Internal Medicine

MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)

Summarized Notes

ENDOCRINOLOGY

I. Thyroid Gland
Disease Manifestations Pathophysiology Diagnostics and Results Management and
Treatment
Hypothyroidism Hyporeflexia (most • Primary: autoimmune • Unexplained • Levothyroxine 12.5 –
consistent), dry skin, cold (Hashimoto), hyponatremia 25 mcg
intolerance, coarse skin, congenital, iodine • Increased creatinine
puffiness, sweating, weight deficiency phosphokinase
changes, paresthesia, • Transient: silent, • Increased LDH
constipation, hoarseness subacute • Macrocytic anemia
• Secondary: • Decreased T4 with
hypopituitarism, increased TSH
bexarotene,
hypothalamic
Hyperthyroidism • Primary: Grave’s, toxic
multinodular goiter, toxic
adenoma, struma ovarii,
iodine excess
• Without: subacute, silent
• Secondary: TSH-secreting
adenoma, CGH-tumor, TH
resistance

Grave’s disease Symptoms: Hyperactivity, • Female > male • Low TSH • Anti-thyroid drugs:
irritability, dysphoria, heat • Stress: environmental • Increased T3, T4 PTU, carbimazole,
intolerance and sweating, factor • Increased RAIU methimazole
palpitations, fatigue and • Smoking • Propanolol
weakness, weight loss with • IFN-alpha, TNF, IL-1 (supportive)
increased appetite, • High-dose
diarrhea, polyuria, glucocorticoids,
oligomenorrhea, loss of sometimes combined
libido with cyclosporine
• Radioiodine (1311)
Signs: tachycardia; atrial treatment
fibrillation in the elderly, • Thyroidectomy
tremor, goiter, warm, moist
skin, muscle weakness,
proximal myopathy, lid
retraction or lag,
gynecomastia
Thyrotoxic crisis Fever, delirium, seizures, Life-threatening Burch-Wartosky scoring • PTU (600 mg loading
coma, vomiting, diarrhea, exacerbation of • Body temperature dose and 200-300 mg
and jaundice, cardiac hyperthyroidism • Heart rate and every 6 hours)
failure, arrhythmia, or presence of HF and • Stable iodide,
hyperthermia arrhythmia propranolol,
• GI manifestations glucocorticoids
• CNS manifestation
Thyroiditis • Acute: bacterial,
fungal, radiation
therapy
• Subacute: viral,
silent, mycobacterial
• Chronic:
autoimmunity,
parasitic, traumatic
Diffuse nontoxic goiter Normal thyroid Suppression therapy,
thyroidectomy (seldom)
Nontoxic multinodular Radioiodine,
goiter glucocorticoids or surgery
Toxic multinodular goiter Jod-Basedow Increased RAIU Anti-thyroid drugs + beta-
blockers

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

II. Pituitary Gland

Disease Manifestations Pathophysiology Diagnostics and Results Management and
Treatment

Hyperprolactinemia Males: PRL attenuates LH • Pregnancy • Elevated PRL • Cabergoline

secretion, leading to low • Lactation • Decreased bone • Bromocryptine
testosterone levels. • Nipple stimulation mineral density mesylate
diminished libido and • Chest wall lesions • Gonadal dysfunction
diminished sexual potency, • PRL-secreting • Galactorrhea
oligospermia, and lowered adenoma
ejaculate volume; up to • Medications
about 30% may have • Compromised
galactorrhea pituitary stalks
Females:
hyperprolactinemia leads
to loss of pulsatile LH
secretion, blunting of the
LH peak, hypoestrogenism
and anovulation,
oligomenorrhea and
amenorrhea, vaginal
dryness, dyspareunia, loss
of libido, and infertility.
Adult GH deficiency Impaired quality of life, Somatotroph damage and Elevated GH GH is started at a dosage
body composition changes, the subsequent of 0.15 to 0.2 mg/day and
decreased exercise development of pituitary titrated to a maximum of
capacity tropic hormone deficiency 1.25 mg/day, to maintain
follows a sequential pattern midrange age- and
in which loss of adequate sex-matched IGF-I levels
GH reserve usually
foreshadows subsequent
deficits of other pituitary
hormones
Acromegaly Acral bony overgrowth, Elevated GH Stereotactic ablation of
frontal bossing, increased GH-secreting adenomas
hand and foot size, and by gamma-knife
mandibular enlargement radiosurgery
with prognathism and a
widening of incisor spaces,
soft tissue swelling results
in coarse facial features;
increased heel pad
thickness; and
enlargement of feet and
hands
Diabetes insipidus Polyuria, preference to • Central: partial/ Water deprivation test • Chlorpropamide
cold beverages complete vasopressin • Severe: intranasal or
deficiency oral DDAVP
• Nephrogenic: • Others:
vasopressin carbamazepine,
resistance of the clofibrate, thiazides,
kidney tubules indomethacin
• Dipsogenic:
oversensitivity of the
thirst center
SIADH • Neoplasms: lung, • Significant expansion
duodenum, pancreas and dilution of body
etc. fluids (only if water
• Head trauma intake exceeds rate of
• Infections insensible loss and
• CV: thrombosis, urinary output)
occlusions • Excess intake often
• Neurologic: GBS, MS, caused by: defect in
ALS osmoregulation of
• Drugs: anti-thyroids, thirst, psychogenic or
oxytocin, etc. iatrogenic factors,
administration of IV
fluids

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Summarized Notes

• Extracellular volume
expansion produces
increase in ANP,
suppression of
plasma renin activity
and a compensatory
increase in urinary
sodium excretion
(reduce the
hypervolemia but
aggravates
hyponatremia)
Pituitary adenoma Structural compression or Surgery, irradiation/
hormonal balance medical
Hypercalcemia • Recurrent • PTH immunoassays • Medical: hydration
nephrolithiasis (more combined with • Surgical: subtotal
common) simultaneous calcium parathyroidectomy
• Osteitis fibrosa measurements
cystica • Elevated
• Howship’s lacunae immunoreactive PTH
(pathognomonic • Shortened QT interval
features)
• CNS, PNS, GIT and
muscle dysfuctions
Hypocalcemia • Symptoms: perioral • PTH absent: • Decreased Ca (I
numbness, hereditary hypopara, mean--)
paresthesia, muscle acquired hypopara, • Prolonged QT interval
spasm hypomagnesemia
• Signs: Chvostek sign, • PTH ineffective:
Trousseau sign, chronic renal failure,
Prolonged QT interval active Vitamin D
lacking (dietary intake
or sunlight, defective
metabolism-
anticonvulsant
therapy or Type 2
vitamin D-dependent
rickets), active vitamin
D ineffective
(intestinal
malabsorption or
Type 2 vitamin D-
dependent rickets)
• PTH overwhelmed:
severe, acute
hyperphosphatemia
(tumor lysis
syndrome, acute renal
failure,
rhabdomyolysis0

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

III. Adrenal Gland

Disease Manifestations Pathophysiology Diagnostics and Results Management and
Treatment

Cushing’s syndrome Central obesity, increased • Adrenal hyperplasia • Refer to table below • Neoplasm: miitotane,
body weight, fatigability • Adrenal micronodular glucocorticoids and
and weakness, hyperplasia mineralocorticoids
hypertension, hirsutism, • Adrenal neoplasia pre- and post-op,
amenorrhea, broad • Exogenous, iatrogenic platinum therapy
violaceous striae, causes
personality changes,
ecchymoses, proximal
myopathy, edema,
polyuria, polydipsia,
hypertrophy of clitoris

Diagnostic tests to determine the type of Cushing’s syndrome

Test Pituitary Macroadenoma Pituitary microadenoma Ectopic ACTH or CRH Adrenal tumor
production
Plasma ACTH level Increase + or ++ N to increase + Increase Decrease
% who respond to high- <10 95 <10 <10
dose dexamethasone
Percent who respond to >90 >90 <10 <10
CRH

Disease Manifestations Pathophysiology Diagnostics and Results Management and

Treatment
Primary aldosteronism Diastolic HPN, muscle • With tumor: Criteria: • Surgical excision of
weakness and fatigue, excessive • Diastolic HPN without the adenoma
polyuria, polydipsia, left inappropriate edema • Dietary sodium
ventricular enlargement, aldosterone • Hyposecretion of restriction
prominent U waves, production à Conn’s renin that fails to • Aldosterone
proteinuria, renal failure • Without: unknown increase appropriately antagonist e.g.,
during volume spironolactone 25-100
depletion mg every 8 h
• Hypersecretion of • Eplerenone, a less
aldosterone that does potent but more
not suppress specific MR antagonist
appropriately in 50-150 mg every 8
response to volume hour
expansion • Triamterene
• Amiloride
Laboratory findings
• Impaired ability to
concentrate the urine
in overnight
concentration test
• Alkaline urine
• Hypokalemia
• Hypernatremia
• Hypomagnesemia
• Metabolic alkalosis
and elevation of
serum bicarbonate
Secondary Increased production of • Hypokalemic alkalosis
aldosteronism aldosterone in response to • Increased plasma
activation of RAAS renin
• Moderate to marked
increase in
aldosterone
Primary Adrenocortical Insidious onset of • Progressive • Adrenal stimulation • Hydrocortisone
deficiency (Addison’s fatigability, weakness, destruction of the with ACTH (cortisol) is the
disease) anorexia, nausea and adrenals, which must • Serum sodium, mainstay of treatment:
vomiting, weight loss, involve 0% (you need chloride, and two-thirds of the dose
cutaneous and mucosal to destroy 90% before bicarbonate levels are is taken in the
pigmentation, hypotension, it can manifest) reduced morning, and the
remaining one-third is

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

and occasionally • Frequent site for • Serum potassium taken in the late
hypoglycemia chronic level is elevated afternoon
From mild chronic fatigue granulomatous • Elevated plasma • Mineralocorticoid
to fulminating shock diseases, vasopressin and supplementation is
associated with acute predominantly angiotensin II levels usually needed
destruction of the glands, tuberculosis but also • Mild to moderate • Daily replacement with
as described by histoplasmosis, hypercalcemia 25-50 mg of DHEA PO
waterhouse and coccidioidomycosis, • Hypoglycemia may improve quality of
friderichsen and cryptococcosis life and bone mineral
density
• Periodic
measurements of body
weight, serum
potassium level, and
blood pressure

Pheochromocytoma • Great masquerader • Associated • Measurement of • Complete tumor

• Labile HPN syndromes: MEN, catecholamines: removal: ultimate
• Triad: palpitations, MEN1, MEN2A (Ret), elevated plasma and therapeutic goal
headaches, severe neurofibromatosis urinary levels of • Alpha-blockers
sweating (NF1), Von Hippel- catecholamines and (phenoxybenzamine):
Lindau syndrome the methylated low doses
(autosomal dominant) metabolites,
metanephrines,
• High-performance
liquid
chromatography,
enzyme-linked
immunosorbent
assay, other
immunoassays:
increased two to three
times the upper limit
of normal,
• Urinary tests for
VMA,
metanephrines (total
or fractionated), and
catecholamines
• Plasma
metanephrine
measurements are
most sensitive and
are less susceptible
to false-positive
elevations from
stress, including
venipuncture

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

IV. Diabetes Mellitus

Criteria ADA 2020

1. Symptoms (polyuria, polydipsia, unexplained weight loss); casual plasma glucose >200 mg/dL
2. Fasting plasma glucose >126 mg/dL
3. 2-hour plasma glucose of >200 mg/dL during OGTT
4. HbA1c >6.5

Levels of Glycemia

Disease Manifestations Pathophysiology Complications Management and

Treatment
Type 1 • Chromosome 6
• Autoimmune
destruction of
pancreatic beta cells
• Absolute insulin
deficiency
Type 2 Ominous octet • Insulin resistance and • Microvascular: • Medical nutrition
• Increased lipolysis relative insulin retinopathy, therapy
• Increased glucose deficiency neuropathy, • Sulfonylureas: acts
reabsorption neuropathy on beta cells only (we
st
• Decreased glucose • Macrovascular: don’t use the 1 gen
st
uptake CAD, PAD, CVS anymore) (1 gen –
nd
• Neurotransmitter • Nonvascular: “ide”, 2 gen – G +
dysfunction gastroparesis, “ide”)
• Increased hepatic infection, hearing • Biguanides:
glucose production loss, skin changes stimulate AMP kinase
• Increased glucagon (metformin)
secretion • Alpha-glucosidase
• Increased insulin inhibitors: inhibits the
secretion enzyme to cleave
• Decreased incretin complex
effect carbohydrates into
sugar (e.g. acarbose)
• Thiazolinediones:
PPAR gamma
receptor agonist à
act on DNA
transcription and
increase
subcutaneous
adipose tissue
• Incretin hormones
(GLP-1 and GIP):
stimulate insulin
secretion
• DPP-4 inhibitors:
increases active GLP-
1
• SGLT-2 inhibitors
(Dapagliflozin and

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

Empagliflozin):
reduces renal glucose
reabsorption and
increases glucose
elimination

Insulin regimens
• Split-mixed: 2/3
prebreakfast, 1/3
predinner or 50-50
distribution
• Basal insulin + OHA
• Multiple-component
insulin
regimens/multiple
daily injections/basal
bolus regimen
• Basal plus regimen
• Continuous insulin
pump
• Type 1 DM: 0.5-1
u/kg/d
• Type 2 DM 0.3-0.4
u/kg/d
Diabetic ketoacidosis Exaggerated increase in • Blood glucose >250 • Correction of
glucagon, catecholamines, mg/dl dehydration
cortisol and growth • Arterial pH <7.3 • Correction of
hormones and reduced • Bicarbonate <15 hyperglycemia
level of insulin mEq/L • Correction of
• Moderate ketonuria or electrolyte imbalances
Ketonemia • Identification of
Hyperosmolar • Blood glucose >600 comorbid precipitating
hyperglycemia mg/dl events
• Arterial pH >7.3 • Frequent patient
• Bicarbonate monitoring
>15mEq/L
• Effective serum
osmolality >320
mOsm/kg H2O
• Mild ketonuria or
ketonemia
Gestational DM • Any degree of • initial testing by 50 g
glucose intolerance GCT
with onset or first • Perform a 100-g
• recognition during OGTT on the subset
pregnancy of individuals with
• Associated with GCT value of > 140
increased perinatal mg/dl
morbidity and
mortality
• 6 weeks or more after
pregnancy ends, the
woman should
be reclassified
• High risk for type 2
DM

