (though the alkaline phosphatase is only very mildly elevated).
Since the patient is an elderly, it is likely that the increase of calcium is
associated with aging.
FURTHER TESTING
Additional testing should directly address the possibility of Grave's disease and
should also determine the nature of the nodule associated with the thyroid (testing
so far has been inconclusive regarding the nodule). Grave's disease is strongly
associated with the presence of anti-thyroid microsomal antibodies, while other
antibodies against thyroid epitopes (e.g., thyroglobulin) occur in Hashimoto's
thyroiditis. Furthermore, the thyroid hyperfunction that occurs in Grave's disease
can be assessed directly by measuring the rate radio-iodine uptake into the thyroid
gland.
Serum was obtained for anti-thyroid antibody testing and the following results
were obtained:
Patient
Normal
Antithyroglobulin Ab.
neg.
neg.
Antimicrosomal Ab.
pos. (1:1280)
neg.
A thyroid scan to evaluate the uptake of radioactive iodine into the thyroid gland
showed 68% uptake at 6 hr and 54% uptake at 24 hr after treatment with iodine123 (normal 5 - 28% uptake at these time points). The radio-iodine uptake was
homogeneously increased over the entire gland except in the area of the palpable
nodule, where uptake was decreased.
INTERPRETATION OF THE ABOVE RESULTS
The anti-thyroid antibody tests and radio-iodine uptake results make a
diagnosis of Grave's disease solid at this point. However, the finding that radioiodine uptake is decreased in the area of the nodule suggests that there is an
additional problem in the thyroid gland that is separate from Grave's disease.
DIAGNOSIS AND COURSE
The finding of a low radio-iodine uptake into the palpable nodule suggests that a
thyroid neoplasm might be present. A tissue diagnosis is needed to fully evaluate
that possibility, so a fine needle aspirate (FNA) of the nodule was made and the
cytology of the recovered cells was examined.
The diagnosis from the FNA was papillary carcinoma of the thyroid, and the
final diagnosis for the patient was:
Grave's disease with papillary carcinoma
Course
The patient underwent surgical thyroidectomy followed by thyroid hormone
replacement therapy. Later, he was scanned for residual thyroid tissue, which was
ablated with iodine-131. He underwent periodic serum thyroglobulin analysis and
iodine-131 scans, which remained negative over a two-year course.
Recently, ocular tearing and itching with proptosis were noted on physical exam.
COMMENT
It is important to remember that Grave's disease is a systemic autoimmune
process that has hyperthyroidism as one of it's manifestations. The removal of the
thyroid gland cures the hyperthyroidism, but not the other symptoms of Grave's
disease--which include the ocular symptoms.
4.7 CASE STUDY # 7
Patient history : C.D is a 74 years old male.
Three months ago, the patient experienced a mottled, blue coloration of his
left toe; a few weeks later, he noted similar changes of his right toes. His
past medical history includes a myocardial infarct, four-vessel coronaryartery bypass-graft surgery, non-insulin-dependent diabetes mellitus,
hypercholesterolemia, hypertension, peripheral vascular disease, a cerebral
vascular accident, and former tobacco use. His medications include
amiodarone, diltiazem, hydrochlorothiazide, and simvastatin.
He was admitted to the peripheral vascular service at the New York Harbor
Health Care System Medical Center and was started on clopidogrel. He
later underwent axillo-bifemoral bypass surgery with resection of the
common iliac arteries and partial amputation of the left second toe.
Physical examination
Mottled, reticulated, violaceous coloration involved his left toes, most
prominently on the plantar aspects of the medial toes and the distal plantar surface
of his left foot, with milder involvement of his right toes. All toes were tender to
palpation. His distal left second toe exhibited a black coloration. Pitting edema
involved his lower legs. Dorsalis pedis and posterior tibial artery pulses were not
palpable in either foot.
Laboratory data
A complete blood count was normal except for a hematocrit of 37.8%. An
erythrocyte sedimentation rate was 118 mm/hr, and a C-reactive protein 11.2
mg/dl. A blood chemistry profile, C3 and C4 proteins, and protein C and S
activities were normal. Antinuclear antibody, lupus anticoagulant, and hepatitic
serologies were negative.
Arteriograms showed ulcerated plaques in the right common iliac artery and
stenosis of the left popliteal artery. An abdominal computed tomography
scan showed atherosclerotic disease of the abdominal aorta and iliac arteries,
with a thrombus in the distal abdominal aorta.
