CPC-Patho Version 6
CPC-Patho Version 6
CPC-Patho Version 6
Name: G.C.
Age: 55 years old
Gender: Female
Civil Status: Married
Occupation: Unemployed
Address: Tondo Manila
Others: Right handed
Admission history: Admitted for the first time
Chief Complaint
Generalized body weakness
History of Present Illness
4 months prior to admission, the patient noticed gradual onset of generalized
body weakness. This was associated with on and off low-grade afternoon fever, gradual
onset of weight loss, anorexia and pallor. Persistent of symptoms prompted the patient
to seek consult with a general practitioner who diagnosed anemia. The patient was
prescribed with ferrous sulfate tablets with note of some improvement.
2 months prior to admission, there was note of palpable nodules on the right side
of the neck as well as at the axillary and inguinal areas, and on the right wrist. There
was also note of slight limitation of movement of the wrist.
A few hours prior to admission, there was an increase in body weakness with
associated dizziness prompting consult at the emergency room of this institution.
Review of Systems
(+) weight loss, 50% in 4 months
(+) fever
(+) anorexia
(+) dyspnea
(+) abdominal pain
(+) vomiting
(+) dizziness
(+) pallor
(-) bone pain
(-) polyuria
(-) chills
(-) cough/colds
(-) hemoptysis
(-) orthopnea
(-) palpitations
(-) constipation
(-) hematuria/dysuria
(-) seizures
(-) jaundice
(-) polydyspia
(-) bleeding
(-) chest pains
(-) edema
(-) diarrhea
(-) melana
(-) hematochezia
(-) headache
(-) behavior change
(-) LOC
(-) polyphagia
Family History
(+) hypertension in a brother
(+) cough and occasional fever in the husband
Patient denies history of diabetes mellitus, goiter, allergies, cancer, tuberculosis,
and asthma in the family.
Personal/Social History
Patient is a housewife, married and has one child
The husband is an itinerant laborer who is currently unemployed
Family rents a small room in a house in a crowded community
Patient denies smoking, illicit drug use and alcoholic beverage drinking
OB-Gyne History
G1P1 (1001)
Delivered by spontaneous vaginal delivery by a midwife in a lying-in clinic.
No pre-natal check-ups were done.
No maternofetal complications were reported.
Menarche was at 12 years old, 3-5 days per episode, consuming 2-3 pads er
day, at regularly monthly intervals
Initial PE at Emergency Room
Pale conjunctiva, anicteric sclera
(+) bilateral neck lymphadenopathies, firm, non tender, and slightly movable
Dry oral mucosa
Equal chest expansion, clear breath sounds, no subcostal retractions, rales or
wheezes
Distinct heart sounds, normal rate, regular rhythm, no murmurs
Flabby tender abdomen with slight guarding, liver edge not palpable, no masses
or organomegaly
Pale nail beds, full equal pulses no cyanosis
Assessment at the Emergency Room
To consider hypovolemic shock, probable causes are
1. Dehydration
2. Ongoing blood loss (rule out intra-abdominal bleeding)
To consider lymphoma
Aspiration pneumonia
Anemia probably secondary to
1. Chronic disease
2. Blood loss
General Data
Name: G.C.
Age: 55 years old
Gender: Female
Civil Status: Married
Occupation: Unemployed
Address: Tondo Manila
Others: Right handed
Admission history: Admitted for the first time
Chief Complaint
Generalized body weakness
History of Present Illness
4 mos PTA:
Gradual onset and generalized body weakness
On/off low grade fever
Gradual onset of weight loss
Anorexia and pallor
Diagnosis of anemia
Rx ferrous sulfate
2 months PTA
Palpable nodule on the K side of the neck, axillary, inguinal area
Slight limitation of movement of the wrist
Few hrs PTA
Increase in weakness of associated dizziness
Past Medical History
No previous hospitalizations and surgeries
Denies history of bronchial asthma, diabetes mellitus, hypertension, tuberculosis,
goiter, allergies, cancer, kidney disease
Personal/ Social History
Married, housewife, 1 child
Rents small house in a crowded community
Denies smoking, illicit drug use and alcoholic beverage drinking
OB Gyne History
G1P1 (1001)
Delivered by spontaneous vaginal delivery by a midwife in a lying-in clinic.
No pre-natal check-ups were done.
No maternofetal complications were reported.
Menarche was at 12 years old, 3-5 days per episode, consuming 2-3 pads per
day, at regularly monthly intervals
3rd Day
weaned off from the mechanical ventilator
Vital signs were stable.