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

V. Hypoglycemia and Obesity

Disease Manifestations Pathophysiology Diagnostics and Results Management and
Treatment
Hypoglycemia • Neuroglycopenic: • Treatment of DM • Plasma glucose <70 • 20 g glucose per
decreased CNS mg/ dl orem if conscious
neuronal glucose, • Whipple’s triad: • IV D50 (250 g
behavioral changes, palpitations and glucose)
confusion, seizure, sweating, low plasma • IM/SQ glucagon
death glucose, relief of
• Neurogenic: symptoms after
adrenergic glucose is corrected
(palpitations, tremor),
cholinergic (sweating,
hunger, paresthesia)
Obesity • Genetic Waist circumference: • Behavior modification
susceptibility: leptin increased risk if >88 cm in • Diet (lower fat intake
gene mutation F, >102 cm in M <25%)
• Environmental: • Exercise
hypothalamic injury • Pharmacologic
intervention
• Bariatric surgery

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

Classification of Obesity

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

VI. Disorders of Lipid Metabolism

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

PULMONOLOGY

I. Disorders of Ventilation
Disease Manifestations Pathophysiology Diagnostics and Results Management and
Treatment
Hypoventilation • Dyspnea during • Reduction of minute • ABG usually shows • Treat the underlying
(Parenchymal lung and activities of daily living ventilation hypercapnia with disease
chest wall diseases, • Orthopnea in • Normal or even normal pH • Supplemental O2
sleep disordered diseases affecting increased minute • Chest X-ray • Correct metabolic
breathing, diaphragm function ventilation • Chest CT Scan alkalosis
neuromuscular disease, • Poor quality sleep • PFT • Phrenic nerve or
respiratory drive • Daytime • Screen for sleep diaphragm pacing
disorder) hypersomnolence disorder breathing • Respiratory stimulant
• Muscle strength medroxyprogesterone,
MIP, MEP, & FVC acetazolamide
• CO2 & O2 challenge • NIPPV
• Mechanical ventilation
(invasive)
Obesity Hypoventilation • Body mass index > 30 • Weight reduction
2
Syndrome kg/m • CPAP
• Sleep disordered
breathing
• Chronic daytime
alveolar
hypoventilation
• PaCO2 > 45 mmHg
and PaO2 <70 mmHg
Central Hypoventilation Neonatal or later in life (2- • Defect in PHOX2B • Increased in PaCO2 • NIPPV
Syndrome 50 years) while awake while 3x • Phrenic nerve/
increase in PaCO2 diaphragm pacing
during sleep
Hyperventilation • Dizziness, syncope, • PaCO2 below the • Reassurance
visual impairment & normal range of 37-43 • Breathing exercise
seizure mmHg and diaphragmatic
• Paresthesias, • Low bicarbonate retraining
carpopedal spasm & • Near normal pH • Beta-blockers if
tetany patient have
• Muscle weakness palpitation and
• Chest pain tremors

II. Sleep Disorders

Disease Manifestations Pathophysiology Diagnostics and Results Management and
Treatment
Obstructive Sleep Apnea • Daytime sleepiness • Apnea is cause by the • Epworth Sleepiness • Weight reduction
Hypopnea Syndrome no. 1 feature upper airway being Score >11 • Alcohol reduction
(OSAHS) • Impaired vigilance, sucked close on • Physical examination • Sedative drug
cognitive performance inspiration during ü Obesity • CPAP (5- 20 mmHg)
& driving sleep. ü Jaw structure the most acceptable
• Depression, mood • Like all striated ü Upper airway • Mandibular Reposition
disturbance muscles the upper ü Blood pressure Splint (MRS)
• Disturb sleep, airway dilating ü Risk factor like • Surgery
unrefreshing sleep muscles relax during hypothyroidism, • Drug – modafinil
• Systemic sleep, in patient with acromegaly
hypertension OSAHS the dilating Surgery
• Difficulty in muscles fail to • Bariatric surgery for
concentrating oppose the negative obesity
• Morning headache pressure within the • Tonsillectomy
• Nocturnal choking, airway during
• Tracheostomy
nocturnal heartburn inspiration
utilized if everything
• Nocturia else fails
• Decrease libido • Jaw advancement
• Dry mouth, surgery
diaphoresis of the • Maxillomandibular
neck and chest osteotomy for
posterior

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

displacement of the
mandible-retrognathia

Uvulopharyngopalatoplasty
removing the uvula, part of
the pharynx,
and soft palate

Central Sleep Apnea • Insomnia • Inhibition of central • Sleep study • Treat underlying
• Daytime sleepiness respiratory drive by • Measurement of cause
upper airway reflexes esophageal pressure • Oxygen supplemeny
ü Esophageal • Respiratory muscle • CPAP?
reflux electromyography
ü Aspiration
ü Upper airway
collapse
• Increase sensitivity to
PaCO2
• Prolong circulation
delay between
pulmonary capillary
and carotid
chemoreceptor
• Due to medications
like opioids and
CPAP

III. Pneumonia

Pattern of pneumonia Description

Lobar • Congestion (edema): 1st 24 hours, grossly appears red and doughy, due to the proteinaceous exudates &
often bacteria in the alveoli
• Red Hepatization: RBC in the cellular intraalveolar exudates, increased neutrophil influx, bacteria are
occasionally seen
• Gray Hepatization: no new RBC are extravasating, & those already present have been lysed & degrades.
Neutrophil is the predominant cell, fibrin deposit is abundant and bacteria have disappeared
• Resolution: the macrophage reappears as the predominant cell in the alveoli, & the debris of neutrophils,
bacteria and fibrin has been cleared, as has the inflammatory response
Bronchopneumonia Margin usually poorly demarcated, neutrophilic infiltrates center in bronchi and bronchioli (usually due to
Staphylococcal inf.)
Interstitial pneumonia Inflammation in the insterstitial space, alveolar wall & connective tissue space (usually caused by viruses or
atypical microorganism
Military pneumonia Spread widely all over both lung-field usually due to hematogenous spread (TB is common in our country)

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

Radiographic Pattern
Pattern of pneumonia Species
Focal opacity • Streptococcus pneumoniae (Most common)
• Mycoplasma pneumonia
• Legionella pneumophila
• Chlamydia pneumoniae
• Mycobacterium tuberculosis
• Blastomyces dermatitidis
• Staphylococcus aureus
Interstitial • Viruses
• M. pneumoniae
• Pneumocystis jiroveci
• C. psittaci
Interstitial pneumonia with • Epstein-Barr virus
lymphadenopathy • Francissella tularensis
• Fungi
• C. psittaci
• M. pneumoniae
Cavitation (lung abscess) • Mixed aerobic-anaerobic
• Aerobic gram (-) bacilli
• M. tuberculosis
• L. pneumophilia
• Cryptococcus
• Nocardia asteroides anaerobic
• Actinomyces israelli
• Coccidioides immitis
• P. jiroveci
Bulging fissure • Klebsiella pneumoniae
• Legionella pneumophila
Multi-focal opacities • S. aureus (highly suggestive)
• Coxiella burnetti
• L. pneumophila
• S. pneumoniae
Miliary • M. tuberculosis (most common)
• Histoplasma capsulatum
• C. immitis
• B. dermatitidis
• Varicella zoster
st
Segmental or Lobar with • M. tuberculosis (1 infection)
Lymhadenopathy • Atypical rubeola
Pneumatocoeles • S. aureus (highly suggestive)
• S. pyogenes
• P. carinii
Round pneumonia • C. burnetii
• S. pneumoniae
• L. pneumophila
• S. aureus

Microbial causes of Community-Acquired Pneumonia by site of Care

Hospitalized Patients
Outpatients Non-ICU ICU
S. pneumoniae S. pneumoniae S. pneumoniae
M. pneumoniae M. pneumoniae M. pneumoniae
H. influenzae Chlamydia Legionella spp.
Respiratory viruses H. influenza H. influenzae
Legionella spp.
Respiratory viruses

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

Risk Stratification for Community Acquired Pneumonia

Risk Clinical Features Chest X-ray Diagnostic Work-up Potential Empiric Treatment
Pathogens
Low Risk • RR < 30/min • Localized • Chest X-ray • S. pneumoniae • Previously
• PR < 125/min infiltrates • Sputum GS/CS (optional) • M. pneumoniae healthy:
• SBP >90 mmHg • No evidence of • M. catarrhalis amoxicillin,
• DBP >60 mmHg extrapulmonary • H. influenzae azithromycin
• No or stable co- sepsis • Chlamydia dehydrate,
morbid • No progression pneumoniae clarithromycin
conditions within 24 hours • Enteric gram- • With stable co-
• No evidence of negative bacilli morbid illness:
extrapulmonary co-amoxiclav or
sepsis sultamicillin or
nd
• No evidence of 2 gen
aspiration cephalosporin
or extended
macrolides
Moderate • Unstable vital • Multilobar • Chest X-ray • Strep IV nonpsuedomonal
signs: RR > infiltrates • Blood CS pneumonia b-lactam with or
30/min, PR • (+) pleural • Sputum GS/CS • M. pneumoniae without b-lactamase
>125/min, Temp effusion • Particle agglutination (PA) • Chlamydia inhibitor plus
0 0
<35 C or <40 C • Progression of test for M. pneumoniae pneumonia macrolide
• Unstable findings to > • Microimmunofluorescence • H. influenzae OR
comorbid 50% in 24hrs (MIF) test for C. • M catarrhalis Antipneumococcal
condition: pneumoniae (for elderly • Enteric gram (- fluoroquinolone (FQ)
Uncontrolled and ) bacilli
DM, active immunocompromised) • Legionella
malignancy, • Urine Ag test for L. pneumophila
neurologic pneumophila • Anaerobes
disease in • Direct fluorescent Ab (among those
evolution, CHF (DFA) test for L. with risk of
class IIIV, pneumophila aspiration)
unstable
coronary artery
disease, renal
failure on
dialysis,
uncompensated
COPD,
decompensated
liver disease
• Evidence of
extrapulmonary
sepsis hepatic,
hematologic,
gastrointestinal,
endocrine
• Suspected
Aspiration
High Risk Any of the clinical Same as in moderate • Chest X-ray • Strep No Risk for P.
feature of moderate risk CAP • Blood CS pneumonia aeruginosa
risk CAP plus any of • Sputum GS/CS • M. pneumoniae a. IV
the following: • ABG • Chlamydia nonpseudomonal b-
1. Shock or signs of • Particle agglutination (PA) pneumonia lactam with or
hypoperfusion test for M. pneumoniae • H. influenzae without b-lactamase
2. Hypoxia • Microimmunofluorescence • M. catarrhalis inhibitor plus IV
(MIF) test for C. • S. aureus macrolide
1. Shock or signs of pneumoniae (for elderly • P. aeroginosa b. IV
hypoperfusion and antipneumococcal
• Enteric gram (-
hypotension (BP < immunocompromised) fluoroquinolone
) bacilli
90/60 or > 20 mmHg • Urine Ag test for L. • Legionella
drop from usual) pneumophila With Risk of P.
pneumophila
altered mental state aeruginosa
• Direct fluorescent Ab • Anaerobes
urine output < 30 a. IV
(DFA) test for L. (among those
ml/hr antipseudomonal b-
pneumophila with risk of
2. Hypoxia (PaO2 < lactam with or
60 mmHg) or Acute aspiration) without b-lactamase
hypercapnea (PaCO2
> 50 mmHg)

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Summarized Notes

inhibitor plus IV
macrolide or IV
antipneumococcal
fluoroquinolone +/-
aminoglycoside or IV
ciprofloxacin

Antibiotics
Antipneumococcal fluoroquinolone Levofloxacin
Moxifloxacin
Nonpseudomonal B-lactam IV B-lactams
2nd generation cephalosporin (cefuroxime)
3rd generation cephalosporin (ceftriaxone,
cefotaxime)
those with anaerobic activity (cefoxitin, ceftizoxime,
ertapenem (only effective against gram +)

IV B-lactams with B-lactamase inhibitor

1. ampicillin-sulbactam
2. amoxicillin-clavulanic acid Antipseudomonal
Antipseudomonal Antipneumococcal B- IV B-lactams Those without anaerobic activity
lactam 4th generation cephalosporin (Cefepime)
those with anti-anaerobic activity
Carbapenem (Imipenem-cilastatin, Meropenem)

IV B-lactams with B-lactamase inhibitor

Cefoperazone-sulbactam
Ticarcillin-Clavulanic acid
Piperacillin-tazobactam

Empirical Antibiotic Treatment of CAP

Category Treatment
Outpatient Previously healthy & no antibiotics in past 3 months
1. A macrolide (clarithromycin 500 mg PO bid or azithromycin 500 mg PO once, then 250mg qd) or
2. Doxycycline 100 mg PO bid

Comorbidities or antibiotics in past 3 months: select an alternative from a different class

1. A respiratory fluoroquinolone (moxifloxacin 400 mg PO qd; gemfloxacin 320 mg PO qd, levofloxacin 750 mg PO qd
or
2. A beta-lactam (preferred: high dose amoxicillin 1 g tid or amoxicillin/clavulanate 2g bid; alternatives: ceftriaxone 1-
2 g IV qd, cefpodoxime 200 mg PO bid, cefuroxime 500mg PO bid plus a macrolide

In regions with high rate of high-level

Pneumococcal macrolides resistance, consider alternatives listed for patients with comorbidities
In-patient Non-ICU • A respiratory fluoroquinolone (moxifloxacin 400 mg PO or IV qd, gemifloxacin 320 mg PO qd, levofloxacin
750 mg PO or IV qd
• A beta-lactam (cefotaxime 1-2 g IV q 8 hrs, ceftriaxone 1-2 g IV qd, ampicillin 1-2 g q 4-6 hrs, ertapenem 1
g IV qd in selected patient plus a macrolide (oral clarithromycin or azithromycin or IV azithromycin 1 g once
then 500 mg qd
In-patient ICU A beta-lactam (ceftriaxone 2 g IV qd, ampicillin-sulbactam 2 g IV q8h or cefotaxime 1-2 g IV q 8h plus
Azithromycin or fluoroquinolone as listed for in patients, non-ICU
Special Considerations If Pseudomonas is a consideration
• An antipneumococcal, antipsuedomonal blactam (piperacillin/tazobactam 4.5 g IV q6h, cefepime 1-2 g IV
q12h, imipenem 500 mg IV q6h, meropenem 1 g IV q12h, plus either ciprofloxacin 400 mg IV q12h, or
levofloxacin 750 mg IV qd
• The above b-lactam plus aminoglycoside (amikacin 15mg/kg qd or tobramycin 1.7mg/kg qd & azithromycin
• The above b-lactam plus aminoglycoside plus an antipneumococcal fluoroquinolone

If CA-MRSA is a concern
Add linezolid 600 mg IV q12h or vancomycin 15 mg/kg q 12h initially with adjusted doses plus clindamycin 300 mg q
6h

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

Hospital/ Ventilator-Associated Pneumonia (HAP/VAP)