Diagnosis : cholestrol emboli
Cholesterol emboli are a common complication of advanced atherosclerotic
disease. Cholesterol crystals dislodged from plaques travel through the
circulation until they become trapped in smaller vessels, which leads to
ischemia and infarction. Risk factors include older age, male sex, hypertension,
diabetes mellitus, smoking, and aortic aneurysms. Precipitating factors include
anticoagulation, thrombolysis, invasive vascular procedures, and vascular
surgery; clinical signs of embolization usually occur within days after a
vascular procedure.
Typically, one or both distal lower extremities are involved. Purple-blue toe
syndrome presents as the sudden appearance of a small, cool, cyanotic and
painful area of the foot, usually a toe. Pulses may remain normal. Pain and
myalgias are common. Other sites of involvement include the buttocks, lower
back, and lower abdomen. Extracutaneous manifestations include acute or
progressive renal failure, with refractory hypertension. Abdominal discomfort,
nausea, vomiting, diarrhea, and gastrointestinal bleeding may occur; less
frequently, intestinal infarction and perforation develop, and rarely, hepatitis
and pancreatitis. Transient ischemic attacks, cerebral infarcts, amaurosis fugax,
paralysis, altered mental status, and gradual deterioration of neurologic
function may occur. Other systemic manifestations include retinal ischemia
and infarction, fevers, and weight loss.
Diagnosis may be challenging because embolization has a random and
variable distribution and may mimic a variety of disorders, which include
thrombotic arterial or septic embolic occlusion, vasopastic disorders, and
vasculitis.
Histological confirmation is made by biopsy of the target organs, which
include kidneys, muscle, and skin. Skin biopsy specimens show cholesterol
clefts in dermal arterioles that are associated with amorphous eosinophilic
material or foreign-body giant-cell reactions. Vascular walls demonstrate
intimal fibrosis and often obliteration of lumina in older lesions. Fibrin
thrombi also may be noted.
Drug-drug interaction when viewing his medications:
1) Amiodarone when taken with Deltiazem will increase the risk of
Bradycardia, AV block and myocardial depression
2)
When taking Amiodarone with thiazides we must be very careful
and avoid the occurrence of hypokalemia as it increases cardiac toxicity.
3)
Diuretics with calcium channel blockers enhance hypotensive effects.
4)
With all the above medications it is not advisable to include anticoagualnts as they may cause severe drug-drug interactions like:

The metabolism of anti-coagulants will be inhibited by
Amiodarone.

With Clopidogrel their effects will be enhanced.

Simvustatin enhances the anticoagulant effects.
Management : is directed towards limiting progression of tissue ischemia
and prevention of further embolism. Currently, there are no effective
therapies. Anticoagulation should be avoided as it is not preventative and
may precipitate or exaggerate the degree of embolization. HMG-CoA
reductase inhibitors may stabilize and induce regression of atheromatous
plaques. The value of antiplatelet agents and pentoxifylline has not been
extablished. Surgical and invasive vascular procedures should be limited as
much as possible. The prognosis of cholesterol emboli is quite poor, with
one year mortality rates ranging between 64 and 87 percent. Causes of
death are most commonly related to cardiac disease, ruptured aortic
aneurysms, and central nervous system and gastrointestinal ischemia
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4.8 CASE-STUDY # 8
Case and Patient History:
A 70-year-old man is brought to the clinic by his daughter. Since the death
of his wife 7 months ago he has lost 15 pounds of weight. He does not
eat or sleep well and has stopped playing golf with his friends - something
he had loved doing since his retirement. He spends most of his time
repeatedly cleaning out the attic and rearranging the contents of the trunks
there.
He denies smoking or alcohol. Review of systems is otherwise negative.
Past medical history is significant for a supraventricular tachyarrhythmia for
which he takes atenolol, and seizures, of which the last episode was 3 years
ago.
Physical examination reveals a somewhat emaciated male, but is otherwise
unremarkable.
Discussion.
The presence of severe symptoms extending beyond 3-6 months is suggestive of
an abnormal grief reaction.
Depression is not a diagnosis of exclusion. While it is a good idea to keep a high
level of suspicion for malignancy, this patient has enough clues to suggest
depression that treatment should be started.
The atenolol that he takes could be an important factor in this scenario.
Beta-blockers can cause or aggravate depression, especially in the elderly. If his
depression is difficult to treat or the need for beta-blockers is not absolute, one
may consider stopping or changing medications.
The sleep and appetite disorders are common presentations of depression in the
elderly.
Elderly patients often present with vegetative symptoms as the first signs of
depression. Younger patients are more likely to present with subjective dysphoria
or a feeling of sadness.
Medications that can be given and the consequences:
Doxepin has anticholinergic side effects which make it a less optimal choice in
this elderly patient. The history of arrhythmia further rules it out.
While bupropion has few side effects, it does lower the seizure threshold and so
it would be contraindicated in this patient.
