FINAL NOTES FOR APMC-SN CPC National Convention

Right sided body weakness Neurological localization

• In general, the right hemisphere is dominant for tasks requiring spatial and constructional skills, as well as for directed attention and body image, while
the left hemisphere is dominant for language and motor functions, as well as linguistic thought and reasoning, analytic and mathematical skills, and the
temporal sequencing of stimuli.

• Characteristic of cortical lesions are (a) seizures and (b) multimodal motor and sensory deficits, such as aphasia and apraxia. Although subcortical
lesions may cause aphasic symptoms, these are seldom as pronounced or long lasting as they are with cortical lesions.

• Characteristics of white matter lesions are (a) weakness, (b) spasticity, (c) visual field deficits, (d) “pure†motor syndromes, and (e) urinary
incontinence.

• The cortex in the posterior portion of the inferior (and middle?) frontal gyri (Broca area), cause a true language disturbance. Patients with true Broca
aphasia usually have extensive damage involving not only Broca area (the inferior left frontal gyrus, which contains areas 44 and 45) but also the
surrounding frontal fields (the external aspects of area 6 and areas 8, 9, 10, and 46) and the underlying white matter and basal ganglia. Although the
patient knows what he or she wants to say and can recognize an appropriate sentence, he or she cannot produce the appropriate sounds or write a
meaningful sequence of letters. There is a drastic loss of speech fluency, with speech becoming effortful and often slow, with pauses between words
often outnumbering the words themselves

• Area 312 (Primary somatosensory cortex or postcentral gyrus): they are responsible of touch, temperature, vibration and pain. Sensory perception
especially the legs, trunk, arms, hands, face and the lips. Skilled and coordinated orofacial movement and motor learning. Leions in this area causes loss
of vibration, proprioception and fine touch.

• Area 4 (Primary motor cortex or the precentral gyrus): responsible for executing motor movements, contralateral. Lesion in this area would cause
paralysis in the contralateral side of the body.

• Area 44, 45 (Broca’s area): Motor speech area. Lesion in this area causes a deficit in the ability to speak and produce the proper words/sounds even
though the patient maintains the ability to comprehend language and mentally fomulate proper sentences.
In transit: projective • Vomiting: second stage of the progression of increased ICP
vomiting, aphasic but • Aphasic but shouting: not clear if the “shouting” includes words or just moaning
shouting
CHECK VID DIFFERENTIATE Infarct and Hemorrhagic
WOULD THIS BE JUST A LARGE INFARCT? MOST OBVIOUS IS BLEEDING
SIGNS OF INCREASE ICP: NO 1 CAUSE IS BLEED; so CT SCAN!!!!!!
FUNDOSCOPY: IF CHRONIC MAG (+), PAPILLEDEMA, GRADING CHERVS NA NAMAN
CLINICAL AND HISTORY: CANNOT DIFF JUD SO CT SCANNNNNN
FUNDOSCOPY: OH MAY BLOOD, PERO INFARCT PALA; NOT ALL BLEED WOULD CAUSE OF BLEEDING; RETINA BECAUSE OF ELEVATED BP OR SUPER INC ICP;
BLEEDING IN FUNDO NOT REALLY = TO ICH; SAH YESSSSS COS ________ ; ______ SCORING??? NOT USED
MAIN REASON FOR CT SCAN FOR STROKE;
INFARCT:
1. Thrombolysis: nth hours; to rule out bleed; you wont find infarct or locate bleeding
BLEED: NOT TO CONFIRM LOCALIZATION
1. based on history and pe; check the location and severity of the bleed. quantify the bleed; refer
MEASURE pothari method?????

STROKE IS A CLINICAL DIAGNOSIS

DAY 1 ROS: symptoms; to establish pertinent positives and pertinent negatives to clarify the diagnosis. A question answered by a yes or no, there’s no details about the OLDCAARTS;
uncover problems unrelated to the present illness

• Headache: the first sign of inc ICP. This is followed by vomiting. In this case, The patient showed these two signs already in the first hospital day, causing us to
suspect for a lesion in the brain which could have caused the increase in the intracranial pressure

• Projectile vomiting: vomiting withour nausea; CHECK VID

• Cough: we dont know oldcaarts

• Nape pains: we dont know oldcaarts — NO ONSET

• Chills: we dont know oldcaarts — NO ONSET

• Headache, R occipital area: we dont know oldcaarts

• Irritable: we dont know oldcaarts

 LABS:

• INCREASED WBC: shifts the hemostatic balance in favor of coagulation (Morotti); expected highest WBC in hemorrhagic stroke; Check WBC in GTN; If infection,
what is present and what to request? JUST CHECK RECORDED VID. ALWAYS SUGGEST TEST. NO MENTION IF ANTIBIOTICS IS GIVEN. INCREASED WBC RELATED
TO COUGH? > PNEUMONIA > NEED FURTHER WORK UP
• VIRAL HERPES ENCEPHALITIS: CHECK VID GIRL > TEMPORAL LOBE > MODE OF EXIT: UNCAL HERNIATION
• MORE ON MYCOTIC ANEURYSM: X-RAY!
• PARASITIC
• O
• DECREASED RBC: due to ongoing hemorrhage
• DECREASED HEMOGLOBIN DAW?????: RBCs lysis occurs within 24 h of ICH and induces the release of Hb and heme, which are taken up by microglia and neurons; All of
Hb, heme and iron causes significant brain edema after the first 24 h, which is related to a threefold increase of BBB permeability (Zheng)
• DECREASED HEMATOCRIT: due to ongoing hemorrhage; the plasma volume has compensated for fluid loss while the red blood cells that have been lost cannot be replaced
for days
• INCREASED MCV: due to ongoing hemorrhage; the plasma volume has compensated for fluid loss while the red blood cells that have been lost cannot be replaced for days
• INCREASED MCHC: due to ongoing hemorrhage
• INREASED RDW: due to RBC lysis
• INCREASED NEUTROPHILS: Neutrophils or polymorphonuclear leukocytes (PMNs) are the first leukocytes to infiltrate the nervous system within 4-5 h after ICH, and reach a
peak value at 3 days (Zheng); promote a procoagulant state that limits hematoma expansion.
• DECREASED LYMPHOYCTE: Because of the bleeding, there is decreased in RBC, an increased in neutrophils to promote coagulation and an increased in platelets to promote
hemostasis; Pluripotent stem cell would favor the production of myeloblasts than lymphoblasts.
• NORMAL GLUCOSE: we can note in the history that the patient had vomiting after eating, so this might be a random blood sugar reading. If we are suspecting, a DM, FBS is
needed.
• FBS normal <126 mg/dL (<7.00 mmol/L) RBS normal <200 mg/dL (<11.1 mmol/L) without DM classic symptoms (weight loss, polyuria, polyphagia and polydipsia)
• NORMAL BUN:CREA RATIO
• SLIGHTLY INCREASED Na+: this might because of the administration of a hyperosmotic solution for management; to be searched
• SLIGHTLY INCREASED CHLORIDE: this might because of the administration of a hyperosmotic solution for management; to be searched
• DECREASED ALBUMIN: Due to vasogenic edema; A redistribution from the intravascular to the interstitial space, due to increased capillary permeability
RULE OUT OTHERS ROM VITAMIN C D
Go back to intracranial bleed
Localization Headache: the first sign of inc ICP. This is followed by vomiting. In this case, The patient showed these two signs already in the first hospital day, causing us to suspect for a lesion
in the brain which could have caused the increase in the intracranial pressure.