Risk Factors Pathogenesis Clinical Diagnosis Empirical Treatment Complications and
Manifestations Prognosis
• Endotracheal tube • Colonization of • Fever; Quantitative culture No Risk factors for • Prolong
• Colonization by the oropharynx leukocytosis approach resistant Gram- mechanical
pathogenic with pathogenic • Increase in Clinical approach negative pathogen ventilation &
microorganism microorganism respiratory • Piperacillin- ICU days
• Aspiration • Aspiration of secretions tazobactam (4.5 • Necrotizing
• Immunosuppression these micro- • Pulmonary g IV q 6h) pneumonia
organism consolidation of • Cefepime (2 g • General
• Compromise of physical IV q 8h) debilitation
the normal host examination • Levofloxaxin • Mortality rate 50
defense • New or (750 mg IV q -70%
mechanism changing 24h)
rediographic • Risk for MRSA:
infiltrate Linezolid (600
• Tachycardia; mg IV 12h) or
tacypnea adjusted dose
• Worsening Vancomycin
oxygenation (trough level
• Increased 1520mg/dl)
minute
ventilation Risk factors for
resistant Gram-
negative pathogen
• Piperacillin -
tazobactam (4.5
g
• IV mg/kg IV q
6h)
• Cefepime (2 g
IV q 8h)
• Ceftazidime (2 g
IV q 8h)
• Amikacin (15-20
mg/kg q 24 h)
• Gentamycin (5-7
mg/kg IV q
• 24h)
• Tobramycin (5-7
mg/kg IV q 24h)
• Imipenem (500
mg IV q 6h)
• Meropenem (1 g
IV q 8h)
• Ciprofloxacin
(400 mg IV q 8h)
• Levofloxacin
(750 mg IV q
24h)
• Colistin (loading
dose of 5 mg/kg
IV followed by
maintenance
doses of 2.5 mg
x (1.5xCrCl +
30) IV q 12h)
• Polymyxin B
(2.5-3 mg/kg per
day IV in 2
divided doses)

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

IV. Bronchial Asthma

Risk factors Pathophysiology Effects of Clinical features Diagnosis Treatment
inflammation
Endogenous (host) Allergen will • Damage in the • Wheezing, • Lung function tests Bronchodilators
Factors stimulate a lot of airway dyspnea, (Spirometry) B2 agonists
• Genetic inflammatory cells. epithelium coughing- vary • Airway • SABA
predisposition Dendritic cells and • Fibrosis overtime and hyperresponsiveness: (albuterol,
• Atopy mast cells will be • Airway smooth intensity, methacholine or terbutaline): 3-
• AHR activated once the muscle spontaneously histamine challenge 6 hrs duration of
• Gender allergen triggers the • Vascular and with (also known as broncho action
• Ethnicity immune system. responses therapy provocation test) • LABA
• Obesity Mast cells will then • Mucus • Worse at night, • Hematologic tests: not (Salmeterol,
• Early viral recruit hypersecretion early morning usually helpful. (usually Formoterol): 12
infections neutrophil and • Neural awakening eosinophilia) hrs
eosinophils. And regulation • Increased • Total serum IgE and • LABA
Environmental dendritic cells will • Airway mucus specific IgE to inhaled (Indacaterol,
Factors recruit T-helper cells Remodeling production allergens Olodaterol and
and eosinophils • Non-pro variant (radioallergosorbent Vilanterol):
• Indoor allergens
as well. Eventually • Inspiratory, test [RAST]) may be given OD
• Outdoor
producing expiratory measured in some
allergens
hypersecretion, wheezes, patients Anticholinergics
• Occupational vasodilatation,
sensitizers rhonchi, • Imaging CXR: normal, • SAMA
bronchoconstriction hyperinflation hyperinflation (Ipratroprium
• Passive and also damage to
smoking • Increased • Skin tests to allergens bromide)
the epithelial cells. ventilation, use Fractional Exhaled • LAMA
• Respiratory Then also resulting
infections of accessory Nitric oxide (FENO) (Tiotropium
to nerve activation muscles bromide,
• Diet and Glycopyrronium
• Acetaminophen subepithelial fibrosis bromide,
(paracetamol)
Aclidinium,
Umeclidinium)
Methylxanthines
• IV:
Aminophylline
• Oral:
Theophylline
and Doxofylline

ICS: the most

effective controllers
for asthma
• Mode of
Action: Reduce
inflammatory
cell numbers
and their
activation. eos.,
activated T
lymph. and mast
cells in the
airway mucosa.
• AHR with
chronic ICS
treatment

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

I. Chronic Obstructive Pulmonary Disease

Components Risk factors Pathogenesis Pathologic Clinical Features Diagnosis Treatment
Types
• Emphysema: • Tobacco 1) Chronic Centrilobular • Dyspnea *Refer to Group A -
char. by smoking exposure to emphysema ü Progressive GOLD’s BRONCHODILATOR
destruction of • Air pollutants cigarette smoke • Most (worsens criteria • A short- or long-
lung alveoli • Occupational in genetically frequently over time) acting
with air space dusts susceptible associated ü Persistent bronchodilator
enlargement • Chemicals individuals à with (present • Long-Acting
• Chronic • Infections triggers cigarette everyday) Muscarinic
Bronchitis: • Genetic - inflammatory smoking, ü Worse on Antagonist
clinical alpha 1- and immune • Char. by exercise (LAMA) or
condition of antitrypsin cell recruitment enlarged air ü Worse • Long-Acting
chronic deficiency in the airways spaces in during resp. Beta2 Agonist
cough and and alveoli respiratory infections (LABA)
phlegm bronchioles • Exercise • Recommended
• Small 2) Inflammatory prominent in intolerance based on their
Airway cells release the upper • Fatigue effects on
Disease: proteinases lobes and • Chronic cough patients'
small damaging the superior with or without breathlessness.
bronchioles extracellular segments of sputum
narrowed and matrix lower lobes • Reduction in
reduced in supporting • Often focal activities of daily Group B - LABA or
number airways, living LAMA
vasculature, and Panlobular There is evidence
alveoli • Refers to Physical findings monotherapy is
abnormally • Early stages of sufficient at symptom
3) Cell death large air COPD: normal PE control and
occurs through: spaces • Prolonged expiratory combination therapy
oxidant-induced evenly phase is not twice as
damage, cellular distributed • Expiratory wheezing effective
within and

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

senescence, across • Hyperinflated lung: Group C - LAMA

and acinar units barrel shaped chest, LAMAs are superior
proteolytic loss • Observed in poor diaphragmatic to LABAs regarding
of cellular-matrix •
patients with excursion COPD exacerbations
attachments à alpha-1-anti- (percussion)
Leads to trypsin • Use of accessory Group D - LAMA
extensive loss of deficiency muscles LABA + LAMA (in
smaller airways, • Has a • “Tripod” position addition to symptoms
vascular predilection• Cyanosis and CAT >20), or
pruning, and in lower ICS + LABA
alveolar lobes Advance disease (depending on
destruction • Cachexia, specific lab values).
Paraseptal bitemporal
• occurs in 10- wasting, diffuse
4) Disordered 15% of loss of
repair of elastin cases subcutaneous
and other • distributed adipose tissue
extracellular along the • Associated with
matrix pleural inadequate oral
components margins, intake and
contribute to air sparing the elevated levels
space central areas of inflammatory
enlargement • associated cytokines (TNF-
and with alpha)
emphysema significant • Paradoxical
airway inward
inflammation movement of the
and with rib cage with
centrilobular inspiration
emphysema

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

V. Pleura and Mediastinum

Classify as transudate or exudate
• Transudate: systemic factors that influence formation & absorption of fluid are altered à May be due to LV or cirrhosis
• Exudate: local factors that influence the formation and absorption of fluid à Pneumonia, PTB, malignancy, viral infection or pulmonary
embolism

Diagnostic Criteria
Exudate - one or more of the ff:
• Pf/serum protein > 0.5
• Pf/serum LDH > 0.6
• Pf LDH > 2/3 N serum LDH (250iu)
Exudate - requires further analysis: description, glucose, cell count & diff. count, G/S, C/S, cytology

PNEUMOTHORAX
Spontaneous Traumatic Tension Treatment
• Primary spontaneous: no • Penetrating • Positive pleural space • Aspiration: for mild
underlying lung disease, • Non-penetrating chest injury pressure, life threatening à pneuomothorax
rupture of subapical blebs, • Iatrogenic decrease • CTT: for secondary
smokers • Venous return, therefore spontaneous pneumothorax
• Secondary spontaneous: decreasing the preload, • Pleurodesis: used to prevent
underlying lung disease, decreases CO, leading to recurrence
more life threatening, high hypotension ü Chemical you instill
recurrence rate (COPD, • PE: absent BS, doxycycline or
asthma, pneumonia) hyperresonance, mediastinal tetracycline mix with
shift NSS in order to induce
• Death secondary to fibrosis of the pleura
hypotension/hypoxemia ü Surgical
• VATS: done to repair the
tears in the pleura.
• Thoracotomy

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

MEDIASTINITIS
Evaluation of Mediastinal Masses Diagnosis Types
Anterior • Mediastinoscopy: for anteriorly located and 1. Acute mediastinitis
• Thymoma right sided lesions • Cause by Esophageal perforation or
• Teratoma • Mediastinotomy: more open procedure, median sternotomy
• Thyroid wherein you do a large incision in order to • Symptoms: Chest pain & DOB due to
• Lymphoma see the content of mediastinum. Usually infection in rupture
done for posteriorly located and left sided • Treatment: mediastinal exploration &
Middle lesions. repair. Antibiotics
• Vascular • FNAB
• LN enlagement (mets granulomas), • EBUS ultrasound guided bronchoscopy 2. Chronic mediastinitis
• Pleuropericardial cysts • VATS • Range from granulomatous
• Bronchogenic cysts inflammation of lymph nodes to
fibrosing mediastinitis
Posterior • Causes: TB, histoplasmosis; others:
• Neurogenic tumors sarcoidosis, silicosis
• Meningocoele • Fibrosing mediastinitis can leads to
• Meningomyelocoele compression
• Gastroenteric cyst
• Esophageal diverticula

VI. Acute Respiratory Syndrome

CRITERIA FOR DIAGNOSIS OF ARDS
Clinical Presentation Clinical Setting Radiologic Lung Mechanics Gas Exchange Normal Vascular
appearance Pressure
• Tachypnea • Direct lung injury • Diffuse alveolar • Diminished • Refractory • PCWP < 18
• Dyspnea pneumonia infiltrates compliance hypoxemia mmHG
• Crackles on • Indirect lung (peripheral) • < 40 ml/cm H2O • Pao2/Fio2 < 200 • Low pressure
auscultation injury - sepsis • Absence of pulmonary
pleural effusion edema

PHASES OF ARDS
Exudative Phase Proliferative Phase Fibrotic Phase
• Alveolar capillary endothelial cell & type I Most patient recover rapidly, histologically, the Requires long term support on mechanical
pneumocyte injury first signs of resolution are evident in this phase ventilation
• Loss of the tight alveolar barrier à with the initiation of lung repair. Histologically, there is extensive ductal &
accumulation of protein rich edema fluid in 1. organization of alveolar exudates interstitial fibrosis, acinar architecture markedly
the interstitial and alveolar spaces 2. shift from neutrophils to lymphocyte disrupted, leading to emphysema-like changes
• Increased concentration of cytokines (IL-1, predominant infiltrates with large bullae.
IL-8 & TNF) & lipid mediators (LT B4); 3. proliferation of type II pneumocytes along
neutrophils in the interstitium & alveolar alveolar The physiologic consequences include:
spaces basement membranes -these cells synthesize 1. an increase risk of pneumothorax
• Hyaline membrane whorls new 2. reduction in lung compliance
• Pulmonary vascular injury pulmonary surfactant & differentiate into type I 3. increase in pulmonary dead space
• Alveolar edema pneumocytes
Intimal fibroproliferation in the microcirculation
Despite the improvement, many still experience leads to progressive vascular occlusion &
dyspnea, tachypnea & hypoxemia pulmonary hypertension
Some develop progressive lung injury and
pulmonary fibrosis.
Histologically, the presence of alveolar type III
procollagen peptide, a marker of pulmonary
fibrosis, is associated with a protracted clinical
course & increased mortality from ARDS

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

VII. Acute Respiratory Failure

Types Description
I Occurs when there is alveolar flooding (pulmonary edema, pneumonia or alveolar hemorrhage) and subsequent
intrapulmonary shunt physiology occurs à decreased PaO2
II Occurs as a result of alveolar hypoventilation and results in the inability to effectively eliminate carbon dioxide à
Increased PaCO2 with or without decreased PaO2
III Occurs as a results of lung atelectasis. Because atelectasis occurs commonly in the perioperative period, this is also
called perioperative respiratory failure à Post-op pain, anesthesia are causative
IV Patients in shock. Normally, respiratory muscles consume <5% of the total cardiac output and oxygen delivery. Patient
in shock often suffer respiratory distress due to pulmonary edema, lactic acidosis, and anemia. In this setting, up to
40% of the cardiac output may be redistributed to the respiratory muscles

Respiratory Failure Based on Physiologic Principles

Controller Dysfunction Pump Dysfunction Airway Dysfunction Pulmonary Vascular
Dysfunction
• Least common primary cause • Common cause of respiratory • P.E. findings of: stridor; • Distended jugular vein
of respiratory failure failure in ICU and is usually Rhonchi; Wheezes; dynamic • Prolonged or delayed
• Most common cause is due to multifactorial hyperinflation pulmonic component of S2
medications that impairs • Conditions that affect the • In intubated patient, airway • Right sided S3
respiratory drive respiratory muscles resistance can be estimated • Murmur of tricuspid
• Defect in regulatory drive do ü Prolonged periods of by determining the plateau regurgitation
not have elevation in mechanical ventilation pressure & dividing it by the
respiratory rate and not use ü Polyradiculopathy end inspiratory flow rates • Diagnostic test: ABG, Chest
accessory muscle inspite of associated with critical (normal value: 3 to 8 cmH2O) X-ray, 2-D Echo, Right heart
significant hypercarbia or illness • Pneumotachography: lung catheterization, contrast
hypoxemia. With normal • Sign of respiratory muscle impedance, airway resistance enhanced CT scan of the
AsDO2 weakness abdominal: and dynamic compliance chest
paradoxical breathing
• Diagnostic test • Diagnostic test: chest X-ray,
ü Carbon dioxide • Diagnostic test ABG, lung compliance
challenge test: ü Measurement of
inhalation of 5% CO2 & muscle strength: VC &
15 % of O2 (normal MIF
response is an increase ü Other breathing
of RR to at least 25/min) indices: RSBI (rr/Vt);
ü P0.1 test: measuring the transdiaphragmatic
pressure generated 0.1 pressure measurment;
s after the start of § EMG and nerve
inhalation conduction study
§ Respiratory muscle
insufficiency
indicated by: VC <
10 ml/kg; MIF < 20
cmH2O