Due to his obsessive behavior pattern, fluoxetine would be a good choice for this
patient. Fluoxetine has been found to be useful in patients with obsessivecompulsive disorder. Being an SSRI it is safer in older patients. Thus it may be
the ideal antidepressant in this patient
Patient counselling
-Take the medication every day
-Expect noticeable improvement from the medication in 2 4 weeks
-Continue taking the medication even if you feel better
-Do not stop taking the medication without notifying your physician
-Contact your physician with any question
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4.9 Case-study # 9
Discharge Diagnosis:
1. Chronic obstructive pulmonary disease.
2. Pulmonary embolism.
3. Hypothyroidism.
4. Degenerative joint disease.
History of Present Illness:
This patient is an 83 year old white female who presents with a chief
complaint of increasing dyspnea on exertion over the past 7 days, in
addition to a dry cough. She denies any history of chest pain, PND,
orthopnea, fever, chills, nausea or vomiting. In addition, she denies any
history of cold or flu exposure. The patient does have a significant history
of prior tobacco use of approximately 80 pack years, however, she states
she quit smoking 10 years prior to admission. The patient was seen in the
Outpatient Clinic on the day of admission and was found to be in
respiratory distress with an
ABG of 7.46,
PCO2 of 38,
PO2 52 and 88.6% on room air.
Therefore, she is being admitted for COPD exacerbation, rule out
pneumonia, and rule out MI.
Past Medical History
1. Graves' disease with diplopia in 1969 treated with iodine. Also has a
history of Hashimoto's disease.
2. History of stroke in 1989 which was determined to be in the right
cerebellar distribution.
3.
Obscure history of dyspnea on exertion in 1989 at the time of the
stroke workup. ABG at that time was 7.36, 38, 60, PO2 of 91% post
exercise.
Past Surgical History
1. History of DJD, L2-L5 surgery in 1961 and 1985.
2. History of TAH/BSO in 1956 secondary to menorrhagia.
3. Hemorrhoidectomy in 1965.
4. Left shoulder surgery years ago.
Past Social History
She has an 80 pack year history of smoking. She quit 10 years ago after her
husband's death secondary to throat cancer. She has a history of occasional
alcohol. She received a flu shot in 10/93. She is an ex-nurse pulmonary technician
at a health insitute. She currently lives alone, is in close contact with her niece
and nephew and has many friends.
Past Family History
Her husband passed away of throat cancer and father passed away of pernicious
anemia
Physical Exam
In general, she is a well developed, well groomed, elderly white female, alert
and oriented times 3, pleasant and a good historian.
Temperature 36.8,
heart rate 80,
respirations 24,
blood pressure 150/70.
Oropharynx clear
Positive dentures. Neck supple. No bruits. No JVD.
Lungs: Positive expiratory wheezes throughout.
Heart: Regular rate and rhythm. No S3, S4. No murmurs or rubs.
Abdomen: Positive bowel sounds, nontender, nondistended, no organomegaly.
Well healed midline scar.Femoral pulses 2+ bilaterally. Extremities: 2+ DT
pulses. No clubbing. Positive varicosities noted in the distal lower extremities. 1+
edema in the medial malleolus area bilaterally.
Neuro Exam: Alert and oriented times 4. Cranial nerves II-XII intact.
Reflexes bilaterally symmetric and 1+ throughout.
Motor Exam: Upper extremities 5/5 bilateral, lower extremities 4/5 bilaterally.
Sensory: Proprioception and light touch sensation intact.
Cerebellar: Normal finger-to-nose.
Rectal Exam: Two small external hemorrhoids, no inflammation. Stool brown,
guaiac negative.
Lab Data
CBC: White count 6.1, H&H 12.8/37.7.
Sodium 142,
potassium 3.8,
chloride 103,
bicarb 29,
BUN 18, creatinine 0.8.
Chest x-ray without evidence of infiltrate. Small blunting of the right costophrenic
angle.
EKG: Normal sinus rhythm. No evidence of acute ST changes. Poor R wave
progression in V2, V3.
Hospital Course
The patient was admitted to the ICU with probable COPD exacerbation with
admission blood gas of 7.46, 38, 52 and 88% sat on room air. She was
aggressively treated with IV Solu-Medrol, Atrovent, albuterol, Azmacort.