INTERNAL CAPSULE AND CORONA RADIATA

Increased ICP MECHANISMS OF Increased ICP

I. NORMAL PHYSIOLOGY

a. ICP
1. Skull as a rigid container, inelastic, closed
2. Pressure is distributed evenly throughout the intracranial cavity
3. Modified Monroe-kellie hypothesis
- sum of intracranial volumes of blood, CSF, brain parenchyma and other components = constant
- increased 1 component = dec in other components to keep ICP normal
b. Normal values of ICP, Foramen monroe, recumbent

mm CSF mmHg
Adult 90-200 6.6-16 (<10-1%)
Young children 3-7
Term infants 15-80 1-6

c. Compliance of intracranial contents

-compressibility of intracranial contents
-change in pressure as a function of change in volume
-describes effect of volume on ICP
-higher compliance, more able to accommodate volume with minimal increase in ICP
d. Vascular physiology
Cerebral blood flow (CBF)

-Paramater for brain function and survival

CPP (cerebral prefusion pressure)

=—————————————————-
CVR (cerebral vascular resistance)

MAP (mean arterial pressure) - ICP

= ———————————————
CVR

Normal CPP adult >50mmHg

Average: 50 mL/100g brain tissue/min

(75-80 gray matter/20-30 white matter)

Cerebral blood flow compromised when

CPP(MAP-ICP) <40 mmHg

CEREBRAL AUTOREGULATION - CBF constant with MAP 40-140 mmHg (modify CVR)

Effect of CBF on Cerebral function:

(ml/100g brain tissue/min)

16-18cc —EEG Flatline

15cc — Physiologic paralysis
12cc — Loss of evoked potentials
10cc — Cell death

Therefore the ultimate effect of progressive, increasing, untreated pathologic increased intracranial pressure (ICP) is decreased cerebral blood flow (CBF) > Decreased CMRO2
(cerebral metabolic rate of oxygen / rate of oxygen consumption) demands > Cell death
INCREASED ICP (IC-HTN)

a. Increased ICP due to:

1. Cerebral edema — increased in brain water > tissue swelling

a. Cytoxic edema

- intracelullar, gray matter (cell bodies/conducts, process, and sends information to various part of the body), loss of intracelullar K

- strokes

b. Vasogenic edema

- extracelullar, white matter (axons/interprets sensory information from various parts of the body), increased permeability of blood vessels

- tumor, brain abscess

c. Interstitial edema

-brain parenchyma

2. Increased CSF volume

-hydrocephalus

-communicating vs obstructive (non-communicating)

3. Hyperemia

-increased cerebral blood volume

-loss of cerebral autoregulation

-commonly seen in children even with mild head injuries

4. Space occupying lesion (mass) - tumors, abscess, etc.

b. Symptoms of Increased ICP
1. Headache - with nausea and vomiting
-warning signs: morning, Valsalva maneuver
-posture related, blurring of vision, diplopia
2. Transient visual loss
3. Change in intellect or development of lethargy
4. Symptoms related to cause of increased ICP
-numbness, weakness
c. Signs of Increased ICP

1. Severe papilledema
2. Cushing’s triad = hypertension, bradycardia, respiratory irregularity
3. Nuchal rigidity
4. CN VI palsy
5. Setting sun sign
6. Increased head circumference
7. Herniation syndromes
d. Diagnosis
1. Physical signs and symptoms
2. Direct ICP monitoring
2. Direct ICP monitoring
a. Type of monitors:
-intraventricular catheter
-intraparenchymal monitor
-subarachnoid, subdural, or extradural sensor
-infants: fontanometry, aplanation principle
b. ICP wavefroms
1. Lundbergh A waves (plateu waves)
-elevations >50mmHg for 5-20 min
2. Lundbergh B waves (pressure waves)
- 10-20mmHg, for 3s to 2min
3. Lundbergh C waves (Traube-Hering waves)
- low amplitude, 4-8/min
- May be normal ICP waveform
c. Complications of ICP monitors
1. Infection - average 4-17%
2. Hemorrhage - average of 0-2.8%
3. Malfunction and obstruction - average of 6.3-40%
4. Malposition - 3% of IVC require repositioning
Progression Headache > Vomiting > Decreased sensorium > Brain herniation syndrome > Coma

Increased ICP (Harrison’s)

• Commonly the focal deficit worsens over 30-90 minutes = headache, vomiting decreased sensorium
• 5-30 minutes = face sags
• 12-72hours = edema in adjacent brain tissue may cause progressive deterioration
• Pontine hemorrhages = deep coma with quadriplegia often occurs over a few minutes
COMA

RAS

• Activates cortex which gives us wakefullnes

• Melatonin shuts down RAS for sleep to occur

• Located in the tegmentum of the midbrain and pons

• Responsible for wakefullness

• Activates the cortex

• Awake: open eyes spontaneously

• Drowsy: open eyes upon verbal commands and light sensation

• Stupor: open eyes upon pain

• COma: close despite pain

- Purposeful withdrawal to pain

- Non-purposeful withdrawal to pain

- Decorticated

- Decerebrate

- Unresponsive coma
Herniation 2 components

1. Opening

2. Something that enters through the opening: parenchyma

• Lowest part of the termporal lobe - uncus

• Medial lower cerebellum - tonsills of cerebeullum

Openings

• Tentorial notch: diec connect with midbrain - uncus

• Tentorium cerebelli

• Foramen magnum - medulla to sc; tonsils

• Temporal lobe above the tentotium; uncus

UNCAL HERNIATION: caused by pressure; finding a way out

• Decreased sensorium

adducts the eye, pupillary constriction and opening the eyelids (CN III normal)

• Ipsilateral medial rectus palsy

• Ipsilateral dlating pupil, not reactive to light

• Ipsilateral ptosis: cannot be seen because coma na



CENTRAL HERNIATION

• Decreased sensorium

• Bilateral medial rectus palsy

• Bilateral non-reactive pupil

SIGNA OF TONSILLAR HERNIATION: increased ICP in the infratentorial

• Apnea

• Decreased sensorium
 FACTORS THAT INCREASE ICP

• Increased CBF -> more edema -> control bp and inc icp

• Hypercapnia -> when breathing slows down in cases of decreased sensorium

• Fever ->

• Hypervolemia ->

• Restlesssness

CONTROL OF ICP

• Elevated head 15-30 - bad: too high, decrease blood flow, brain cells lack o2

• Control fever

• Ventilatory support: one of the fastest ways, blow off CO2; hyperventilate; works 5-10 minutes only; immediate but not sustainable

• Osmotic diuretics mannitol/hypertonic saline: diuresis, remove fluid out of the area/remove edema; osm 280 (make the osm on bv 1000-9000 )