Management
• Non-invasive
ü CPAP
ü BIPAP
• Invasive
ü Mechanical Ventilation
§ Controlled: takes over in case the patient stops breathing
§ Assist/control: you have spontaneous breathing, which is augmented by the ventilator
§ SIMV (Synchronized Intermittent Mechanical Ventilator): combination of spontaneous breathing and assisted mechanical
ventilation
§ PCV: a certain pressure is set to limit the ventilation. Best used by patients with barotrauma or who had thoracic surgery.
§ PSV (Pressure Support Ventilation): stops when a certain pressure is reached. This method is best used when weaning the
patient
• Management of ARF
ü Identify & treat the cause
ü Identify & treat the complications
§ Pulmonary: VAP, barotrauma, tracheal stenosis, respiratory muscle atrophy
§ Cardiac: hypotension
§ GI: jaundice
• Once the cause and complication are treated and ventilator support is minimal and the patient is stabilized à Weaning from the ventilator is started

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

NEUROLOGY

I. Stroke
Types Clinical Manifestations Pathophysiology Diagnostics Management and
Treatment
Ischemic Anterior cerebral artery •
Lack of circulating blood
CT scan IV RTPA
• Hemiparesis, sensory deprives the
• neurons
MRI of • Clinical diagnosis of
loss (leg more affected oxygen and nourishment stroke
than arm) • Onset of symptom to
• Impaired time of drug
responsiveness administration <3 h
(abulia, akinetic • CT scan showing no
mutism), esp. bilateral hemorrhage or
• Left sided ideomotor edema of >1/3 of the
apraxia or tactile • MCA territory
anomia • Age 18 years
• Consent by patient or
Middle cerebral artery surrogate
• Main trunk
ü Hemiplegia Platelet inhibition:
ü Hemianesthesia aspirin, dipyrimadole,
ü Hemianopsia clopidrogel, cilostazol
ü Aphasia (D)
ü Hemineglect(ND)
• Upper division Anticoagulant: tx for
ü Hemiparesis cardioembolic stroke
ü Sensory loss
(arm, face> leg)
ü Broca aphasia
ü Hemineglect
• Lower division
ü Wernicke aphasia
ü Behavior disorder

Posterior circulation
• Ataxia, gait
abnormalities
• Diplopia, oscillopsia,
nystagmus
• Dysconjugate eye
movements
• Nausea and vomiting(
area postrema)
• Crossed hemiparesis,
hemisensory deficits
• Headache more
common
Thrombotic • Atherosclerosis
• Lipohyalinosis
Cardioembolic • Thrombotic material
from atrial or
ventricular wall or left
heart valves
• Emboli from heart
usu. lodge over MCA,
post. cerebral artery
• infrequent ACA
• Most common cause
nonvalvular AF; other
causes MI, prosthetic
valves, RHD,
ischemic
cardiomyopathy
Transient Ischemic • Looks like a stroke
Attack but, symptoms
improve in 1-24hours

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

• Temporary disruption
of blood flow to the
brain
• Like Unstable Angina
of the brain
• Warning sign (15% of
strokes have TIA first)
• Mimicked by low
blood sugar (> blood
sugar signs and
symptoms go away)
• 1 in 20 patients will
have a true stroke in
3 months
Hemorrhagic • Primary ICH (78-88%
case) spontaneous
rupture of small
vessels damaged by
ü Hypertension
(basal ganglia,
thalamus, pons,
cerebellum) the
usual part of
hypertensive
bleed.
ü Cerebral Amyloid
Angiopathy
• Basal ganglia (50%):
contralateral
hemiparesis, sensory
loss, conjugate gaze
• Lobar regions (20-
50%): contralateral
hemiparesis or sensory
loss, aphasia, neglect,
or confusion
• Thalamus (10-15%):
contralateral
hemiparesis, sensory
loss, gaze paresis
• Pons (5-12%):
quadriparesis, facial
weakness, decreased
level consciousness
• Cerebellum (1-5%):
ataxia, miosis, vertigo,
gaze, paresis

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

II. Subarachnoid hemorrhage

Types Clinical Manifestations Pathophysiology Diagnostics Management and
Treatment
Subarachnoid • Loss of consciousness • 3rd nerve palsy: • CT scan: • Clip: open surgery
hemorrhage • Worst headache PCA aneurysm hyperdensity • Coil: interventional
• Sudden in onset no • 6th nerve palsy: • MRI • To avoid vasospasm,
focal neurologic deficit cavernus sinus • 4-vessel allow HPN; CCB can
• Meningeal signs • Visual field defect: angiography: gold also be given
ACA or supraclinoid standard (nimodipine)
Delayed neurologic ICA
deficits • Pain behind the eye
• Rerupture: first month or low temple: MCA
30% peak first seven aneurysm
days
• Hydrocephalus
• Vasospasm: 30%
appears 4 to 14 days,
most often at 7 days
• Hyponatremia: atrial
and brain natriuretic
factor

III. Seizures
Types Clinical Manifestations Pathophysiology Diagnostics Management and
Treatment
Simple partial seizures With motor symptoms • Foci in the Criteria for starting
• Focal motor sensorimotor cortex antiepileptic drug
without march • Consciousness is therapy
• Focal motor with retained • Diagnosis of epilepsy
march must be firm
(Jacksonian) • Risk of recurrence of
• Versive seizures must be
• Postural sufficient
• Phonatory • Seizures must be
(vocalization or sufficiently
arrest of speech) troublesome
ü Types of
With somatosensory or seizures
special sensory ü Frequency of
symptoms seizures
• Somatosensory ü Severity of
• Visual seizures
• Auditory ü Timing of
• Olfactory seizures
• Gustatory ü Precipitation of
seizures
• Vertiginous
• Good compliance
With somatosensory or must be likely
special sensory • Patient has been fully
symptoms counseled
• Somatosensory
First generation
• Visual
• Phenobarbital
• Auditory
• Phenytoin
• Olfactory
• Carbamazepine
• Gustatory
• Valproate
• Vertiginous
• Clonazepam
Somatosensory Numbness, tingling, or a Seizure focus in the
“pins and needles” postcentral • Primidone
Visual Usually produce elemental Foci near the striate cortex • Ethosuximide
visual sensations of of the occipital lobe
darkness or sparks and Second generation
flashes of light • Gabapentine
Auditory Buzzing and roaring sound, Foci in the superior • Lamotrigine
or a human voice temporal convolution • Topiramate
Olfactory hallucinations Perceived odor is Pahippocampal or • Tiagabine
exteriorized uncinate • Felbaramate

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

Vertiginous sensation Superoposterior temporal • Vigabatrin

region or the junction
between parietal and Third generation
temporal lobes • Oxcarbazepine
Gustatory hallucination Temporal lobe, insula and • Levitiracetam
parietal operculum • Zonisamide
Complex partial Automatisms • The aura may be
• Oro-alimentary: either a focal
chewing, lip smacking seizure of simple
• Mimicry: anger, joy type or a
• Gestural: clapping, hallucination or
scratching perceptual illusion,
• Ambulatory: walking, indicating a
riding a bicycle temporal lobe origin
• Verbal • Instead of complete
loss of control of
thought and action,
there is a period of
altered behavior
and consciousness
Generalized seizures • Prodrome
(grand mal) • Tonic phase
ü Extension and
piercing cry
ü Pupils dilated and
unreactive to light
ü Lasts for 10 to 20
seconds
• Clonic phase
ü Repetitive
relaxation of tonic
contraction
ü Autonomic signs
(rapid pulse,
elevated BP,
pupils dilated,
salivation and
sweating
profusely)
• Terminal phase (post-
ictal confusion)
Generalized epilepsy EEG
• Tonic phase
ü Repetitive spike
or spike-wave
discharges
lasting a few
seconds
ü Followed by an
approximate 10
s period of 10
Hz spikes
• Clonic phase
ü Spikes become
mixed with slow
waves
ü Followed by
polyspike and
wave pattern
• Terminal phase
ü Nearly flat for a
variable time
ü Brain waves
resume their
preseizure
pattern
Atonic seizure It is when the patient
suddenly lose tone. The
patient will suddenly

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

collapse. Then they stand

up eventually. This event is
also recurrent. It doesn’t
mean that the whole body
loses tone, sometimes it is
partial.
Idiopathic nonconvulsive • Petit mal or pykno
seizures (absence epilepsy
seizures) • Sudden interruption of
consciousness
• Resemble a moment of
absentmindedness or
daydreaming
• Brief burst of fine clonic
movements
• Minor automatisms
• Rarely begin 4 years of
age or after puberty
• Can be induced by
voluntary
hyperventilation for 2-3
minutes

Choice of AED for adult type seizure

Choice of AED for childhood type seizure

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

Types Clinical Manifestations Pathophysiology Diagnostics Management and

Treatment
Status epilepticus Single seizure lasting at • Convulsive status
least 30 minutes or recurrent ü Generalized
seizures tonic-clonic
lasting > 30 minutes without seizures
fully regaining ü Partial motor
consciousness seizures
between episodes. • Non-convulsive
status
ü Absence status
ü Complex partial
status
ü Partial sensory
status

IV. Dementia
Types Clinical Manifestations Pathophysiology Diagnostics Management and
Treatment
Dementia • Behavior and mood: • Increasing age: Routine Evaluation
noradrenergic, single strongest risk • History
serotonergic, factor • Physical examination
dopaminergic • Factors affecting • Laboratory Tests
• Attention and frequency: ü Thyroid function
memory: cholinergic ü Age group (TSH)
• Alzheimers Disease: ü Access to ü Vitamin B12
transentorhinal region medical care ü CBC
> hippocampus > ü Country of origin ü Electrolytes
Lateral and posterior (Western AD; ü CT/MRI
temporal and parietal ASEAN VD)
neocortex > ü Ethnic
widespread background
• Vascular Dementia:
focal, random, cortical • Most common
or subcortical causes
• Fronto-temporal ü Alzheimer's
Dementia: frontal and Disease
temporal lobes ü Vascular
• Corticostriatal dementia
pathway: behavior § Multi-infarct
• Dorsolateral § Binswanger
prefrontal-central (diffuse
band of caudate: poor white
organization and matter
planning disease)
• Lateral orbitofrontal ü Alcoholism
ventromedial ü Parkinson's
caudate: disease
impulsiveness, ü Drug/medication
distractability, intoxication
disinhibition
• Anterior cingulate
cortex-nucleus
accumbens: apathy,
poverty of speech,
akinetic mutism
Alzheimer’s disease • Insidious onset of Atrophy of medial • Long term
memory loss followed temporal, medial and amelioration of
by slowly progressive lateral parietal, and lateral behavioral and
dementia over several frontal cortex neurologic problems
years atrophy of medial • Providing caregiver
temporal, medial and support
lateral parietal, and • Donepezil -10 mg
lateral frontal cortex daily – ACHase inh
• Microscopically: • Rivastigmine 6 mg
neuritic plaques daily
containing Ab • Galantamine 24 mg
neurofibrillary tangles daily

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

NFT’s; accumulation of • Memantine 10 mg

amyloid in blood vessel bid- blocks NMDA
walls glutamate rec.
• Tacrine- hepatotoxic
• Gingko Biloba-
improvement in
cognitive fxn
• Antidepressant
Vascular Dementia • Mild confusion, apathy,
anxiety, psychosis
• Memory, spatial or
executive deficits
• Euphoria, elations,
depression, aggressive
behavior
• Pyramidal and cerebral
signs may be present
• Advance disease -
urinary incontinence,
dysarthria, dysphagia,
pseudobulbar features
• Seizures, myclonic
jerkings in minority

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

V. Parkinsonism
Types Clinical Manifestations Pathophysiology Diagnostics Management and
Treatment
Parkinson’s disease Cardinal Features Loss of cells in the • History and PE • Levodopa/ carbidopa
• Bradykinesia substantia nigra • Imaging • Dopamine agonist:
• Rest tremors enhance the effect of
• Rigidity levodopa
• Gait disturbance • COMT inhibitors:
• Postural instability inhibit the
degradation of
Minor Motor Features dopamine
• Micrographia
• Masked facie
(hypomimia)
• Reduced eye blink
• Hypophonia
• Dysphagia
• Freezing

Non-motor Features
• Anosmia
• Sensory disturbances
• Mood disorders
(depression)
• Sleep disturbances
• Autonomic
disturbances
• Cognitive impairment/
dementia
Atypical Parkinsonism • Multiple- system
atrophy
ü Cerebellar type
(MSA-c)
ü Parkinson type
(MSA-p)
• Progressive
Supranuclear Palsy
• Corticobasal ganglionic
degeneration
• o Frontotemporal
dementia
Secondary Parkinsonism • Drug-induced
• Tumor
• Infection
• Vascular
• Normal-pressure
hydrocephalus (due to
dilatation of lateral
• ventricles)
• Trauma
• Liver Failure
• Toxins (CO, Mn, MPTP
Cyanide, Hexane, CS2,
methanol)

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

VI. Diseases of the Peripheral Neuropathy

Types Clinical Manifestations Pathophysiology Diagnostics Management and
Treatment
Peripheral Motor symptoms Damage to the nerves of History and PE (7 • Pregabalin 50-
neuropathy • Positive: muscle cramps, fasciculations, the PNS, which may be questions) 100 mg TID
myokymia, tremor inherent to the nerves or • Gabapentin
• Negative: weakness in the distal toe and from involvement in a 1. Systems (fibers) • Tricyclic
ankle extensors, atrophy, gait disturbance systemic illness involved? antidepressant
2. Distribution? s
Sensory symptoms 3. Nature of • Lidoderm 5%
• Loss of function (negative): large fiber sensory/motor/ patch
(decreased vibration, proprioception, reflexes, autonomic • Duloxetine
(+) Romberg’s), small fiber (numbness on involvement?
pain and temperature) 4. Evidence of umn
involvement?
5. Temporal
involvement?
6. Evidence for
hereditary
neuropathy?
7. Associated medical
conditions?
Mononeuropath Focal involvement of a
y single nerve
Due to local process
1. Direct trauma
2. Compression or
Entrapment
3. vascular lesions
4. Neoplastic
compression or
Infiltration
Mononeuropath Simultaneous/
y simplex sequential damage to
multiple noncontiguous
nerves
Due to:
• Ischemia caused by
vasculitis
• Microangiopathy
(DM)
Polyneuropathy • Evolution is centripetal- spread up legs early
symptoms- usually sensory
• Usually depressed ankle jerk
• Poor- walking on heels
• Distally predominant
• Usually symmetrical
• Stocking- glove sensory loss
• Distal muscle wasting and weakness
Diabetic • Large fiber: proprioception, vibration and light
nephropathy touch, (+)
• Small fiber: impaired pain/temperature
• Autonomic: cardiovascular and GI
• Commonly presents with slow onset
numbness and tingling then pain in distal
extremities, feet before hands à sensory
early absence of
DTR