4th Day
Back to the wards
4 am: cyanosis, asystole cardiac monitoring
Intubated
Three episodes of cardiac arrest
Death
I. Salient Features
Prior to admission
Generalized body weakness
On and off low-grade afternoon fever
Weight loss (50% in 4 months)
Anorexia
Pallor
Diagnosed with anemia (prescribed with ferrous sulfate tablets)
Palpable nodules
- Right side of the neck
- Axilla
-Inguinal area
-Right wrist
Slight limitation of movement of the right wrist
Dizziness
Dyspnea
Abdominal pain
Vomiting
Emergency Room
Pale conjunctiva
(+) bilateral neck lymphadenopathies
- Firm, non tender, and slightly movable
- 5x5 cm tender left submandibular mass
- 3x3 cm tender right submandibular mass
Dry oral mucosa
Flabby tender abdomen with slight guarding
Pale nail beds
Hypotension (70/50)- continuous despite interventions
2 episodes of vomiting
Sudden dyspnea with cyanosis thus patient was intubated
Aspiration due to presence of food particles per suction tube
LABORATORIES:
CBC
1ST HOSPITAL
DAY
WBC
Hgb
48 (low)
Hct
0.145 (low)
Pit
Seg
Ly
Stabs
Retics
2ND HOSPITAL
DAY
4.3 (slightly low)
93 (low)
0.163 (low)
307
0.84 (high)
0.09 (low)
0.7
0.012 (normal)
URINALYSIS
Appearance
Specific. Gravity
pH
Sugar
Albumin
RBC
6
(-)
+1
0-2
NORMAL VALUES
4.4-11x 10^3/L
140-175g/l
123-153g/l
0.415-0.504
0.359-0.446
0.56
0.34
0.005-0.015
NORMAL VALUE
After 12 hr fluid restriction:
>1.025
After 12hr deliberate fluid
intake: </= 1.003
5-9
0-2
WBC
Cast/Crystals
Mucus Threads
Epithelial cells
8-15 (high)
(-)
(-)
Few
ABG
pH
pCO2
pO2
HCO3
TCO2
BE
O2Sat
NORMAL VALUES
7.35-7.45
32-45 mmHg
72-104 mmHg
22-30 mEq/L
95-100%
1ST HOSPITAL
DAY
4.97
91
2ND HOSPITAL
DAY
Sodium
Potassium
Chloride
Uric Acid
127 (low)
2.8 (low)
97
133 (low)
3.6 (low)
LDH
326
BLOOD CHEMISTRY
Glucose
Crea
0.18
Control
Patient
Act
INR
1ST HOSPITAL
DAY
12.7s
12.3s
0.78
1.22
Control
Patient
44.8s
45.8s
PT
NORMAL VALUES
53-106 umol/L
27-53 umol/L
136-142 mmol/L
3.8-5.0 mmol/L
95-103 mmol/L
0.24-0.51 mmol/L
0.16-0.43 mmol/L
NORMAL VALUES
11-14s
0.8 to 1.2
PTT
25-25 s
Non hodgkin
lymphoma is
malignancy of the
lymphocytes. A
proliferation of any
one of the three
predominant
lymph cell typesnatural killer cells,
T cells or B cells
may be included in
the category of
NHL. Clinically
NHL can be
classified into two
different groups:
1) Nodal and
Extra nodal
2) Indolent
aggressive
and very
aggressive
Patients with
indolent lymphoma
may present with
mild or no
symptoms and
seek medical
attention for a
swollen lymph
node whereas the
aggressive and
very aggressive
lymphomas create
easily noticeable
symptoms such as
pain, swelling due
to obstruction of
vessels, fever and
night sweats.
RULE IN
RULE OUT
(+) peripheral
adenopathy;axillary
& inguinal
lymphadenopathy,
later cervical
lymphadenopathy
No organomegaly;
splenomagaly and
hepatomegaly
NHL is
predominantly
found in females
(+) B symptoms;
on and off low
grade afternoon
fever, gradual
onset of weight
loss.
(+) anemia, pallor.
Anorexia and
fatigue
(+) increase of
serum lactate
dehydrogenase
Absence of night
sweats
Sarcoidosis
Is an inflammatory
disease with an
unknown etiology
characterized by
the presence of
non-caseating
granulomas. The
disease is often
multi system and
requires the
presence of
involvement of 2 or
more organs for a
specific diagnosis.
Sarcoidosis is an
inflammatory
disease that
affects multiple
organs in the
body, but mostly
the lungs and
lymph glands.
Chronic
myelogenous
leukemia ( CML)
Myeloproliferative
disorder
characterized by
increased
proliferation of the
granulocytic cell
line without the
loss of their
capacity to
differentiate. CML
are insidious,
changing
symptoms as the
disease
progresses
through 3 phases:
chronic,
accelerated and
(+) bilateral
infiltrates with
nodular masses
(stage II Bilateral
Hilar
Lymphadenopathy
with infiltrates)
(-) arthalgia
Presence of
normochromic
normocytic
anemia, with
normal platelet
count.
Absence of
leukocytosis.