• Mannitol (1 gm/kg/maintain at .25-.5 gm/kh q 4 = woeks well with vasogenic

• Hpertonic saline 1-1.5cc/kg q4 = works well with all edema

=only 4 houts

=based on weight

• Dexamethasone for vasogenic edema

=risk for gi bleeding and infection

=for tumors

=no effect on cytotoxic effect on strokes infarct

Diagnosis

Management

WHAT LABORATORY CT MRI TUMOR

TESTS SHOULD HAVE MRI: better resolution; clearer infratentorial structures; can view old blood/previous hemorrhages; CVM: check for old blood; if you're not sure of the ct scan
BEEN REQUESTED? MRA and CTA: better resolution in MRA

IN THIS PATIENT
WOULD YOU DO MRI? Is it economical? Will it change your management? Yes, because of cavernous malformation. Academically, yes. But economically, noooo!
MRI: recurrent bleeding because hemosiderin deposits are seen.; silent bleeds can be seenl those that are not big to cause clinical manifestation.
WHAT SHOULD HAVE
BEEN THE PROPER
MANAGEMENT FOR DAY
1
DAY 2 Neurologic findings

• Can follow commands, moans mean that the patient can comprehend but is incapable forming the right words. This is typical of Broca’s aphasia. So
location fo the lesion if Left, frontoparietal.

• Pupils are 3-4 mm, which is at the normal state. Preferential gaze, Left. Here, the lesion can be either at the left frontal lobe (contralateral) or at the right
pontine area (ipsilateral). But the problem is there is no examination of the extraocular muscles which could grreatly help in distinguishing the two
lesions. But in conjunction to the aphasia of the patient, the lesion leans toward the left frontal lobe since lesions in the brocas area could affect the
surrounding frontal eye fiels which are the areas 8, 9, 10 and 46.

• Diminished sensation on the right side of the face. The are 312 or the primary somatosensory area in the postcentral gyrus is affected. And since the
manifestation is contralateral, the leion is in the Left Parietal lobe.

• Weak gag reflex: Probably secondary to facial palsy in the right.

• Weak shoulder shrug, right: probably secondary to right sided weakness.

• Tongue deviation, right: Can be fake, because the mouth should be in midline in testing this.

• Motor strength. 0/5 in Right UE, 1/5 in Right LE. This shows a lesion in the precentral gyrus or the primary motor cortex.

• FINAL Assessment based on Neuro examination on 2nd day: Left, frontoparietal hematoma. Why hematoma or bleeding? The clue is the projectile
vomiting of the patient. This follows the increased ICP progression. Headache>Vomiting>decrease in sensorium>Herniation syndromes>brain death
LABS

INCREASED BUN:CREA RATIO: Higher BUN is associated with upper GI bleeding (González-González JA); A BUN/Cre ratio > 30 is a useful metric by which to diagnose upper
GI bleeding (Tomizawa)

Localization

History of AUB

Transvaginal ultrasound

GTN Etiology
Pathogenesis
Diagnosis
Management
Theca lutein cyst Etiology
Pathogenesis
Diagnosis
Management
WHAT SHOULD HAVE
BEEN THE PROPER
MANAGEMENT FOR DAY
2

DAY 3 2:30PM

DAY 3 9:30PM

Clinical manifestation Hypertension

Abdominal (Cheyne Stokes): DOC G: CHEYNE; DOC C: NO IT’S NOT; can be metabolic for compensation; just check the vid; ventilatory failure = pco2; check the vid!!!!!!
ALWAYS GO BACK TO THE PATIENT AND THE INFO GIVEN
Decreased sensorium
Anisocoria
Neuro

• New findings: Anisocoria and decreased sensorium: This is parallel to the progression that was previously mentioned. Decreased sensorium is a sign or a raised
intracranial pressure. Anisocoria is noted with dilated left eye. Anisocoria is already a sign of an impending uncal hernitaion. In this manner, the herniation of uncus may
have compressed the third nerve causes dilation of the ipsilateral pupil.
• Increased BP: This is the body’s compensatory mechanism to the increased intracranial pressure. As the ICP increases, the CPP declines because the ICP is increasing
up to the level of the MAP. Here, the body tries compensate by increasing the blood pressure and dilate the arteries in the brain.
• Stuporous and no eye opening: These are two conflicting principles since stupor is eye opening due to vigorous stimulation. But they said there is no eye opening.
• Flexion of the upper extremities: Decorticate. This, together with anisocoria and decreased sensorium are already signs of the brain herniation syndromes. This is still in
congruent with the progression of raised ICP.
• (+) shoulder shrug: Maybe secondary to right sided weakness and (+) flesion of the upper ex
• Abdominal breathing: The patient is most probably having Cheyne Stokes respiration since the patient is experiencing a brain herniation syndrome. This type of
respiration consists of brief periods of hyperpnea alternating regularly with even shorter periods of apnea. After the apneic phase, the amplitude of respiratory movements
increases gradually to a peak and then slowly wanes to apnea. During the hyperpneic stage, the patient becomes more alert, the pupils may dilate toward normal from
the miosis characteristic of diencephalic dysfunction, and the motor behavior reflects control by higher centers (e.g., decorticate posturing yields to semipurposeful
movements). The eyelids may open during the rapid breathing phase and close during the slow breathing phase.
• (+)Corneals and gag reflex: They are intact.
Cranial CT Requested to confirm 1. expanding hematoma, 2. new onset hematoma, 3. Perihematomal edema, 4. Intraventricular hematoma
IVH:
SAH (Grade III): Fissure grade: thickness of SA blood; >5mm ang III; to predict the risk of vasopasm; IDK IF Hunts and Hess ba sya or Fissure; III daw ang patient girl; Find:
Structural daw if SAH — based on the clinical manifestation: the patient did not present with nuchal rigidity and sudden worst headache of my life with or without local deficits and
with or without _______; the headache and nape pains in the history has no ONSET of nape pains and headache; NUCHAL RIGIDITY ABSENT WHEN = If small amount of SAH
Focal deficit: cant if SAH alone; __________ check vid
Intraparenchymal: check vid
DEMYER’S neurologic exa, 7th edition???????: meningeal irritation no = 1. very young very old 2. comatose 3. acute ___ of corticospinal tract 4.
The usual meningeal irritatio signs may fail to occur in five circumstances: 1.
Laboratory

WHY IS THERE A NEW

BLEED

SMASH U

Structural LAW OF PARSIMONY — A principle in science and philosophy, much applied in medicine, that one should try to account for an observed phenomenon in the simplest possible
way and should not look for multiply explanations of its different aspects.

LOOK FOR SOMETHING TO EXPLAIN IT AS A WHOLE

IF WE CANNOT LOOK FOR SOMETHING THEN SEPARATE

RULE IN:
RULE OUT:

AVM
Etiology
Pathogenesis
Diagnosis
Management
 RULE IN:
RULE OUT:

PUFF OF SMOKE: CT ANGIO

Moya Moya
Etiology
Pathogenesis
Diagnosis
Management
RULE IN: GINAGMAY NA RECURRENT
RULE OUT: not massive bleeding

POP CORN: CAN BE COVERED BY THE BLEEDING; calcifications/popcorn appearance can be seen

CVM
Etiology
Pathogenesis
Diagnosis
Management
Hypertension ADDRESS BP READING ON THE DAY 3
CHECK VID GIRL
Basal ganglia (55%): putamen
Cannot be ruled out because other structural cause should still be ruled out
COULD BE ONE ENTITY OR COMBINED?????