• Cranial nerve deficits; EOM, with pupillary

sparing
• Focal entrapments or ischemic neuropathies
• Amyotrophy: asymmetrical proximal leg
weakness and pain
Demyelinating • Myelin sheath à most vulnerable to injury
neuropathy • Seen in immune mediated disorders
• Faster recovery than axonal disorder

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

• Mild sensory loss with prominent muscle

weakness which can start proximally
• Absent reflexes, neuropathic Tremors/
palpably enlarged nerves
Guillain Barre • Areflexic motor paralysis with or without • C. jejuni isolates • Elevated CSF IVIg total dose 2g/kg
Syndrome sensory disturbance from patients protein without body weight (0.4
• Ascending paralysis proceeding from hours to express pleocytosis g/kg/day) for 5 days
days lipooligosaccharide • Electrodiagnosti initiated in patients
• Legs> arms s (LOS) that mimic c abnormalities seen within 14 days
• Facial diplegia in 50%; lower CN involvement the carbohydrates (slowing of of symptom onset
(dysphagia); of gangliosides conduction
• Pain in the shoulder/ back/ neck/ leg GM1 (ganglioside- velocity,
• Proprioceptive sense affected like LOS) à reduced
• Plateau (within 4 weeks of onset) antigenic cross amplitude of
reaction à local action
complement potentials)
activation at the
damaged nerve à
clinical symptoms
• Cellular and
humoral immunity
Myasthenia • Weakness and fatigability à diurnal variation 1. Symptomatic
Gravis • Weakness increase with use of the muscle; treatment:
improve with rest acetylcholinesterase
• Myasthenic crisis: provoked by infection or inhibitors
systemic disorders 2. Rapid short-
• Cholinergic crisis: caused by excessive term:
medication plasmapheresis and
• Crisis: requires ventilatory assistance intravenous
• Ocular weakness affects more than one immunoglobulin
EOM; diplopia, and ptosis 3. Chronic long
• 85% manifest with generalized weakness, term:
with limb weakness (proximal & asymmetric) immunomodulating
treatment -
Bulbar Weakness glucocorticoids &
immunosuppressive
• Weakness of face and throat muscles
drugs
ü Dysphagia
4. Surgical
ü Dysarthna
treatment
ü Dysphonia
• Limb muscle weakness
ü Neck extensors > flexors
ü Upper limbs > lower limbs
Myopathy • Hypothyroidism: weakness, cramps, pain
and stiffness, muscle hypertrophy slow
contraction and relaxation (25%); CK elevated
• Hyperthyroidism: proximal weakness with
atrophy may affect bulbar muscles, CK levels
normal
• Hyperparathyroidism: proximal muscle
weakness, brisk reflexes, CK normal or
slightly elevated
• Hypoparathyroidism: symptoms due to
tetany, hyporeflexia, CK levels elevated
Trigeminal • Unilateral, paroxysmal Carbamezapine
neuralgia • Second and 3rd division of cn 5. (maxillary
and mandibular)
• Presence of an initiating or trigger point
• No sensory or motor dysfunction
• Usually idiopathic
• Disorder of middle age and later life
• Compression by superior cerebellar artery
• Age related brain sagging
• Increased vascular thickness and tortuosity
Bell’s palsy • Abrupt onset maximal weakness in 48 hours Prednisone 60-80
• Preceded by ear pain mg during the first 5
• Hyperacusis, loss of taste days and tapered in
the next 5 days

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

GASTROENTEROLOGY

I. Liver Function Tests

Excretory Function (Bilirubin) Isolated increase in unconjugated bilirubin is due to
Conjugated bilirubin (<0.3mg/dl): soluble in water 1. Hemolytic disease
so excreted by kidney 2. Genetic disorders: Crigler Najjar and Gilbert's syndrome
Unconjugated bilirubin: insoluble in water so 3. Neonatal jaundice/physiological jaundice
bound to albumin in blood
Isolated increase in conjugated bilirubin is due to
4. Cholestasis
5. Genetic disorders: Dubin johnson syndrome and Rotor's
syndrome

Increase to both conjugated and unconjugated bilirubin due

to
1. Intrahepatic /liver disorders

Detoxification function (Ammonia) • Liver à converted to urea à excreted by kidneys

• Striated Muscles à combined with glutamine à forms glutamate à organ trafficking à
hepatic encephalopathy
Synthetic Function (Plasma proteins and Albumin
Prothrombin time) In hepatitis - <3g/dl of albumin: possibility of chronic fiver disease
Non-hepatic causes of Hypoalbuminemia: protein losing enteropathy, nephrotic syndrome

Globulins
Cirrhosis: increased gamma gloulins
Increased IgM: primary biliary cirrhosis
Increased IgA: ALD

Alfa feto protein: HCC

AST/ALT Ratio • Normal ratio is 0.7 to 14
• Useful in Wilson disease, chronic liver disease and alcoholic liver disease
• AST/ALT ratio of > 2:1 is suggestive of and >3:1 is highly suggestive of ALCOHOLIC
liver disease
• AST in alcoholic liver disease is rarely >300 IU/L
• ALT is usually normal in alcoholic liver disease; can be sometimes low due to an alcohol
induced deficiency of pyridoxal phosphate
• AST/ALT <1 is seen in NASH and viral hepatitis

Isolated rise of ALT is seen in

1. Chronic HepC infection
2. Fatty liver

Isolated AST elevation

1. Alcohol -related
2. Drug -induced liver injury,
3. Hemolysis
4. Myopathic processes

ALP >4 times the Normal is seen in

1. Cholestatic liver disease
2. Infiltrative liver disease such as cancer and amyloidosis
3. Paget's disease of bone
Cholestasis ALP, 5’NT, GGT

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

II. Liver Cirrhosis

Causes Clinical Pathophysiology Diagnosis Management Complications
Manifestations and Treatment
• Alcoholic Liver • Spider • Reversible • Enzyme tests (principally • Other Pulmonary
Disease angiomas chronic injury the Syndromes
• Hepatitis C and • Palmar of the hepatic serumaminotransferases, ü Hepatic
B erythema of parenchyma alkaline phosphatase, hydrothorax
• Chronic the thenar and • Extensive and gamma glutamyl ü Portopulmonary
Autoimmune hypothenar fibrosis - transpeptidase), the HTN
Hepatitis part of the distortion of serum bilirubin • Hepatic
• Inherited palm the hepatic encephalopathy
Metabolic • Nail changes: architecture Morphologic Classification • Hepatocellular
Diseases Muerchke’s • Formation of • Micronodular cirrhosis carcinoma
• Primary Biliary nails, Terry’s regenerativeü Nodules less than 3 mm in
Cirrhosis nails nodules diameter
• Nonalcoholic • Gynecomastia ü Believed to be caused by
Steatohepatitis • Testicular alcohol, hemochromatosis,
atrophy cholestatic causes of
cirrhosis, and hepatic venous
outflow obstruction
• Macronodular cirrhosis
ü Nodules larger than
3 mm
ü Believed to be
secondary to
chronic viral
hepatitis

Complications of Liver Cirrhosis

Complications Clinical Manifestations Pathophysiology Diagnostics Management and
Treatment
Ascites • Fever • Accumulation of fluid • Grading • Combination of
• Abdominal pain within the peritoneal ü Grade 1: mild. single morning oral
• Abdominal cavity Detectable only by doses of
Tenderness • Most common US Spironolactone and
• Mental status change complication of ü Grade 2: moderate. Furosemide,
• Ileus cirrhosis Moderate beginning with 100
• Hypotension symmetrical mg and 40 mg
distension of the
abdomen
ü Grade 3: large or
gross ascites with
marked abdominal
distension

• Routine test
ü Cell count and
differential
ü Albumin
concentration
ü Total protein
concentration Culture
in blood culture
bottles

• Optimal Tests
ü Glucose
concentration
ü LDH concentration
ü Gram stain
ü Amylase
concentration

• Usual test
ü Tuberculosis smear
and culture
ü Cytology

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

ü Triglyceride
concentration
ü Bilirubin
concentration
Spontaneous bacterial • Fever • Infection of ascitic fluid • A positive ascitic fluid
peritonitis • Abdominal pain • Almost always seen in bacterial culture
• Abdominal tenderness the setting of end- • Elevated ascitic fluid
• Altered mental status stage liver disease absolute
polymorphonuclear
leukocyte (PMN) count
(>250 cells/mm3)
Hepatorenal • Oliguria • Acute renal failure • Major diagnostic criteria
syndrome • Benign urine sediment coupled with advanced for hepatorenal
very Iow rate of hepatic disease (due to syndrome
excretion cirrhosis or less often ü Cirrhosis with ascites
• Progressive rise in the metastatic tumor or ü Serum creatinine >
plasma creatinine severe alcoholic I.5 mg/dL
concentration hepatitis) ü No improvement in
serum creatinine
• Reduction in GFR (decrease to a level
often clinically masked of <1.5 mg/dL) after
• Prognosis is poo/ at least 2 days with
unless hepatic function diuretic withdrawal
improves and volume
• Nephrotoxic agents expansion with
and overdiuresis can albumin. The
precipitate HRS recommended dose
of albumin is 1 g/kg
of body weight per
• Type 1 hepatorenal day up to a
syndrome maximum of 100
ü The serum g/day
creatinine level ü Absence of shock
doubles to greater ü No current or recent
than 2.5 mg/Dl treatment with
within 2 weeks nephrotoxic drugs
ü It is characterized ü Absence of
by its rapid parenchymal kidney
progression and disease as indicated
high mortality, by proteinuria >500
with a median mg/day.
survival of only 1 microhematuria (<50
to 2 weeks RBC/high power
ü It can be field) and/or
precipitated by abnormal renal
spontaneous ultrasonography
bacterial
peritonitis and • Minor diagnostic criteria
variceal for hepatorenal
hemorrhage syndrome
ü In some cases of ü Urine volume < 500
acute hepatic mLJ24 h
injury, ü Urine sodium <10
superimposed on mEq/L
cirrhosis, may ü Urine osmolality
lead to liver failure greater than plasma
and HRS osmolality
ü Urine red blood cells
• Type 2 Hepatorenal < 50 per high power
Syndrome field
ü Serum creatinine ü Serum sodium <130
increases slowly mEq/L
and gradually
during several
weeks or months
ü Many patients
with type 2 HRS
eventually
progress to type 1

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

ü HRS because of a
precipitating factor
ü The median
survival of type 2
HRS is about 6
months

• Type 3 hepatorenal
syndrome
ü 85% of end-stage
cirrhotics have
intrinsic renal
disease on renal
biopsy
ü Patients with long-
standing diabetic
nephropathy,
obstructive renal
disease, or
chronic
glomerulonephritis
can develop HRS
from a
precipitating event
or worsening liver
failure
ü More than half of
patients with ALF
develop HRS,
although the
frequency varies
depending on the
ALF etiology

• Type 4 hepatorenal
syndrome
ü More than half of
patients with ALF
develop HRS,
although the
frequency varies
depending on the
ALF etiology
ü The
pathophysiology
of HRS in ALF is
believed to be
similar to that
postulated for
HRS occurring in
cirrhosis
Varices • History: • Treat underlying
Hematemases, disease
melena • Endoscopic
• Physical examination banding protocol
• Ultrasound abdomen • B-blockers
• Endoscopy • Shunt surgery (only
if no cirrhosis)
• Liver
transplantation
Hepatopulmonary • Hepatic Hydrothorax
syndrome ü Pleural effusion in
a patient with
cirrhosis and no
evidence of
underlying
cardiopulmonary
disease

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

ü Movement of
ascitic fluid into
the pleural space
through defects in
the diaphragm,
and is usually
right-sided
ü Diagnosis -
pleural fluid
analysis reveals a
transudative fluid
serum to fluid
albumin gradient
greater than 1.1

• Portopulmonary HTN
ü Refers to the
presence of
pulmonary
hypertension in
the coexistent
portal
hypertension
ü Prevalence in
cirrhotic patients
is approximately
2 percent
ü Diagnosis:
Suggested by
echocardiography
ü Confirmed by
right heart
catheterization
Hepatic • Reversal of sleep • Spectrum of potentially • Monitoring for
encephalopathy pattern reversible events likely to
• Disturbed neuropsychiatric precipitate HE
consciousness abnormalities seen in ti.E.variceal
• Personality changes patients with liver bleeding, infection
• Intellectual dysfunction (such as SBP), the
deterioration administration of
• Fetor hepaticus sedatives,
• Astrexis hypokalemia, and
• Fluctuating hyponatremial
• Reduction of
ammoniagenic
substrates
• Lactulose/ lactitol
• Dietary restriction
of protein
• Zinc and melatonin
(zinc enchances
urea cycle)
Hepatocellular • Pain, early satiety. • Patients with cirrhosis • MELD (model for end-
carcinoma obstructive jaundice, have a markedly stage liver disease)
and a palpable mass increased risk of ü Identify patients
developing whose predicted
hepatocellular survival
carcinoma postprocedure would
• Incidence in well be three months or
compensated cirrhosis less
is approximately 3 ü MELD = 3.8[serum
percent per year bilirubin (mg/dL)] +
11.2(lNRl +
9.6[serum creatinine
(mg/dL)] + 6.4

• Child-Turcotte-Pugh
(CTP) score

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

ü Initially designed to
stratify the risk of
portacaval shunt
surgery in cirrhotic
patients
ü Based upon five
parameters: serum
bilirubin, serum
albumin, prothrombin
time, ascites and
encephalopathyGood
predictor of outcome
in patients with
complications of
portal hypertension

• Serum AFP greater than

500 micrograms/I in a
patient with cirrhosis are
virtually diagnostic

III. Gallbladder
Disease Clinical Manifestations Pathophysiology Diagnosis Treatment and
Management
Cholelithiasis • Gross malabsorption
of bile acids from the
intestines, as seen in
patients with severe
ileal disease
• Obstruction of the
biliary tract,
interrupting the
enterohepatic
circulation
• Severe hepatic
dysfunction, leading
to decreased
synthesis of bile salts,
or other abnormalities
in bile production
• Excessive feedback
suppression of bile
acid synthesis as a
result of an
accelerated rate of
recycling of bile acids.
Gallstones • More common in There is supersaturation or
females too much cholesterol, then
• Classified as: it will undergo
cholesterol, pigment, crystallization and stone
calcium growth, which reduces the
contractility of the
gallbladder.
Pure • 90-100%
• Solitary, whitish
• >2.5 cm