(-) dermatologic
findings:
Systemic
(-) lowercomplains of fever
extremity
and anorexia
panniculitis
with painful,
(+) fatigue
erythemato
us noduloes
Pulmonary findings
( often with
can be normal in
Logren
sarcoidosis
syndrome)
(-) erythema
(+) heart block and
nodusum
sudden death
(-) lupus
pernio
Anemia
(-)
violaceous
rash on
cheeks or
nose
(-) ocular
involvement
Patient manifested Absence if
symptoms such as granulocytes and
generalized body
immature
weakness, low
precursors (blast
grade fever and
cells) in peripheral
gradual weight loss blood smear
(50% in 4 months. indicative of CML.
Marked
lymphadenopathy
located in neck
Intact traubes
space indicative of
no splenomegaly
(which is typical of
CML)
No hepatomegaly.
blast phase.
The diagnosis is
based on
histologic findings
in the peripheral
blood,
Philadelphia(Ph)
chromosome in
bone marrow cells
using workup such
as CBC, peripheral
blood smear and
bone marrow
analysis
Miliary
Tuberculosis
Miliary TB is the
widespread
dissemination of
Mycobacterium
tuberculosis via
hematogenous
spread. Miliary TB
can arise as a
result of
progressive
primary infection
or via reactivation
of a latent focus
with subsequent
spread.
(bilateral), axilla,
inguinal suggestive
of early sign of
blast crisis in
chronic phase
CML.
Physical
examination
reveals slight
tenderness at the
upper abdominal
area which may
indicate
enlargement of
spleen
Advanced age
accounts for
progressive
secondary
tuberculosis.
(+) bilateral
infiltrates
(+) fever, anorexia,
weight loss,
weakness
(+)
lymphadenopathy
(+) anemia w/
lymphopenia
(+) hyponatremia
due to adrenal
insufficiency (can
occur due to an
acquired
disturbance of
neurohypophyseal
function resulting in
unregulated
antidiuretic
hormone (ADH)
No hematologic
signs of bleeding,
petechiae,
echymosis, and
bone pain.
release; an
antidiuretic
principle in the lung
tissue affected by
TB that may either
produce ADH or
absorb an
inappropropriately
release hormone
from the posterior
pituitary)
(+) DIC
III. FINAL DIAGNOSIS
Miliary Tuberculosis
IV. PATHOPHYSIOLOGY
Uninfected (70%)
Progressive primary
Miliary TB
Wall of primary
lesion loses its
integrity. Tubercle
bacilli proliferate
more rapidly and
escape scar tissue
Reactivation of the
infection
Re-exposure
Massive lymphohematogenous
dissemination and embolization to
vascular beds of various organs
Post-primary
Miliary TB
Re-infection
Patients Manifestations
Systemic
Generalized body weakness
On and off low-grade
afternoon fever
Weight loss (50% in 4
months)
Anorexia
Dry oral mucosa
Lymphatics
Bilateral neck
lymphadenopathies:
Firm, non tender, and slightly
movable
5x5 cm tender left
submandibular mass
3x3 cm tender right
submandibular mass
Gastrointestinal
Flabby tender
abdomen with slight
guarding
Abdominal pain
Vomiting
Hematologic
Anemia
Pallor
Dizziness
Pale conjunctiva
Pale nail beds
Palpable nodules:
Axilla
Inguinal area
Right wrist
Musculoskeletal
Limited movement of
right wrist
Endocrine
Capillary blood
glucose= 125mg%
Cardiovascular
Hypotension (70/50)
continuous despite
interventions
Respiratory
Dyspnea
Endotoxin or lipopolysaccharides of
bacteria
Neurological abnormalities
( dizziness )
Re-routing of vomitus
to the air passages via
the trachea & into the
lungs
Aspiration
Nitric oxide
synthesis
Vessel wall
vasodilation
hypotension
Cellular hypoxia/
low vascular
resistance/ ischemia
Hypokalemia
Aspiration
Pneumonia
Lactic acidosis
Septic
Shock
SEPTIC SHOCK
Miliary TB
Gram (+) Bacilli
Septic Shock
Compensatory
Vasoconstriction
H2O retention
Arterial pressure
RAAS
Maintain CO +
Perfusion to
heart & brain
Baroreceptors
Carotid sinus
Aortic arch
Compensatory
mechanism
activated
Dec. BP
Peripheral
resistance
Reduced
blood flow
kidney
Release of
Nor/Epi
BP
Myocardial
contractility
Tissue Hypoxia
Cell death
Progressive
Stage
Release of
lysosomal enzymes
ATP depletion
Anaerobic
metabolism
Damaged cell
membrane
Lactic acid
accumulates
Inadequate
perfusion
Inc. Risk
for DIC
Vascular endothelium
ARDS
Inc. capillary
permeability
MI
Movement of
fluid from
vascular space
Venous pooling
Inc. capillary
permeability
Lactic acid
accumulation
Alveolar epithelium
Hypotension
Interstitial
space
Pulmonary
Gas,...