HOW TO DIAGNOSE CHRONIC HYPERTENSION????????: CHECK VID GIRL //

RULE IN:
RULE OUT:

Etiology
Pathogenesis
Diagnosis
Management
Non-stroke Tumor
Primary tumor bleed RULE IN:
RULE OUT:

Oligodendroma
Etiology
Pathogenesis
Diagnosis
Management
Glioblastoma
Etiology
Pathogenesis
Diagnosis
Management
Metastatic tumor bleed PERCENTAGE BLEED COMPARED TO PRIMARY

Bronchogenic carcinoma Etiology

Pathogenesis
Diagnosis
Management
Melanoma Etiology
Pathogenesis
Diagnosis
Management
Renal cell cancer Etiology
Pathogenesis
Diagnosis
Management
Choriocarcinoma BECAUSE OF THE ULTRASOUND AND OBGYNE HISTORY
PERCENTAGE PLZ

It is preceded by several clinical conditions, it is observed that about 50% arise in molar pregnancies, 25% arise after previous abortions, 22.5% arise in normal pregnancies, and
2.5% arise subsequent to ectopic pregnancies

The favoured sites are the lung (94%), vagina (44%), liver (28%), and brain (28%), followed by the skin, gastrointestinal tract, kidney, breast, and bones

Approximately 30% of patients with choriocarcinoma show metastasis at the time of diagnosis, generally associated probably with the higher affinity of trophoblasts to blood
vessels.

Because choriocarcinomas are very vascular lesions and are often perfused by fragile vessels, as well as due to the tendency of trophoblastic cells to invade and erode vessel
walls, they are frequently haemorrhagic. Thus, intraparenchymal bleeding in any woman of child-bearing age with this malignancy is well explained
Etiology
Pathogenesis
Diagnosis
Management
WHY D&C Indication
Contraindication
RECURRENCE OF BLEED

MANAGEMENT OF Acute and long-term management: CHECK VID

CHORIO WITH BRAIN
DAY 3 MANAGEMENT Hyperventilation:

Subsequent intubation: protect the airway

SUGGEST POSSIBLE EXPLANATION AND MENTION JOURNALS

Maybe aspiration: check vid;
Maybe lungs infection:+hemoptysis
Maybe central: related to stroke
WHAT LABORATORY
TESTS SHOULD HAVE
BEEN REQUESTED?
WHAT SHOULD HAVE
BEEN THE PROPER
MANAGEMENT IN DAY 3
DAY 4 CLINICAL MANIFESTATION

• Comatose (GCS 3), no response to pain.

• Fever; central fever: This is a poor prognostic factor for patients with ICH. They are common after spontaneous ICH especially those with largeICH. Mechanisms include
disruption of mesecephalic-diencephalic mechanisms responsible for inhibition of thermogenesis. PGE2 is released acting in the preoptic area of the hypothalamus
leading to an increase body temperature. Systemic pyrogens, IL 1 appear on the area where there is incomplete BBB thus they act on the preoptic area inducing fever.
• Coffee-ground material in NGT: Cushing’s ulcer is a gastro-duodenal ulcer produced by elevated ICP. This increase in ICp may cause overstimulation of the vagus nerve
or paralysis of the sympathetic system leading to increased secretion of gastric acid causing formation of gastroduodenal ulcerations.
• Tachycardia: The first stage of Cushing’s reflex is tachycardia as a compensatory mechanism in the elevating ICP.
CUSHING ULCER
Etiology
Pathogenesis
Diagnosis
Management
ACUTE CUSHING REFLEX
Etiology
Pathogenesis
Diagnosis
Management
CENTRAL FEVER
Etiology
Pathogenesis
Diagnosis
Management
LABORATORY INCREASED WBC
DECREASED RBC
INCREASED HEMOGLOBIN
DECREASED HEMATOCRIT
DECREASED MCHC
INCREASED RDW

INCREASED NEUTROPHIL
DECREASED LYMPHOCYTES

INCREASED ESR
LABORATORY CSF
PARAMETERS WITH NO ABG
RESULTS URINALYSIS
MANAGEMENT DOPAMINE

WHAT LABORATORY
TESTS SHOULD HAVE
BEEN REQUESTED?
WHAT SHOULD HAVE
BEEN THE PROPER
MANAGEMENT IN DAY 4

DOC MAU
what do you think are the cough and chills in the ROS? What is cough? Where does it manifest
What is chills? Where does it manifest?
What is ROS?
Present the patient
Relate patient to the definitions above
Provide if cough is, ____ it should be related to ________ and the data of __________ should be congruent or requested.
Provide if chills is _________
what do you think of pulmo mets before brain mets? In metstatic choriocarcinoma, ____ of the cases go to lungs then brain; but there are also case reports that do not have pulmo.
What in the case can allow us to consider If there is, the symptoms are:
The patient has
We cannot conclude because the patient do not have ____
Is the chills in the ROS possibly related to possible Chills is _____
febrile episode; or afebrile chills or shivering? ROS is _____
Chills associated with febrile
Afebrile chills are seen in
Shivering is
Patient presented with
We dont know the old caarts
We need _____ to know its significance.
Is the course of ti,e fro, primary to pulmo to brain In metstatic choriocarcinoma, ____ of the cases go to lungs then brain; but there are also case reports that do not have pulmo.
compatible with a 4 month history Common course if alone
Common course if with pulmo
The patient
We need info _____ to know
FIGO staging and classifcation
FIGO on prognostic factors
Leukocytosis Leukocytosis is ________
It is related to _______
ICH is __________
GTN/Chorio is ____
Patient is
We cannot relate it to ROS cause we dont know the old caarts and there are no other test that can supprort. We need too request.
Elevated glucose on admission Elevated glucose in
RBS is
FBS is
The patient is
Therefore
What do you think of the hypernatremia, increased
chloride
BUN Crea ratio + sensi and speci
Decreased hemoglobin
DOC CLARION
What is the importance of specifically classifying
vomiting as projectile and non-projectile
What is the beta HCG Is normal, what is your next step?
What explains elevated BUN but normal crea? What is
the BUN:crea reatio?
In the abscence of cerebral angio, can you rule out AVM
based on CT scan?
What is the typical CT scan finding of
oligodendrolioma? Glioblastoma multiforme?
Without the benefit of MRI or CT angio, what findings in
the CT scan that makes you suspect AVM?
Other than elevated beta HCG, are there any other
possible cause of theca lutein cyst?
The increased in sodium and chloride was noted on the first hospital day. The patient in this case presented with headache, vomiting and Broca’s
aphasia which are consistent symptoms of a frontoparietal hemorrhage and an increased in intracranial pressure. Part of the management of this is
the administration of a mannitol and a hypertonic solution which can increase sodium and chloride. We cannot commit to other reasons like
dehydration or diarrhea or fever because those were not mentioned upon admission.
Na
Cl
we dont know if this is baseline
If iatrogenic
If baseline:
First explanation
Possible reason connected to the case: BLEED WITH INCREASED PRESSURE mamangement give hper and mannitol that can increase sodium
We cannot commit to to other reasons like, Dehydration - was not mentioned
Dystrophic (with calcifications) vs Metastatic
oligodendrolioma: Lots of calci in CT
Glioblastoma multiforme: most common primary tumor; vasogenic/finger like edema
EDEMA IN CT: hypodense
MRI: dinger like; hyperintensity of edema
Without the benefit of MRI or CT angio, the CT scan findings that can make AVM suspicious are:
________ can be a possible cause of Theca Lutein cyst. Insert physio how
Other than GTN, what are other possible causes of Other than GTN, the possible causes of theca lutein cyst are:
theca lutein cyst?
What are the UTZ findings of GTD and GTN? Ultrasound is _____ for GTD and GTN
the UTZ findings of GTD and GTN are:

For this patient

What are the mimickers of GTN with UTZ? With clinical The mimickers of GTN with UTZ sre
manifestation?
_______ has the ff clinical manifestations:
Is anemia contributory to the demise of the patient? Yes. Anemis is. The patient has a ____ _____ anemia caused by ___ and ____. This can physio

What explains the elevated WBC? Leukocytosis is ________

It is related to _______
ICH is __________
GTN/Chorio is ____
Patient is
We cannot relate it to ROS cause we dont know the old caarts and there are no other test that can supprort. We need too request.
If you are the AP, will you start the patient with Antibiotics is indicated in
antibiotics? The patient _______
I will __ or not start antiobiiocs upon admission because
If you are the attending physician, will you do surgical Surgical intervention is indicated durign.
intervention? What procedure, when and why? If I am the AP, I will or not on ____ because________
Do you think lumbar tap should be done to this patient? Lumbar tap is____
Why? For this patient he has an inc in
So not
Why do you think lumbar tap was done lumbar tap is indicated in ________. The patient has ______. It is needed post mortem in order to________ The possible findings are:

In what instance of CNS bleed will you do lumbar tap Lumbar tap is ______; I will do lumbar tap in a CNS bleed
What explains her cough and fever?
What will you do or request to rule in or rule out
infection as cause of fever?
In this cause cough was presented upon admission through the in Review of Systems. We still need to know the onset, duration, characteristic of
cough and conduct furtherer work-up like CBC and chest x-ray in order to explain the cough.
In the case, the patient presented with fever at temperature of 40.4C on the 4th hospital day. In order to investigate if it was caused by an infection,
complete blood count (CBC), blood culture, CSF culture, India ink, AFB staining and chest radiograph should be requested. It is infection if there is
an increased in WBC count, depending on the causative agent, a positive blood or CSF or India ink or AFB culture, and depending on the site of
infection, it mat have a positive or negative chest radiograph. However in the case of the patient, there was only fever and leukocytosis and lumbar
tap is contraindicated since the ICP of the patient is elevated.
Honig (2015): With the given clinical presentation of the patient, a diagnosis of exclusion can be made. CF occurs early, typically within 72 hours of
admission after acute brain injury. All the cultures are negative and the chest radiograph is normal. Fever is disproportionately high and persistent.
The temperature peak is higher when the fever starts earlier, and will be higher when compared to infectious fever.
In the case, the patient presented with fever at temperature of 40.4C on the 4th hospital day.
In order to investigate if it was caused by an infection, complete blood count (CBC), blood culture, CSF culture, India ink, AFB staining and chest
radiograph should be requested. It is infection if there is an increased in WBC count, depending on the causative agent, a positive blood or CSF or
India ink or AFB culture, and depending on the site of infection, it mat have a positive or negative chest radiograph. However in the case of the
patient, there was only fever and leukocytosis and lumbar tap is contraindicated since the ICP of the patient is elevated.
Honig (2015): With the given clinical presentation of the patient, a diagnosis of exclusion can be made. CF occurs early, typically within 72 hours of
admission after acute brain injury. All the cultures are negative and the chest radiograph is normal. Fever is disproportionately high and persistent.
The temperature peak is higher when the fever starts earlier, and will be higher when compared to infectious fever.
The patient in this case does not have any info if she was given an antibiotic or not.
Increased WBC to cough = pneumonia = presentation: tahycardia and hypoxemia; Xray? ABG?
Increased WBC and pulmo mets + pneumonia = inc wbc
CNS infection + bleeding = viral herpes encephalitis; temporal lobe; fever, headache, seizure, behavioral changes; toxic outset; mode of exit: uncal
herniation
More on mycotic aneurysm sya kung bleeding =
How do you diagnose central fever? How does central Hocker, 2013:
fever happen?
Central Fever (CF) is defined as peak fever measurement ≥ 38.3°C without evidence of infection.

Overall in the intensive care unit (ICU), at least 50% of fever are reported to be due to noninfectious causes. (Dimopoulos 2009)
The incidence of noninfectious fever in the neurology ICU is 23% while in the neu- rosurgical ICU it is 47% (Kilpatrick, 2000)
Of these, the highest rates of febrile episodes occur in patients with subarachnoid hemorrhage (SAH; 50% to 65%), followed by traumatic brain
injury (TBI; 4% to 40%) and intracerebral hemorrhage (ICH; 31%), with no cause of fever identified in 28% of patients, suggesting fever of central
origin . (Goyal, 2020)

Intraventricular hemorrhage (IVH) is thought to elevate the tem- perature set point in the hypothalamus by direct damage to the thermoregulatory
centers in the preoptic region, stimulation of prostaglandin production, or decreased inhibitory feedback from the lower midbrain which suppresses
thermogenesis (Shibata, 1998)

Honig (2015): This is a diagnosis of exclusion. CF occurs early, typically within 72 hours of admission after acute brain injury. All the
cultures are negative and the chest radiograph is normal. Fever is disproportionately high and persistent. The temperature peak is
higher when the fever starts earlier, and will be higher when compared to infectious fever

rule-out fever
do not respond to paracetamol
Bromocriptine helps in treating……

Central fever vs Malignany Fever

Naproxen test: if it would lyse = malignant fever

Hocker, 2013:

They are common after spontaneous ICH especially those with large ICH. Mechanisms include disruption of mesecephalic-diencephalic
mechanisms responsible for inhibition of thermogenesis. PGE2 is released acting in the preoptic area of the hypothalamus leading to an increase
body temperature. Systemic pyrogens, IL 1 appear on the area where there is incomplete BBB thus they act on the preoptic area inducing fever.

Central fever tends to appear within 72 hours of admission, persists longer, and is present on more days after accounting for NICU length of stay.
The combination of negative cultures; absence of infiltrate on chest radiographs; diagnosis of SAH, IVH, or tumor; and onset of fever within 72
hours of admission predicted central fever with a probability of .90
If after autopsy, the demise is not CNS. What are the HYPERCOAG, ___, ____, ____ > DVT > PULMO EMBO >
possible cause or causes of death in this case?
TUMOR CELLS SECRETE PROCOAG, INFLAM CYTOKINES, -> HYPERCOAGUABLE STATE

TUMOR ITSELF SAMA SA CIRCULATION > SADDLE EMBOLUS

MASSIVE PULMO EMBO > OBSTRUCTIVE CHERVS > CHECK VID

BLEED AND HYPERCIAGULABLE STATE CAN CO-EXIST > BLEED > CEREBRAL THROMBOSIS

UTERINE RUPTURE = CHECK VID

===
Buza (2010) and Berkowitz (2009): The most common metastatic site for choriocarcinoma is the lung (80%).