Mixed • 50-90%
• Multiple, small, variety
of shape
Pigmented Brown
• Calcium Bicarbonate
• Ca Soap
• Bacteria has role in
the synthesis
• In Asia
• Mainly at the bile duct

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

• Periumpullary
duodenal diverticula

Black
• Excess in bilirubin
• In elderly, chronic
hemolysis alcoholic
Acute cholecystitis Murphy’s sign Inflammation of the
gallbladder
Ascending cholangitis Charcot’s triad: pain then Obstruction of the cystic ERCP
jaundice then fever duct
(remember this
chronology)

Reynaud’s pentad (if left

untreated): Charcot’s +
hypotension and
disorientation

IV. Pancreatitis
Types Clinical Manifestations Pathophysiology Diagnostics Management and
Treatment
Acute Reversible pancreatic Activation of Hageman Serum amylase Antibiotics
parenchymal injury factor-XII • Onset: almost • As SIRS may be
associated with • Activation of clotting immediately indistinguishable from
inflammation and complement • Peak: within several sepsis syndrome, so if
systems à hours à 3-4 times infection is suspected,
thrombosis à the upper limit of antibiotics should be
splenic vein normal within 24 given while source of
thrombosis hours (90%) infection is being
• Return to normal in investigated
Trypsinogen à trypsin (3-5 days) • Once blood and other
• Lipase activation à • Normal at a time of cultures are found
triglycerides à admission in 20% negative, antibiotics
glycerol + fatty acids cases should be
à fatty acids + • Compared with discontinued
calcium à lipase, returns more • Few antibiotics
saponification à quickly to normal penetrate due to
hypocalcemia values consistency of
• Elastase activation à • Raised amylase à pancreatic necrosis
digestion of elastic may not be AP • Cefuroxime, or
fibers à capillary • Normal amylase à imipenem, or
leak/rupture may be AP ciprofloxacin plus
pseudoaneurysm à metronidazole
rd
3 space of Serum lipase
sequestration of • More sensitive/ Enteral nutrition
blood/ fluid à specific than amylase Traditionally nasojejunal
hemorrhage + • Remains elevated route has been preferred to
hypovolemic shock longer than amylase avoid the gastric
• Activation of (12days) phase of stimulation BUT
lysolecithinase • Useful in late Nasogastric route appears
(deroved from bile) à presentation and if comparable in efficacy and
membrane damage the cause is high TG safety
à necrosis • Serum indicator of
• Release of highest probability of Mild and self-limiting
inflammatory disease needing only brief
mediators into hospitalization
circulation à IV contrast enhanced • Rehydration by IV
systemic computed tomography fluids
complications scan • Frequent non-invasive
• Indications: observation/monitoring
diagnostic • Brief period of fasting
• Initial assessment of till pain/vomiting
prognosis (CT settles
severity index) • Little physiological
• Perfusion CT at 3rd justification for
day area of ischemia prolonged NPO

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

predicts pancreatic • No medication

necrosis required other than
analgesics (important)
and anti-emetics
• Antibiotics not
indicated in absence
of signs or
documented sources
of infection
• Pain results in ongoing
cholinergic discharge,
stimulating gastric and
pancreatic secretions
• Avoid Morphine
Mild acute • Acute Interstitial
/Edematous
Pancreatitis
• Absence of organ
failure
• Absence of local
complications
Severe acute • Acute Hemorrhagic
Necrotizing (Fulminant)
pancreatitis)
• Local Complications
+/-
• Organ failure defined
as:
ü SBP <90 mmHg
ü PaO2 <60mmHg
ü GI bleed >500
ml/24hrs
ü Creatinine
>2mg/dL after
rehydration
• RANSON SCORE >3
• APACHE >8
Hyperlipidemia induced • In the absence of
gallstones and/or
history of significant
history of alcohol use,
a serum triglyceride
should be obtained
and considered the
etiology if
>1,000mg/dL
• Elevated lipase
without increase of
serum amylase
Post-ERCP • 3rd most common • Cause
cause of AP (after ü Duct disruption,
gallstone and alcohol) enzyme
i.e. 4% extravasation
• Most common
complication of ERCP • Predisposing
factors
ü Sphincter of
Oddi dysfunction
(risk increases)
ü H/O recurrent
pancreatitis
ü Sphincterotomy
ü Balloon dilation
of sphincter
ü Inexperienced
endoscopist
Cutaneous ecchymosis • Grey turner’s Periperitoneal/
(acute hemorrhagic syndrome: flanks retroperitoneal
pancreatitis) hemorrhage à

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

• Cullen’s sign: methalbumin formed from

falciform ligament à digested blood à tracks
around umbilicus around fascial planes à
• Fox sign: below hemorrhagic spots and
inguinal ligament ecchymosis

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

V. Hepatitis
Type Clinical Manifestations Pathophysiology Phases Diagnostics
Hepatitis A • Incubation period of • Naked RNA virus • Prodomal or
(Picornaviridae) 30 days; range 15- 50 (Picornaviridae) preicteric phase
days; <6 years • Transmitted via fecal- ü Abdominal pain,
• Jaundice by 10%; age oral route malaise, fatigue,
group 6-14 y/o • Related to joint pain, high
• Complications: enterovirus grade fever, loss
Fulminant cholestatic • Enterovirus 72 of appetite,
jaundice; relapsing • One stable serotype hepatomegaly
=70-80% and 4 genotypes • Icteric phase
ü Jaundice (skin,
sclera, mucus
Persons at increased risk membranes)
of infection ü Cause: elevated
• Travelers bilirubin
• Homosexual men ü Dark urine
• Injecting drug users ü Pale stool

Hepatitis B High risk • Member of Active viruses survive for • HBsAg

(Hepadnaviridae) • Sexual: hepadnaviridae more than 7 days outside ü After a person is
homosexuals, sex • Double stranded DNA of the human body infected with
workers virus HBV, the first
• Parenteral: IV drug • Replicates using virologic marker
use, health workers reverse transcriptase detectable in
are at risk serum within 1–
• Perinatal: vertical, 12 weeks,
HbeAg positive usually between
mother 8–12 weeks
ü Precedes
• High transmission: elevations of
blood, semen, serum, serum
wound exudates aminotransferase
• Moderate: semen, activity and
vaginal fluids, saliva clinical
• Low: urine, feces, symptoms by 2–
sweat, tears, breast 6 weeks and
milk remains
detectable during
the entire icteric
or symptomatic
phase of acute
hepatitis B and
beyond
ü General marker
of infection
• Anti- Hbs: total
neutralizing
antibodies
• HbsAb: recovery and
immunity
• Anti-Hbc IgM: marker
of acute infection
• Anti- Hbc IgG: past
or chronic infection
• HbeAg: indicates
active replication of
virus and therefore
infectiveness
• Anti-Hbe: no longer
replicating: can still be
(+) for HbsAg
integrated HBV

Hepatitis C (Flaviviridae) • “Non-A, non-B HCV antibody

hepatitis" • Most sensitive
• The only member of indicator of HCV
the genus Hepacivirus infection is the

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 Internal Medicine
MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

in the family presence of HCV

Flaviviridae RNA
• Patient who use IV • Requires molecular
drugs, or illegal drug amplification by PCR
abusers or transcription-
• Tattooing mediated amplification
• NS5A and Protease (TMA)
are hit by the virus
• IP = 6-7 weeks
• Range: 2-26 weeks
• Clinical Illness: 20-
30%
• Chronic Hepatitis:
70%
• Persistent: 85-100%
• Immunity: no
protective Ab
response identified

Screen patient
• With tattooes
• Blood transfusion
History
• IV drug users

Risk factors
§ Transfusion/ transplant
§ Injecting Drugs
§ Hemodialysis
§ Accidental Injury
§ Sexual

Hepatitis D • RNA virus Co-infection

• A defective RNA virus • Infect a person
that coinfects with and simultaneously with
requires the helper HBV
function of HBV (or • Severe acute
other disease
hepadnaviruses) for • Low risk of chronic
its replication and infection
expression
Superinfection
• Superinfect a person
already infected with
HBV
• Usually develop
chronic HDV infection
• High risk of severe
chronic liver disease
which may present as
acute hepatitis
• Fulminant hepatitis
• Problematic and
longer course
Hepatitis E (Calciviridae) • Contamination of
water supplies such
as after monsoon
flooding, but sporadic,
isolated cases occur
• Rarity of secondary
person-to-person
spread from infected
persons to their close
contacts
• Favor young adults
• Prevalence in
endemic area with

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Summarized Notes

antibodies to HEV is
40%
• Non-endemic:
prevalence of
antibodies to HEV is
20%
• Reports suggest a
zoonotic reservoir for
HEV in swine.
• Same with Hep A
• Enteric infection
• Oral fecal
transmission
• Worrisome in
pregnant women with
high degree of
mortality
• IP = 4months
• Jaundice

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VI. Malabsorption
Tests useful for the evaluation of Signs and Symptoms Disorder of Digestion
Malabsorption Disorders
• Stool fat content: Sudan III staining Most frequent • Inadequate digestion: liver and biliary
(qualitative), quantitative stool fat • Malnutrition tract disorders (liver cirrhosis, biliary tract
determination (<6 g/d, >94%) • Weight loss obstruction, pancreatic insufficiency), post-
• Xylose absorption test: xylose test • Diarrhea gastrectomy malabsorption
(normal à 5 hour urine xylose >26 mmol) • Inadequate absorptive of short bowel
• Test for pancreatic insufficiency: Other syndrome
secretin test • Glossitis, cheilosis, stomatitis, anemia-Fe, • Bacterial overgrowth of small intestine:
• Vitamin B12 absorption: Schilling’s test Folate, chronic intestinal pseudobstruction,
• Test for bacterial overgrowth: breath • Vit B12 deficiency tropical sprue, scleroderma, malabsorption
tests (lactulose, glucose-H2), culture of • Bone pains, osteoarthropathy- Vit D, in AIDS
intestinal fluid Calcium • Lymphatic obstruction: Whipple’s
• Serum levels (Ca, albumin, cholesterol, • deficiency disease, intestinal lymphoma
Mg, Fe): carotene, vitamin A, PTT • Night blindness, Xerophthalmia- Vit A • Defects in mucosal structure and
deficiency function: inflammatory bowel disease
• Peripheral neuropathy, Eczema, purpura, (regional enteritis), biochemical or genetic
dermatitis abnormalities (celiac sprue)
• Abdominal pain
• Azotemia hypotension
• Amenorrhea, decreased libido

VII. Diarrhea
Type Clinical Manifestations Pathophysiology Diagnostics Treatment
Acute • Nausea • Most common • Stool exam: 1. Supportive and
• Fever cause: infectious increased PMN, RBC; symptomatic
• Vomiting agents examination of stool • Rehydration:
• Diarrhea (bloody or • Other causes: drugs for ova and parasites cornerstone of
non-bloody) e.g. Mg containing • Bacterial culture of treatment
antacids, toxins, stool: Shigella, • Oral rehydration:
chemotherapy, Salmonella, Cholera mild to moderate
resumption of enteral • Sigmoidoscopy/ dehydration
feeding after a colonoscopy: non- • IV fluid replacement:
prolonged fast, onset improving bloody severe dehydration
of chronic diarrhea, diarrhea rest
marathon runners
2. Antimicrobials
Mode of Transmission • Generally, not
• Fecal-oral route: indicated for mild
most common resolving diarrheas or
• Others: contaminated due to viral agents
food preparing and food poisoning.
surfaces • Considered in
• Improperly cooked immunocompromised
food pts, those with
• Person to person: malignancy, abnormal
aerosol (Norwalk, heart valves,
Astrovirus) orthopedic prosthesis,
• Sexual activity hemolytic anemia,
very young and very
For mechanisms, refer to old.
the table below
3. Anti-cholinergics and
opiates: must be avoided
to prevent ileus/ prolong
colonization

4. Anti-secretory agents:
Acetorphan/Racecadotril
enkephalinase inhibitor

For antimicrobials, refer

to the table below
Chronic
Inflammatory • Fever, abdominal
pain, tenesmus, blood
or PMN in stool

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• inflammatory lesions
in mucosal biopsy
• Damaged mucosa
and submucosal
layers due to
inflammation.
• E.g. IBD, radiation
enterocolitis.
Osmotic • Due to presence of
unusually large
amounts of
nondigested food
particles.
• Diarrhea improves
with fasting
• Bulky, greasy foul,
smelling stools.
• Large stool osmotic
gap
• E.g. lactase
deficiency, pancreatic
insufficiency, bacterial
overgrowth, celiac
disease, Whipple’s
disease
Dysmotility • Due to rapid transit of
intestinal contents
• E.g. hyperthyroidism,
IBS
Factitious • Self-induced, usually
in women
• Watery diarrhea with
hypokalemia,
weakness and edema
• E.g. laxative abuse
Secretory • Secretion>absorption
• Watery diarrhea
which persists with
fasting.
• Normal stool osmotic
gap
• E.g. Carcinoid S.
ZES, VIPoma,
medullary thyroid
carcinoma, villous
rectal adenoma.
cholerrheic diarrhea

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Summarized Notes

VIII. Inflammatory Bowel Disease

Ulcerative Colitis Crohn’s Disease
Etiology and Pathogenesis Genetic
• Predisposing genes identified: chromosomes 16q, 12p, 5q, 19p, 1p, 16p, 3p, 10q, 1p, 2q, 5p
• Families: First degree relative- 10%; 2 parents- 36%
• Other genetic syndromes associated with IBD: Turner’s syndrome, Hermansky- Pudlak, Glycogen
storage disease type IB, Hypergammaglobulinemia, Selective IgA deficiency, Hereditary angioedema

Defective immune regulation

• The GI mucosal immune system is normally unreactive to luminal contents due to oral tolerance.
• Deletion or anergy of antigen reactive T-cell or activation of CD4+ T cells which suppress gut inflammation
thru secretion of inhibitory cytokines (IL10 and TGF-B)
• In IBD, CD4+ T cell activation causes secretion of inflammatory cytokines.
• Macrophages and B cells are also activated. Inflammatory leukocytes and mononuclear cells are also
recruited
Pattern of distribution Continuous Segmental
Involvement Symmetrical; mucosal and submucosal Asymmetrical; transmural
Involvement of rectum Involved Spared
Clinical Presentation Mild disease • Ileocolitis: RLQ pain, diarrhea, palpable mass,
• Rectal bleeding fever, leukocytosis, bowel obstruction, fistula
• Tenesmus formation
• Diarrhea • Jejunoileitis: malabsorption, steatorrhea,
• Passage of mucus diarrhea
• Abdominal pain • Colitis and perianal disease: incontinence,
hemorrhoids, anal strictures, anorectal fistulas,
Moderate to severe disease fever, diarrhea, hematochezia
• Anorexia • Gastroduodenal disease: nausea, vomiting,
• Nausea/vomiting epigastric pain, gastric outlet obstruction, fistulas
• Fever from small bowel
• Weight loss
Complications • Catastrophic illness: massive hemorrhage, toxic • Fistula
megacolon • Perforation
• Strictures • Intra-abdominal and pelvic abscess
• Intestinal obstruction
• Malabsorption
• Massive hemorrhage
• Severe peri-anal disease