Alveoli collapse
Gas exchange and
Dec lung
compliance
fr
Histamine
Inflammation &
damage the
alveocapillary
permeability
Fluids ----
Sufficient O2
can't __ the
alveoli
capillary m..
Pulmonary
edema
V. INCIDENCE
Worldwide Scale:
Of all patients with TB, 1.5% are estimated to have miliary tuberculosis. The
World Health Organization reports that 2-3 million patients die with or from all forms
of TB each year.
About one third of the world's population has latent TB infection (LTBI). Over
95% of TB deaths occur in low- and middle-income countries
TB causes one fifth of all deaths of people with HIV infection
TB is still a leading cause of death, particularly in sub-Saharan Africa. In large
parts of Africa, TB is epidemic because of the increased susceptibility conferred by
HIV infection
TB in children accounts for 20% or more of all TB cases in many countries with
high TB incidence
It is estimated that miliary TB accounts for 1 to 2 percent of all cases of TB in
immunocompetent persons
Philippines
Tuberculosis in all forms is the Top 6 cause of mortality in the Philippines
2009: Number: 25,470 Rate:27.6
5-year average (2004-2008): Number: 25,376 Rate:29.2
The tuberculosis mortality rate has been on a decline for the past decade. This is largely
in part to the intensive effort of the National Tuberculosis Program and various nongovernmental organizations that are pushing to eradicate tuberculosis in the country. It
is a monumental task but it has already been gaining ground in terms of mortality rate.
The World Health Organization (WHO) noted in its Global Tuberculosis Report 2012
that the number of TB cases in the Philippines, China, Cambodia and Vietnam had
been going down from 1990 to 2011. In the Philippines, TB deaths went down by 49
percent while the number of Filipinos with TB decreased by 52 percent.
VI. PROGNOSIS
Firstly, many patients can experience a fever lasting several weeks with daily
spikes in morning temperatures. Secondly, hypercalcemia prevails in 16 to 51% of
tuberculosis cases. Thirdly, Chordial tubercules, pale lesions on the optic nerve,
typically indicate miliary tuberculosis in children. Lastly, between 10 to 30% of adults,
and 2040% of children with miliary tuberculosis have tuberculosis meningitis. This
relationship results from myobacteria from miliary tuberculosis spreading to the brain
and the subarachnoid space; as a result, leading to tuberculosis meningitis.
Miliary tuberculosis can present with: enlarged liver (40%), enlarged spleen
(15%), inflammation of the pancreas (<5%), multiple organ dysfunction with adrenal
insufficiency, unilateral or bilateral pneumothorax rarely. Stool may be diarrheal in
nature and appearance.
Adults 25 to 30%.
Most deaths occur within the first 2 weeks of admission to the hospital.
Relapse rate 0-4% with adequate therapy and directly observed therapy
Most relapses occur during the first 24 months after completion of therapy
VII. COMPLICATIONS
Complications are numerous and may involve any organ. "Sepsis tuberculosis
gravissima" is acute overwhelming septic shock with multiple complications such as
respiratory failure, ARDS, cholestatic jaundice, acute pancreatitis, hepatic and renal
failure, and DIC. A variety of neurological complications have been noted in miliary
tuberculosis patientstuberculous meningitis and cerebral tuberculomas being the
most frequent. Multisystem organ failure has a mortality of up to 90%.
VIII. THERAPY AND PREVENTION
Early empirical therapy for suspected miliary tuberculosis is prudent. A delay of
even 1-8 days contributes to a high mortality rate. Steroids are warranted for
hypotension due to presumed adrenal insufficiency after an adrenocorticotropic
hormone stimulation test.
For susceptible organisms, the treatment period is 6-9 months. For meningitis, it
is 9-12 months. For miliary TB with meningeal involvement, daily medications for the
entire length of therapy are recommended.
Rules that apply in the prevention of resistant TB:
1. Rifampin is the drug of choice for treatment; in most cases, the treatment
duration is at least 18 months without rifampin
2. Ethambutol (EMB) is used to prevent rifampin resistance if the organism is
resistant to isoniazid (INH); EMB can be discontinued as soon as the organism is
found to be susceptible to rifampin and INH
3. Pyrazinamide is used for the first 2 months of treatment to decrease the
treatment duration from 9 months to 6 months if the organism is susceptible to
rifampin and INH
For MDR-TB, use a minimum of 1 susceptible injectable and at least 3 additional
susceptible drug to prevent the development of additional resistance.
IX. CAUSE OF DEATH
Underlying Cause of Death Miliary Tuberculosis
Antecedent Cause of Death Septic Shock
Immediate Cause of Death Acute Respiratory Distress Syndrome (Respiratory
Failure)