Athanassiou et. At (1983): Brain metastases are thought to arise from tumour emboli from the lungs. The tumor emboli could also lodge in the
pulmonary artery.

(Stein, 2007): In patients with recognized pulmonary embolism, the incidence of physical signs has been reported as follows:
• Tachypnea (respiratory rate >20/min) - 96%
• Rales - 58%
• Accentuated second heart sound - 53%
• Tachycardia (heart rate >100/min) - 44%
• Fever (temperature >37.8°C [100.04ºF]) - 43%
• Diaphoresis - 36%
• S3 or S4 gallop - 34%
• Clinical signs and symptoms suggesting thrombophlebitis - 32%
• Lower extremity edema - 24%
• Cardiac murmur - 23%
• Cyanosis - 19%

Patients with massive pulmonary embolism are in shock. They have systemic hypotension, poor perfusion of the extremities, tachycardia, and
tachypnea. In addition, patients appear weak, pale, sweaty, and oliguric and develop impaired mentation.

Signs of pulmonary hypertension, such as palpable impulse over the second left intercostal space, loud P2, right ventricular S3 gallop, and a systolic
murmur louder on inspiration at left sternal border (tricuspid regurgitation), may be present.

In the 45h hospital day, the patient in this case is tachycardic at 180bpm, febrile at 40.4C and hypotensive with a palpatory BP of 30mmHg.

Chung (2017): Therefore, if the patient in this case also has a metastatic pulmonary carcinoma, she could die from a massive pulmonary embolism
which can also be complicated by right ventricular failure and cardiogenic shock which have high short-term mortality (> 25%).
The patient in this case has an explicit increased intracranial pressure. Aside from its effect on the CNS alone, this could affect the GI system by
development of ulcer that is usually single and deep which may involve the esophagus, stomach, and duodenum, called as Cushing’s ulcer.
(Cheung, 1988). among patients with an acute critical illness. (Siddiqui, 2020)

Kamada, 1977: Stress ulcers occur frequently in ICU patients who have intracranial disease. It appears within 24 hours of injury; 17% of these
erosions progress to clinically significant bleeding

Lewis, 1973: Increased intracranial pressure may affect different areas of the hypothalamic nuclei or brainstem leading to overstimulation
of the vagus nerve or paralysis of the sympathetic system. Both of these circumstances increase secretion of gastric acid and the
likelihood of ulceration of gastro-duodenal mucosa.

This is suspected among patients with drop in hemoglobin concentration, decreased hematocrit., Coffee ground vomitus, Hematemesis
Melena, Abdominal pain, Nause, Orthostasis in severe cases. (Siddiqui, 2020)

The increased in BUN:Creatinine ration on the 3rd hospital day, as well as the passage of a coffee-ground ground material in the NGT
indicates that the patient has on ongoing upper gastrointestinal bleeding; it also apparent in the hematologic findings that the patient
has a microcytic, hypochromic anemia; which is most probably caused by Cushing’s ulcer.

This can be confirmed by a esophagogastroduodenoscopy presenting as small superficial mucosal erosions or ulcerations in the gastric
body and fundus. (Siddiqui, 2020)

Therefore the demise of the patient could also be because of hemorrhagic shock caused by a massive upper GI bleeding.
Forrest classification is used to stage gastric ulcers

Acute Hemorrhage
• Forrest Ia Active spurter
• Forrest Ib Active oozing
Signs of recent hemorrhage
• Forrest IIa Non-bleeding visible vessel
• Forrest IIb Adherent clot
• Forrest IIc Flat pigmented haematin on ulcer base
Lesions without active bleeding
• Forrest III Lesions without active bleeding

Prognosis

Cho (2016) & Pimentel (2000): Patients with stress ulceration usually have poor prognosis secondary to the underlying critical illness. Moreover, GI
bleeds in these patients secondary to stress-related mucosal disease is independently associated with increased morbidity and mortality. More
often, these patients are too unstable for advanced endoscopic or surgical procedures to suppress GI bleed, leading to worse outcomes. Hence,
aggressive prophylactic measures for the appropriate patient population at risk of developing stress ulceration remains the cornerstone in the
management of stress-induced gastropathy.
How will you support your theory that there is already Buza (2010) and Berkowitz (2009): The most common metastatic site for choriocarcinoma is the lung (80%).
pulmonary mets?

Magrath, 1971: The main symptoms among patients with pulmonary involvement were haemoptysis, dyspnoea, pleuritic pain, and cough
without haemoptysis.

The patient in this case had a cough as stated in the review of systems conducted upon admission. However, we don't know the onset,
duration, character, or any other information that can elaborate this clinical symptom. Therefore, if we are suspecting a mestastatic
chorioCA in the lungs, we should order a chest CT scan.

Zhang 2017: The chest imaging manifestations of pulmonary metastatic choriocarcinoma vary. Metastatic lesions may be isolated or
multiple observed and expressed as flaky, patchy, or cotton-like lesions. “canon-ball appearance”

Morgan, 2008: Trophoblastic cells possess an affinity for blood vessels; therefore trophoblastic tumors exhibit a tendency to metastasize via the
hematogenous route

The most common metastatic sites were the lungs (80%), vagina (30%), brain (10%), and liver (10%).

A total of 75% of FIGO stage IV choriocarcinoma patients are expected to achieve complete or prolonged remission when treated with multiagent
chemotherapy regimens, including MAC (methotrexate, actinomycin-D and cyclophosphamide) and CHAMOCA (cyclophosphamide,
hydroxycarbamide, doxorubicin, actinomycin D, methotrexate, melphalan and vincristine) (16). Currently, the most commonly used alternatives to
the aforementioned multiagent chemotherapy regimens are EMA-CO or fluorouracil-based chemotherapy regimens. (FIGO Committee on
Gynecologic Oncology, 2009)
Up to 40% of patients with negative findings for lung metastases on a chest radiograph will have metastases diagnosed on a chest CT scan.
(Snyman, 2009)

Athanassiou et. At (1983): Brain metastases are thought to arise from tumour emboli from the lungs, as it is most uncommon for such lesions to
arise in the absence of pulmonary metastases.