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Diagnosis Biochemical
• Acute phase: elevated CRP, ESR, platelet count
• Albumin: decreased in severe disease
• Hemoglobin: decreased
• WBC: increased

Imaging
• Radiography: barium enema, small intestinal series, enteroclysis
• Flexible endoscopy: colonoscopy
• Enteroscopy
• Wireless capsule endoscopy
• CT scan
ü UC: not as helpful as be or colonoscopy
CD: identification of abscesses

Treatment and Management of IBD

Therapy Action
5-ASA • Mainstay for mild-moderate UC
• UC: induction, maintenance of remission
• CD: induction, maintenance (?)
• Regulates NF-KB (n cadherin mucus glycoprotein)
• E.g. Sulfasalazine, mesalamine, olsalazine
Glucocorticoids • Induction of remission
• For moderate to severe UC and CD: Prednisone: 40-60 mg/d,
Budesonide
• No role for maintenance of remission
Antibiotics • UC: no role except for pouchitis
• CD: active, fistulous and perianal disease.
• Prevent recurrence after ileal resection
• Metronidazole
• Ciprofloxacin
Azathioprine/ 6 mercapturine • Inhibits immune response
• Steroid sparing agents
• Promising role for maintenance in UC and CD
• Patients treated with this have a 4x increase risk of lymphoma
Methotrexate • Decrease il-1 production
• For induction and maintenance of remission in CD.
Cyclosporine • Inhibit cellular and humoral immune system
• Blocks production of IL-2 by t helper cells
• Inhibits B cell function
• For those refractory to iv steroids
• For induction of remission
• No effect in maintenance if without azathioprine/6 MP.
Tacrolimus • Macrolide antibiotic
• For refractory IBD and those with extensive small bowel involvement
Anti-TNF • Infliximab
• Blocks TNF
• Lyses TNF producing macrophages and T cells.
• For induction and maintenance of remission in cd who are refractory
to steroids, 6 MP, or 5 ASA.
Nutritional therapy • Dietary antigens may stimulate immune response
• CD
ü Bowel rest and TPN
ü For induction of remission, not for maintenance
ü May decrease inflammation in CD
• UC: dietary intervention may not be helpful.
Other immunosuppressive • Thalidomide: inhibit TNF
agents • Adalimumab: binds TNF-alpha
• Certolizumab: anti TNF
Surgery Indications in ulcerative colitis
• Intractable disease
• Fulminant disease
• Toxic megacolon
• Colon perforation
• Massive colon hemorrhage
• Extracolonic disease

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• Colonic obstruction
• Colon cancer prophylaxis
• Colonic dysplasia or cancer

Indication in Crohn’s disease

• Small bowel
ü Stricture or obstruction unresponsive to medical therapy
ü Massive hemorrhage
ü Refractory fistula
ü Abscess
• Colon and rectum
ü Intractable disease
ü Fulminant disease
ü Perianal disease unresponsive to medical treatment
ü Refractory fistula
ü Colon obstruction
ü Colon cancer prophylaxis
ü Colon dysplasia or cancer

IX. Colorectal Cancer

Risk Factors Polyps Clinical Features Diagnosis Treatment Predictors of poor
outcome after
surgery
• High animal fat 1. Hamartomatous • Cecum and Average risk individuals • Surgery: total • Tumor spread
content, red (Juvenile): Non- ascending • Start at age 50 resection to regional
meat, Malignant colon: anemia, • Digital rectal exam • Radiotherapy: lymph nodes
processed meat 2. Hyperplastic palpitation, • Fecal occult blood pre- or post- • Number of
• Insulin Mucosal weakness testing operative; may regional lymph
resistance Proliferation Polyp: • Transverse • Flexible reduce nodes involved
• Dietary fiber Non- Malignant and proctosigmoidoscopy recurrence in • Tumor
• Hereditary 3. Adenomatous descending + DCBE rectal cancer penetration to
factors and Polyp: Potentially colon: • colonoscopy the bowel wall
syndromes Malignant obstruction and Chemotherapy • Poorly
• Inflammatory occasional Surveillance • 5-FU differentiated
bowel disease Probability of perforation • For high risk patients • Leucovorin histology
• Male gender becoming • Recto-sigmoid: • IBD, familial • Irinotecan • Perforation
• Obesity cancerous depends tenesmus, polyposis, family • Oxiplatin • Tumor
• Smoking on: narrowing stool history, history of • Monoclonal adherence to
• Physical activity A. Histologic type caliber, colorectal adenoma antibodies: different organs
• Villous -3X hematochezia or carcinoma Cetuximab, • Venous
higher than Panitumumab, invasion
tubular polyp Metastasis Bevacizumab • Pre-op elevation
Route of spread of CEA (>5.0
B. Size • Regional lymph ng/ml)
• <1.0 cm: nodes • Aneuploidy
negligible (<2%) • Liver • Specific
• 1.5-2.5 cm: • Lungs or chromosomal
intermediate (2- supraclavicular deletions (allelic
10%) lymph nodes via loss)
• >2.5 cm: paravertebral veins-
substantial distal rectal cancer
(>10%)

C. Gross
appearance: Sessile
> Pedunculated

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X. Colonic Diverticula
Type Clinical manifestations Evaluation Treatment and Management
Uncomplicated diverticulitis • Fever Plain abdominal films Medical
• Anorexia • Detect perforation: • Asymptomatic
• LLQ pain, tenderness pneumoperitoneum diverticulosis: dietary
• Obstipation • Bowel dilatation: ileus alteration
• Rectal exam: (+) tenderness • Soft tissue mass: abscess • Symptomatic
• Increased WBC ct. ü Bowel rest
CT scan ü Antibiotics- 7-10 days
• Thickening of the bowel wall ü TMP-SMX OR
• Inflammation within the peri ciprofloxacin +
colic fat metronidazole or
• Collection of contrast material Penicillin + clavulanic
or fluid acid

Colonoscopy/ barium enema Surgery

• Best deferred until after • For low risk patients with 2
resolution of inflammation à documented attacks of
After 6 weeks diverticulitis requiring
hospitalization
• For all low risk patients with
complicated diverticular
disease
Complicated diverticulitis • Generalized peritonitis:
• Abscess: 16%
• Perforation- 10%
• Stricture- 5%
• Fistula- 2%

Painful diverticular disease • Recurrent LLQ colicky pain Barium enema- diverticula without • Anti-spasmodics
without signs of diverticulitis without signs of diverticulitis evidence of Inflammation or • After recovery- high fiber diet
• May be relieved by defecation stricture (+) “saw tooth” • Surgery is not indicated
or passage of flatus Irregularity of the lumen reflecting
• Alternate constipation and muscle hypertrophy and spasm
diarrhea
Bleeding diverticulitis • Most common cause of Mild to moderate bleeding
painless bleeding in patients • Bed rest and blood
>60 years transfusion
• 20% of patients with • May stop spontaneously. (70-
diverticula 80%)
• Most frequently seen in right • May recur. (22-38%)
colon
• Risk factors: hypertension, Moderate to severe bleeding
atherosclerosis, NSAID use • Colonoscopic therapy
• Injection hemostasis
• Heater probe
• Hemostatic clips
• Bipolar probe
• Band ligation
• Fibrin sealant
• Angiographic treatment
embolization

Surgery
• After localization

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Summarized Notes

XI. Irritable Bowel Syndrome

Risk Factors Clinical Manifestations Pathophysiology Diagnosis Management
• Bacterial • Abdominal pain or • Altered intestinal History • High fiber diet
gastroenteritis: discomfort motility • New onset > 50 years • Anti-spasmodics:
Campylobacter • Constipation and • Visceral • Weight loss anti-cholinergics for
• Affluent childhood diarrhea hypersensitivity • Blood in stool spastic pain
environment • Bloating and • Abnormal gas • Fever • Laxatives
• Post-menopausal abdominal distention propulsion and • Night time symptoms ü Osmotic: can
estrogen use • Non-colonic expulsion • Persistent diarrhea aggravate
• Recent antibiotic use symptoms: • Involuntary • Severe chronic bloating and pain
• Food intolerance dyspepsia, headache, suppression of constipation ü Stimulant: can
• Extraintestinal backache, impaired muscle contraction • Recurrent vomiting aggravate
somatic symptoms sleep, fatigue, • Local inflammation • Progressive crampy
increased urinary • Food intolerance and dysphagia abdominal pain
frequency and allergy • Travel history to • Anti-diarrheals
urgency dyspareunia, • Abnormal colonic flora locations with (Loperamide):
anxiety, depression, and bacterial endemic parasitic increase segmenting
fibromyalgia overgrowth diseases colonic contractions,
• Supportive but not • Central dysregulation • Family history of delays fecal transit,
diagnostic: straining • Psychologic factors CRC, IBD or celiac increase anal
during defecation, • Genetics sprue pressures, decrease
urgency, feeling of rectal perception
incomplete Physical exam • Anti-depressants
evacuation, passage • Occult or overt blood ü Tri-cyclic
of mucus, bloating on rectal exam antidepressants
(Desipramine):
• Signs of anemia
slows jejunal
• Abdominal mass
migratory motor
• Signs of bowel complex,
obstruction relieves
• Signs of abdominal pain
malabsorption ü Selective
• Signs of thyroid serotonin
dysfunction reuptake
• Arthritis (active) inhibitors
• Dermatitis (Paroxetine):
herpetiformis or accelerates oro-
pyoderma cecal transit
gangrenosum • Others: citalopram,
mianserin
Laboratory features not • Serotonin receptor
compatible with IBS antagonist
• Anemia • Serotonin type 4
• Increased ESR receptor agonist
• Stool with WBC or (Tegaserod)
blood • Antilatulent therapy
• Stool volume > 200- • Chloride channel
300 ml/day activators
(Lubiprostone)
• Psychological therapy

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Summarized Notes

XII. Upper Gastrointestinal Tract Tumor

Tumor Clinical Features Etiology Diagnosis Management and
Treatment
Esophageal cancer • Squamous cell • Chronic gastric reflux • Barium swallow: • Pre-operative
carcinoma: upper (Barrett’s esophagus) ragged, ulcerating combination
and middle part • Aneuploidy and p53 changes in the chemotherapy and
• Adenocarcinoma: mutations mucosa radiation therapy
lower part • Endoscopy • Surgical resection
• Dysphagia usually • Biopsy: histologic • Palliative
present at the late confirmation
stage of the disease • CT scan: staging
• Difficulty in • Endoscopic
swallowing does not ultrasound: for
occur until >60% of staging
the esophageal
circumference is
infiltrated with cancer.
• Odynophagia, chest
pain, regurgitation,
vomiting, aspiration,
weight loss
• Hypercalcemia for
squamous cell
(parathormonerelated
peptide secreting
tumor cells)
Gastric cancer • Diffuse type: linnitis • Nitrate-containing • Barium study: difficult 1. Complete surgical
plastic or leather food to assess if the ulcer removal of tumor with
bottle appearance • H. pylori is benign or malignant resection of
• Intestinal type: • Menetrier’s disease • Endoscopy with adjacent lymph nodes
cohesive neoplastic • Atrophic gastritis and biopsy: preferred -> possible only in less than
cells that form pernicious anemia diagnostic test third of patients
glandular tubular • Blood type A • Chest X-ray, CT 2. Tumor is radioresistant
structures • Genetics scan: assess extent and chemotherapy alone is
of disease associated with partial
Manifestations • Endoscopic response only
• Early satiety, ultrasound: more 3. Combination
dysphagia, upper accurate in staging chemotherapy prior to
abdominal pain, the diseases than CT surgery + complete
anorexia, nausea, scan surgical resection of tumor +
vomiting post-surgery chemotherapy
• Weight loss and
• IDA, GI bleeding radiation therapy
• Palpable lymph nodes (recommended)
• Palpable mass at the -> reduces recurrence rate
late stage of the and prolonged survival
disease 4. Best form of palliation is
reduction of tumor bulk.
• Unusual: acanthosis
nigricans, migratory
thrombophlebitis,
microangiopathic
hemolytic anemia
Primary gastric Histologically, these • Complete blood • Antibiotic treatment to
lymphoma tumors may range from count; erythrocyte eradicate H. pylori
well-differentiated, sedimentation rate; infection leads to
superficial processes • Chemistry studies regression of about
[mucosa-associated reflecting major organ 75% of gastric MALT
lymphoid tissue function lymphomas.
(MALT)] to high-grade, • CT scans of the • Subtotal gastrectomy
large-cell lymphomas chest, abdomen, and followed by
Most common type of pelvis; and a bone combination
gastric lymphoma is non- marrow biopsy chemotherapy
Hodgkin’s and are of B cell • Waldeyer’s ring is • Chemotherapy: R +
in origin often involved (CHOP) Rituximab +
• Include LDH for NHL cyclosphosphamide,
Symptomatically similar • Diagnosis is by doxuribicin
with gastric endoscopy and (Hydroxydaunomycin),
adenocarcinoma biopsy

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Summarized Notes

Characterized by • Staging: Ann-Arbor vincristine (Oncovin)

ulcerations and ragged, for NHL: International and prednisone
thickened gastric folds Prognostic Index • Better survival rate and
on barium swallow and far more treatable
endoscopy disease than
Infection with H. pylori gastricadenocarcinoma
bacteria increased the risk
MALT (mucosa-associated
lymphoid tissue) lymphoma
is caused by H. pylori
infection
Gastric sarcoma
Leiomyosarcoma • Tumor arising from Surgical resection
the mesenchymal cell
(smooth muscle cell)
• Make up 1-3% of
gastric malignancies
• Most frequently
involve the anterior
and posterior walls of
the gastric fundus
• Ulcer as an
endoscopic finding
• Rarely invade
adjacent organs and
characteristically do
not metastasize to
lymph nodes but to
the lungs and liver.