However, despite aggressive therapy she continued to have difficulty moving
air. She was also treated with IV antibiotics including cefuroxime and
erythromycin for possible infection, although none was ever localized and
the patient remained afebrile with no leukocytosis throughout her hospital
stay. On 1/18 the patient did develop an episode of retrosternal pressure-like
chest pain rated 10/10 which was then relieved with two sublingual
nitroglycerin. Nitropaste was placed, however, the patient developed recurrent
similar chest pain radiating to her back and left side. With that history the
patient was evaluated by the cardiology fellow and was transferred to the
CCU team for further care and rule out MI. Upon arrival in the CCU the patient
described her pain as very pleuritic in nature, so in addition to an echocardiogram
a VQ scan was scheduled. Lower extremity Dopplers were also performed which
were negative. The VQ scan initially came back as high probability. It was then
decided by the attending not to pursue pulmonary angiogram, but treat the patient
for probable pulmonary embolism. A TEE was performed which had no
remarkable findings, however, upon return from this exam on 1/21/94 the patient
did begin complaining of severe abdominal pains. Her exam at that time was
remarkable for positive bowel sounds, but notable rebound in the right lower
quadrant greater than the right upper quadrant in addition to 2+ right lower
quadrant tenderness. Given her history of pulmonary embolus there was concern
of possible ischemic bowel vs. another acute abdominal process. The PS Service
was consulted and followed the patient for her abdominal pain. Serial exams
revealed that the pain eventually resolved on its own. She did obtain an abdominal
CT which revealed no evidence of any abnormalities other than a large
gallbladder. Over time the patient's abdominal pain resolved and her respiratory
status stabilized with inhaler treatments and IV steroids. She was then transferred
to the 5-West Ward for further care.
Upon discharge the patient is much less dyspneic except she does have trouble
when ambulating on her own. It was then decided that although the patient was
living alone prior to her hospital admission that she should be discharged to XXX
for further rehabilitation. Over time the patient's PT did become in the therapeutic
range on Coumadin. Therefore, he patient will be discharged to Country XXXX
for further care.
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5.0 Case- Study # 10
Patient history
A 60-year-old landscape architect was admitted because of a visual defect.
Past history of an irritable bowel syndrome for 1 1/2 years. Three weeks
PTA, because of exacerbation of symptoms, she was placed on azulfadine
for "ulcerative colitis". Two weeks PTA she developed continuous headaches
behind her right eye. One week PTA she first noted visual hallucinations
(stationary colored prisms and flashing lights). One day PTA, she saw an
ophthalmologist who recorded a normal examination and suggested migraine
headaches. On the day of admission, she noticed loss of vision in the left
visual field (115 read as 15) and came to the ER. One month PTA she had
had a dental crown replaced.
Physical exam
On physical exam, she had a temperature of 38.4 degrees C and a normal
neurologic exam except for a left inferior visual field defect. No
papilledema. Stool guaiac positive.
Laboratory findings within normal limits except for a hematocrit 33% and
ESR 50.
Toxoplasma serology negative.
CT SCAN
CT scan with contrast revealed a 2.0cm diameter ring enhancing mass in
the right occipital lobe with edema extending into the posterior temporal
and parietal lobes. Partial opacification of the right maxillary sinus also
noted.
Diagnosis
Brain abscess
Management and discussion
Patient placed on penicillin and chloramphenicol for suspected brain
abscess and dilantin to prevent seizures. Repeat visual field exam revealed
left homonymous hemianopsia. Symptoms of headache and fever improved.
However, two weeks after admission, a repeat CT scan showed enlargement
of the right occipital lobe ring enhancing lesion (3.5 cm diameter) with
angulation of the anterior aspect and increased surrounding edema causing a
mass effect with displacement of the glomus at the lateral ventricle and a
mild midline shift.
The next clinical decision is to place the patient on Decadron. This is so
as to reduce edema. Also, the patient was adviced to perform a right
occipital craniotomy.
At surgery, an abscess containing creamy colored, odorless material was
incised and drained. Gram stain of purulent material showed gram positive
cocci in pairs and chains. Pathology of the surgical specimen revealed acute
and chronic inflammation and a fibrous capsule.
Eradication of the pathogen
Cultures grew Streptococcus anginosis.
Penicilliin and chloramphenicol were continued. The patient did well and
was discharged two weeks postoperative.
Comment on the drugs used in this case
Penicillin, which is a bactericidal and acts by interfering with bacterial cell
wall synthesis. It diffuses well into body tissues and fluids, but penetration
into the cerebrospinal fluid is poor except when the meninges are
inflammed. It is excreted in the urine in therapeutic concentrations.
Chloramphenicol is a potent broad spectrum antibiotic. It must be given
with care as it may cause serious haematological side-effects when given
systemically and should therefore be reserved for the treatment of life
threatening infections.
It interacts with Dilantin and increases its metabolism.
Decadron is a corticosteroid (Dexamethasone) and increases the excretion
of sodium and water hence relieving edema. The metabolism of
dexamthasone is enhanced by anti-epileptics, thus it is useful to increase the
dose of corticosteroids.
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