Suresh 2001: In about 50% of such patients, cerebral metastases may be the first manifestation of the tumor [5] and is uniformly considered as a
poor prognostic factor. (Berkowitz, 1996 and FIGO Committee on Gynecologic Oncology, 2009)

Approximately 30% of patients with choriocarcinoma show metastasis at the time of diagnosis, generally associated probably with the higher affinity
of trophoblasts to blood vessels. Zhou

Because choriocarcinomas are very vascular lesions and are often perfused by fragile vessels, as well as due to the tendency of trophoblastic cells
to invade and erode vessel walls, they are frequently haemorrhagic. Thus, intraparenchymal bleeding in any woman of child-bearing age with this
malignancy is well explained Pulmonart mets is found in ____ and isoloated reports ____. Clinical manifestations are and confirmation si done via z
Pathology of Brain on slides
CSF analysis
Expected CSF finding when lumbar tap is done
Most of the features of trophoblastic neoplasia are explicable on the basis of three major characteristics of trophoblastic tissue. These are its
tendency to invade blood vessels, which leads to early dissemination, its rapid rate of proliferation, and its vascularity. A trophoblastic embolus may
produce a variety of clinical syndromes depending not only on the site of impaction but also on the extent of secondary intravascular thrombosis,
the degree of proliferation into and compression of surrounding tissue, and the extent of local haemorrhage.
Magrath, 1971
Elevated opening and closing pressures
gross: bloody
Increased RBC
Increased WBC
Elevated Protein because of mestatic
Glucose normal or low depending on the activity of tumor cells
May or may not found tumor cells
______ check vid
gram stain:
India ink: cryp
afb: tubercular
Traumatic tap: csf clear gradually; pressnce of cloy.
Cerebral hemorrhage: send the first vial and 4 the vial: RBC; 4th devreased; (no decreasing sa cerebral hemorrhage); micriscipic exam:with
erythrophagocytes.; no clot daw cause clotting factors are diluted
Xanthorcromia: 3rd post-icterus lol; yellowish CSF; same in SAH
Thyroid storm tachy
Jaundice
Irritable
Arthymia
Atrial fib
Hear failure
rales, CHECK CLIPS DAI
JUST FCKN CHECK THE CLIP

SHOUTING - not a behavorial change? It’s not. girl… broca’s aphasia!!!!! Let’s no go there. He’s not aggitataed

______ socring: risk stratify to admit or not; NOT DX

>45: thyroid storm

PATHO:

sustained tachy dawwwwwww

Check clippppppp
Tumor embolization/Parodoxycal embo Check clips
2D echo dawwwww
HOW EMBOLI DAW CHECK CLIPS; GAMITIN DAW ANG 4 MONTH CHERVS

Pulmo Check clips girl kapoy na kaayo pero kaya mo Yan

Hyperthyroidism Explain the manifestation. Ongping herniation, tachy because anemia, 40% drop in hb = massive hemorrhage

Neuro: tremors, irritability, — lala psychosis

It can be hyperthyroidsm/thyroid storm, dapat at the outset nag tachy na daw! Does not happen overnightttttttt

3 hours prior daw!!!!!!!!!!!!!!!! not a thyroid storm daw

Tacchy upon admission

Systolic blood pressure

Widen pulse pressure:

Subclinical hyperthroidism and thyrotoxicosisi

HIE Contributary in devrease sensorium (hb); aggrevate cerebral edema

What accounts for the severe anemia on the 4th day?
Will the ICH (including the rebleeding episode) and
UGIB be enough to explain it?
Why did you consider choriocarcinoma over invasive
mole?
How did you rule out coagulopathy in this patient?

Why did you not consider thyroid storm?
Burch-Wartofsky Point Scale (BWPS) = for risk stratisfication only; if to admit or not the patient.
In 1993, the following scoring system for the diagnosis of thyroid storm was introduced:
• Temperature: 5 points per 1 F above 99 F (maximum 30 points)
• CNS dysfunction: 10 points for mild (agitation), 20 for moderate (delirium, psychosis or extreme lethargy), and 30 for severe (seizure or
coma)
• Tachycardia: 5 (99-109), 10 (110 -119), 15 (120 -129), 20 (130 -139) and 25 (greater than 140)
• Presence of atrial fibrillation:10
• Heart failure: 5 for mild (pedal edema), 10 for moderate (bi-basilar rales), 15 for severe (pulmonary edema)
• GI dysfunction: 10 for moderate (diarrhea, nausea/vomiting or abdominal pain) and 20 for severe (unexplained jaundice)
• Presence of Precipitating factor: 10 points
Diagnosis: A total score of more than 45 is highly suggestive of thyroid storm, 25 to 44 supports the diagnosis, and less than 25 makes the
diagnosis unlikely.
With the available data for the patient in this case, she has a Burch-Wartofsky score of 85 which is highly suggestive of thyroid storm.
However the patient in this case has a specific focal neurologic deficit that is not a characteristic of a thyroid storm. Moreover, Hyperthyroidism and
a precipitating factor precedes thyroid storm. The history and PE of this patient upon admission does not suggest any signs and symptoms of
hyperthyroidism. Hyperthyroidism is diagnosed by a low TSH, Increased T3 and T4, however the levels of this hormone were not mentioned in the
case.

If there is no manifestation of CNS, don’t thyroid storm.

What is the significance of the review of systems?

What explains the cough in ROS?

Nape pain, headache, chills?

MY QUESTION

How was you able to localize the lesion?

What was your parameter in arriving with differentials?

If you are the AP, what laboratory tests would you

request for this patient in order to dx the case earlier?
What should have been done on the recurrence of
bleeding to dx the case early?
What are your suggested managements for this
patient?
Expected ABG of the patient?

Right lower face arm and leg aphasia

Numbness
=left frontoparietal area

=area has propensity to have seizure however it was not mentioned

Seizure

Etiology There are two

• There are two factors that can contribute to the increased in WBC: 1. promote a procoagulant state that limits hematoma expansion in
intracranial hemorrhage. In our patient, she has an ongoing intracranial hemorrhage.

2. Elevated neutrophils are found in advanced cancer. This is because tumors can produce cytokines such as granulocyte colony-stimulating factor
(G-CSF), interleukin- (IL-) 1, and IL-6 which which can induce granulocyte production. The patient in this case have a stage IV choriocarcinoma that
can contribute to leukocytosis. (Uribe-Querol, 2015)

In many patients with advanced cancer, elevated counts of neutrophils in blood are found. How tumors induce neutrophilia is uncertain, but
production of granulocyte-macrophage colony-stimulating factor (GM-CSF) is a possible mechanism in several types of cancer

In addition, other cytokines such as granulocyte colony-stimulating factor (G-CSF), interleukin- (IL-) 1, and IL-6 produced by tumors seem to
contribute to elevated neutrophil numbers in blood

Because neutrophilia is frequently associated with inflammatory responses to infections and tissue damage, neutrophilia represents evidence for
the concept of cancer-related inflammation inducing tumor progression.
Focal with bleed Hypertensive not common here
=subcortical white

AVM =

CVM = rarely large; CT/MRI: popcorn

Traumatic = no history

Gamot = aspiran anticoag walaaaaa

Tumor bleed = caused the kapaspas

Demyelinating = not in the young

Tumifactive tumor necrosis unsa dawwwww =

first onset of focal demyle unsa daw

herpes simplex = wala na kay temporal man ni daw

mycotic aneurysm = no history of chronic fever; no murmur; no __ sa ROS; from infected heart valves

DAVF = but

CAA = ELDERLY!!!! Cognitive changes suggestive of dementia should also be patient.

Metastic= la na daw ginapa opera

if controlled ang primary

and only one area of the brain natamaan which can be easily excised
Chills = generalized seizure

MELANOMA = hahahahahahhahaha

Melanocytes are melanin-producing neural crest-derived cells located in the bottom layer (the stratum basale) of the skin's epidermis, the middle
layer of the eye (the uvea), the inner ear, vaginal epithelium, meninges, bones, and heart.
Thin uterus = hysterectomy because high risk of rupture
Craniotomy =
Craniectomy = remove bone flap; if you cant evacute hematoma; if deep-seated; the swelling of the brain would go there

location is hematoma superficial = craniotomy

we dont know how deep is the hematoma

Within 1cm from the cortex = aspiration; superficial
Fever = <41C; antipyretics effect; change in hypothalamic set point, involves cytokines, diurnal variation. Rarely exceeds 41C, rare complications

Hyperthermia = >41C suggestive; >41.5C = strongly suggestive; antipyretics no effect; failure in the thermoregulation; uncontrolled increased in
body temperature that exceeds the body’s ability to lose heat; can exceed 41C, can be detrimental; absence of diurnal variation (e.g. heat stroke)

Hyperpyrexia = extreme elevation of body temp >/= 41.5 due to high set point.; elevation in the body’s set thermoregulatory point; core temperate is
regulated by the anterior hypothalamus;fever is caused by increased PGE2 synthesis in the hypothalamus

• Fevers, unlike hyperthermias, typically never exceed 40°C.

• Fever is associated with a change to the hypothalamic “Set-point”; Hyperthermia is not.

• Hyperthermias do not respond to antipyretic medication, as there is no cytokine involvement.

• Some diurnal variation is typically seen in fevers. No such variation is seen in hyperthermia.

• Hyperthermia is extremely dangerous and requires intensive care.

Chemo = bagsak ang cbc

and EMACO

Stabilize first
control bleeding
Transfuse blood
correct anemia
Chemotherapy = because the hgb is low
Functional status

Karnofsky score — and blah blah score

Chemotherapy
Infection

Lung metastasis = obstructive pneumonia

Necrotic tissue = nidus for infection
 Venous sinus thrombosis = bilateral, near the midline, headache, seizures, seonsorial changes; by a hypercoagulable state; block absorption of csf;
inc icp; THE ONLY BLEED IN THE BRAIN THAT YOU ANTICOAGULATE; DX = CT VENOGRAM OR MAGNETIC RESONANCE VENOGRAM TO
VISUALIZE

BUNTIS - HYPERCOAG AND WITH MALIGNANCY

MANAGE AFTER D&C patient education!!! > biopsy

lost of follow up
explain properly
BRAIN HISTOPATH Intracranial aneurysms

Infiltrating large and pleomorphic tumor cells into the brain parenchyma with extensive hemorrhage and necrosis (H&E stain-
Intermediate power). a. Multinucleated syncytiotrophoblasts (H&E stain-High power). b. β-HCG immunoreactivity (IHC stain- High power)
Seizure The lesion is the frontoparietal area. She can develop seizure because it is located in the cortical = parietal temporal,
Anticonvulsant drugs???
-no mention of seizure even if high-risk; they wouldn’t but ; prophylactic anticonvulstant to prevent further bleeding
HISTOPATH Syncytiotrophoblasts, large eosinophilic smudgy multinucleated cells with known, large hyperchromatic nuclei, are intermixed with
cytotrophoblasts, polygonal cells with distinct borders, and single irregular nuclei.[7] Additionally, choriocarcinoma is an extremely
vascular carcinoma characterized by necrosis and absence of chorionic villi.[3]
Following chemotherapy, the cytotrophoblasts may predominate, making the diagnosis more difficult. Within the uterus, choriocarcinoma invades
vessels to spread throughout the body, a relatively early finding.[3]
Intra-placental choriocarcinoma demonstrates trophoblast proliferation around villi in a third-trimester placenta, usually otherwise normal in
appearance.[10][11]
In mixed germ cell tumors, choriocarcinoma will also have a mixture of syncytiotrophoblasts and cytotrophoblasts and varying components of other
germ cell tumors.

Grossly, choriocarcinoma is extremely hemorrhagic in both primary and metastatic sites. Histologic examination shows a haphazard
mixture of all types of trophoblast. Intermediate trophoblast tends to be most atypical. No molar villi are seen and their presence
precludes the diagnosi
Choriocarcinoma Trophobalstpure - synccytio and

Invasive mole With chorionic villi

IHC For documentation only; but histopath is already enough;

KI-67 = index of proliferation of tumor cells; intesity of color and number of cells;
Chorioca = 75-90%
PSTT = <50%
Non gestional and Gestational Same histopath; different in utz; same hcg level

Brain gros Bleedddddd; blood clots; fibrin; gelatinous bloody

Placental site tt PSTT leiomyoma; no unsa to check vid; absence of necrosis and hemorrhage

Genes Several molecular studies have been done to establish the expression of tumor-associated proteins in choriocarcinoma. In the p53 pathway,
overexpression of the p53 protein and the p53-associated protein, MDM2, have been detected. Synergistic upregulation of c-MYC, c-ERB-2, c-
FMS, and BCL-2 oncoproteins have also been suggested to have an important role in the pathogenesis of choriocarcinoma. Moreover,
choriocarcinomas have been shown to express increased concentrations of MMP and decreased concentrations of TIMP to help with tumor
invasion and metastasis.
D&C histopath Problem sampling: endometrial daw pero cervical lang

If the specimen is too bloody that the tumor cells are not caught

Sampling is marami

Hydatidiform mole = no necrosis and hemorrhage

CSF check vid

Rare daw makita tumor cells

PSST Intermediate

Chorio no villus

Distal branches of the middle cerebral artery

Chest x-ray
 • Pre-renal azotemia manifests from some insult/injury source before the kidney. Most commonly, we see this in the form of hypoperfusion,
or decreased blood flow, to the kidneys from various etiologies of volume depletion, such as the physiologic state shock,
dehydration, hemorrhage, over-diuresis, burns, and even intravascular depletion from low-oncotic pressure states, such as congestive
heart failure and liver failure.[1]
• Intrinsic azotemia results from damage to the structure of the kidney; the structures affected include glomeruli, renal tubules and
interstitium, and renal vasculature. This can result from inflammatory conditions, such as vasculitis, toxins, drugs, infections, and damage
from hypoperfusion.[2]
• Post-renal azotemia comes from issues in the ureters and bladder. Usually, a patient has some diagnosis of obstruction, seen if a patient
with risk factors such as recurrent urinary tract infections, nephrolithiasis, hydronephrosis, benign prostatic hyperplasia.

Diagnosis of Azotemia can be made by BUN greater than 21 mg/dL

Significant Findings for Pre-Renal Azotemia
• BUN: Cr ratio greater than 20:1
• FeNa less than 1, FeUr less than 35%
• Ur Osmo 500 mOsm/kg
• UA can show hyaline casts[6]
Intra-Renal Azotemia
• BUN: Cr ratio less than 20:1
• FeNa greater than 2, FeUr greater than 50%
• Ur Osmo less than 300 mOsm/kg
• UA: Cellular debris, muddy brown casts red cell casts, eosinophils, + proteinuria
Post-Renal Azotemia
• BUN: Cr ratio less than 20:1
• FeNa greater than 2
• Ur Osmo less than 300 mOsm/kg
• UA: WBC casts
• Imaging findings: pyelonephritis, nephrolithiasis, bladder mass