Gastrointestinal stromal • Express the growth Endoscopic ultrasound • Targeted medical

tumor factor receptor c-KIT determines depth of tumor therapy targets faulty
protein or CD-117 invasion as well as genes or proteins
• 70% of GIST in the GI regional lymph node that contribute to
tract occurs in the involvement cancer growth and
stomach development
• Indolent and slow • Imitanib mesylate
growing (Glivec), a tyrosine-
• Wide spectrum of kinase inhibitor (drug
clinical outcome, can of choice)
be benign to • Sunitinib (Sutent),
malignant like imatinib, is a
tyrosine kinase
inhibitor with
antiangiogenic (a
form of targeted
therapy that stops
tumors from creating
new blood vessels)
properties

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Summarized Notes

XIII. Gastritis and other related diseases

Types Clinical Manifestations Diagnosis Treatment
Acute • Sudden onset of epigastric
pain, nausea, vomiting
• Mucosal histologic studies
demonstrate a marked
infiltrate of neutrophils with
edema and hyperemia.
• If not treated à chronic
gastritis
• Hypochlorhydria lasting for up
to 1 year may follow acute H.
pylori infection
Chronic • Identified histologically by an
inflammatory cell consisting
of lymphocytes and plasma
cell with scanty neutrophil
• Patchy, superficial and
glandular inflammation à
severe glandular destruction,
atrophy and metaplasia
• Intestinal metaplasia:
conversion of gastric glands
into a small intestinal
phenotype with small bowel
mucosal glands containing
goblet cells
Type A (autoimmune) • Involves primarily the fundus • Patients with pernicious
and body, with antral sparing anemia will require parenteral
• Associated with Pernicious • Vitamin B12 supplementation
anemia in the presence of on a long-term basis (For
circulating antibodies against type A)
parietal cell and Intrinsic • Eradication of H. pylori
factor infection (For type B)
• Parietal cell containing gastric
gland is the preferential target
• Destruction of parietal cell à
decrease Intrinsic Factor à
Vitamin B 12 (Cobalamin)
deficiency
• Vitamin B 12 deficiency
(megaloblastic anemia,
neurologic dysfunction)
Type B • Antral-predominant
• More common than Type A
Gastritis
• H. pylori infection
• Converts to pangastritis over
time
• Risk for gastric
adenocarcinoma due to
metaplasia brought about by
chronic H. pylori induced
gastritis
• H. pylori infection is also
associated with low-grade B
cell lymphoma (gastric MALT
lymphoma)
Zollinger-Ellison syndrome • Gastric acid hypersecretion • Elevated fasting gastrin level • Ameliorating signs and
due to unregulated gastrin (>150-200 pg/mL) symptoms related to hormone
release from a non-B cell • Elevated acid secretion overproduction
endocrine tumor measurement (BAO/MAO ü High dose proton pump
(Gastrinoma) >0.6) inhibitor
• Gastrinomas are classified as • Secretin test ü Somatostatin analogue
sporadic tumor or associated • Endoscopic ultrasound: most (Octreotide) as adjunct
with sensitive
• Multiple Endocrine Neoplasia
(MEN) type 1 syndrome

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• Results into aggressive and • Definitive cure

refractory ulceration ü Surgical resection
• More common in male than led to immediate
female cure rates as high
• Majority are diagnosed 30-50 as 60%
years old to 1.0% incidence
with individuals presenting
with PUD
• Mostly malignant (>60%) and
30-50 % have mutiple or
metastatic lesion upon
diagnosis
Stress-related mucosal injury • Mucosal ischemia (due to Proton pump inhibitor
hypotension)
• Breakdown of normal
protective barriers of stomach
• Acid
• Curling’s ulcer: severe burn
• Cushing’s ulcer: head
trauma
Lymphocytic gastritis • Characterized histologically
by intense infiltration of the
surface epithelium with
lymphocytes
• Infiltrative process is primarily
in the body of the stomach
and consists of mature T cells
and plasmacytes.
• A subgroup of patients has
thickened folds noted on
• endoscopy
• These folds are often capped
by small nodules that contain
a central depression or
erosion; this form of the
disease is called varioliform
gastritis.
Eosinophilic gastritis • Marked eosinophilic Antral involvement predominates, Glucocorticoids
infiltration involving any layer with prominent
of the stomach (mucosa, edematous folds being observed
muscularis propria, and on endoscopy
serosa)
• Clinical manifestation of
systemic allergy
• Affected individuals will often
have circulating eosinophilia
• Prominent antral folds can
lead to outlet obstruction
Granulomatous gastritis • Crohn's disease (TB can also
be involved)
• Involvement may range from
granulomatous infiltrates
noted only on gastric biopsies
to frank ulceration and
stricture formation.
• Occurs in the presence of
small-intestinal disease.

Menetrier’s disease • Characterized by large, Large gastric folds on barium Medical Treatment
tortuous gastric mucosal folds swallow and endoscopy (do • Anticholinergics decrease
mostly in the fundus and body biopsy) protein loss
• Histologically, massive • High protein diet
foveolar hyperplasia • Ulcers should be treated with
(hyperplasia of surface and a standard approach
glandular mucous cells) is
noted which replaces most of Surgical
the chief cell and parietal cell Severe disease with persistent and
substantial protein loss

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Summarized Notes

• Over expression of growth may require total gastrectomy

factors such as TGF may be
involved in the process

XIV. Upper gastrointestinal bleeding

• Overt bleeding
ü Melena: black, tarry, foul-smelling stool at least 50 mL of blood
ü Hematemesis: vomitus of red blood or coffee-ground material
ü Hematochezia: reddish blood from rectum
• Occult bleeding: identified in the absence of overt bleeding by fecal occult blood or presence of IDA
• Work-up: assess the hemodynamic stability/ severity of bleeding à resuscitate à identify the cause

Management on other causes of upper GI bleed

Gastroduodenal erosions (involves the PPI
muscularis mucosa/subepithelial level
that is mostly caused by NSAID use)
Mallory-Weiss tear (tear at the GE Supportive: if bleeding stops
junction caused by forceful retching) Endoscopic: if with bleeding
Esophageal erosion and ulcer High dose PPI for reflux esophagitis
Endoscopic treatment for ulcers
Esophageal/gastric/duodenal malignancy Palliative: endoscopic therapy
Definite: surgical resection of tumor
Vascular ectasia (dilatation of blood Endoscopic treatment: argon plasma
vessels) coagulation
Gastric antral vascular ectasia (GAVE) Endoscopic treatment: argon plasma
coagulation
If bleeding is uncontrolled: antrectomy
Dieulafoy lesion (abnormally large Hemoclip application, band ligation, injection
arteriole that retains the large caliber of sclerotherapy
its feeding vessel as it approaches the
mucosa à compresses the mucosa à
small erosion and rupture)

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Summarized Notes

XV. Diseases of the Esophagus

Symptoms: dysphagia, odynophagia, globus sensation, heart burn/pyrosis, regurgitation, water brash, chest pain

Congenital anomalies Manifestations

Esophageal atresia • Most common (1 in 5000 live births)
• Developmental failure of fusion between the proximal and distal esophagus
• Most commonly associated with distal tracheoesophageal fistula corrected surgically within the
first few days of life
• later life complications include dysphagia from anastomotic strictures or absent peristalsis and
severe reflux à post-surgery
Fistula • Open tract between 2 epithelia
• Lined organs or vessels that normally do not connect
• Failure of the lung bud to separate completely from the foregut
Dysphagia lusoria The esophagus is compressed by an aberrant right subclavian artery arising from the descending aorta
and passing behind the esophagus
Heterotropic gastric mucosa • Focus of gastric type epithelium in the proximal cervical esophagus
• The estimated prevalence is 4.5%
• Inlet patch is thought to result from incomplete replacement of embryonic columnar epithelium with
squamous epithelium
• Majority of patches are asymptomatic, but acid production can occur as most contain fundic type
gastric epithelium with parietal cells
Esophageal webs • Congenital or inflammatory in origin
• Characterized by one or more thin horizontal membranes of stratified squamous epithelium
• Located within the upper (common) and mid esophagus (rare)
• Rarely encircle the lumen completely (protrudes from the anterior wall, extending laterally but not
posteriorly)
• Asymptomatic hypopharyngeal webs are demonstrated in
• 10% of normal individuals
• Primary symptom is dysphagia
• Hypopharyngeal webs + iron-deficiency anemia + dysphagia = Plummer-Vinson or Patterson Kelly
syndrome
• Risk factor for squamous cell carcinoma of the esophagus
• Treatment is bougienage or dilatation

Motility Disorder Clinical Features Pathophysiology Diagnosis Management and

Treatment
Achalasia • Affects all ages and • Loss of ganglion cell • Chest X-ray: tubular Medical
sexes within the myenteric mediastinal mass • Nitrates: isosorbide
• Early dysphagia on plexus bedside the aorta; dinitrate (2.5-5
both liquid and solids • Involves both absence of the gastric sublingually or per
• Dysphagia worsen by excitatory air bubble orem) before meal
emotional stress and (cholinergic) and • Barium swallow • Calcium channel
hurried eating inhibitory (nitric oxide) (diagnostic tool of blocker: nifedipine
• Course is usually ganglionic neurons. choice): bird beak (20-30 mg 5L) before
chronic, with • Inhibitory neurons like narrowing at the meal
progressive mediate deglutitive terminal esophagus • Sildenafil
dysphagia andweight lower esophageal • High resolution
loss over months to sphincter (LES) manometry: most Endoscopic
years relaxation and sensitive test • Botulinum toxin
• Relieved by increased sequential • Endoscopy: for ruling • Pneumatic balloon
intraesophageal propagation of out secondary causes dilatation
pressure (i.e., peristalsis. of achalasia • Per Orem Esophageal
Valsalva maneuver, particularly gastric myomotomy
raising the shoulder carcinoma
during swallowing) Surgical
• Regurgitation and • Heller’s extra mucosal
pulmonary aspiration myotomy of LES
• Acid reflux symptom • Laparoscopic
(heart burn) is against myotomy of LES
Achalasia
Durable therapies
• Pneumatic dilatation
• Myotomy
Esophageal spasm Chest pain that mimics • Episodes of • Barium swallow: • Nitrates, Ca channel
angina pectoris dysphagia and chest Corkscrew, Rosary blocker, Botolinium
pain attributable to Beads, toxin,

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• Abnormal esophageal Pseudiverticula or • Anxiolytic (only with

contractions with Curling controlled trial
normal deglutitive • Manometry: showing efficacy)
• LES relaxation diagnostic • Long myotomy or
• Dysfunction of • Endoscopy: to rule even esophagectomy
inhibitory nerves structural or (should be considered
inflammatory lesion only with severe
weight loss or
unbearable pain)

Gastroesophageal Reflux Clinical Features Pathophysiology Diagnosis Management and

Disease Treatment
GERD Heart burn or pyrosis (may Transient LES relaxation History alone Medical
radiate to the sides of the (vasovagal reflex) 2. Therapeutic trial (PPI for 2 1. Lifestyle modification -
chest, o 90% in non-hiatal hernia weeks with 50% decrease in weight reduction, head of bed
neck, angles of jaw). case sx) elevated about 4-6 inches,
Aggravated by bending 2. LES hypotension 3. Endoscopy elimination of factors that
forward, 3. Anatomic distortion of EG 4. Mucosal biopsy increase abdominal pressure -
straining, or lying recumbent junction (hiatal hernia) 5. pH monitoring avoid smoking, fatty foods,
and worse after meal. 6. Bernstein test/Acid perfusion coffee, chocolate, alcohol,
Regurgitation of sour/bitter test mints, citrus fruits, too sweets,
material in the mouth 7. Barium swallow medications that relaxes
Angina-like or atypical chest smooth muscle - avoid lying
pain down
Dysphagia/Choking-like after eating; should eat 4 hours
sensation before lying down
Extraesophageal 2. Medication
manifestation o antacid
o chronic cough, laryngitis, o H2 receptor blocker
pharyngitis, morning (Ranitidine, Famotidine,
hoarseness, dental decay, Cimetidine,
sinusitis Nizatidine)
Recurrent reflux may cause: o Proton-pump inhibitor *
o Asthma, chronic obstructive (Omeprazole, Rabeprazole,
pulmonary disease, Pantoprazole, Esomeprazole,
bronchitis, pneumonia, Lansoprazole,
pulmonary fibrosis Deslanzoprazole)
3. Antireflux surgery for Hiatal
Hernia
o Nissen fundoplication (gastric
fundus is wrapped around
the lower esophagus)
Barrett’s esophagus Metaplasia of esophageal Diagnosed through endoscopy Treatment:
squamous epithelium to and biopsy High grade dysplasia
specialized columnar Salmon colored mucosa esophagectomy, endoscopic
epithelium extending proximally from the mucosal resection,
Specialized metaplastic GE photodynamic therapy
columnar epithelium junction or histologically. No dysplasia and Low grade
dysplasia monitor through
follow-up endoscopy
o 3-5 years for no dysplasia
and yearly for low grade
dysplasia

Structural Disorder Clinical Features Pathophysiology Diagnosis Management and

Treatment
Hiatal hernia Type I or sliding hiatal 1. Transient LES relaxation 1. History alone Medical
hernia (vasovagal reflex) 2. Therapeutic trial (PPI for 1. Lifestyle modification -
• Comprising at least 90% in non-hiatal hernia 2 weeks with 50% weight reduction, head of
95% of the overall case decrease in symptoms) bed elevated about 4-6
total 2. LES hypotension 3. Endoscopy inches, elimination of
• Gastroesophageal 3. Anatomic distortion of 4. Mucosal biopsy factors that increase
junction and gastric EG junction (hiatal hernia) 5. pH monitoring abdominal pressure - avoid
cardia slide upward 6. Bernstein test/Acid smoking, fatty foods,
as a result of perfusion test coffee, chocolate, alcohol,
weakening of the 7. Barium swallow mints, citrus fruits, too
phrenoesophageal sweets, medications that
ligament attaching the relaxes smooth muscle -
gastroesophageal avoid lying down
junction to the after eating; should eat 4
hours before lying down

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Summarized Notes

diaphragm at the 2. Medication

hiatus • Antacid
• Enlarge with • H2 receptor blocker
increased (Ranitidine,
intraabdominal Famotidine,
pressure, swallowing, Cimetidine,
and respiration. • Nizatidine)
• Proton-pump inhibitor
Type II: astric fundus * (Omeprazole,
herniates and the Rabeprazole,
gastroesophageal junction • Pantoprazole,
remains fixed at the hiatus, Esomeprazole,
Lansoprazole,
Type III: mixed • Deslanzoprazole)
sliding/paraesophageal
hernia. 3. Antireflux surgery for
• The stomach inverts Hiatal Hernia
as it herniates and Nissen fundoplication
large paraesophageal (gastric fundus is wrapped
hernias can lead to an around
upside-down the lower esophagus)
stomach, gastric
volvulus, and even
strangulation of the
stomach.
• Surgical repair is
often advocated for
large paraesophageal
hernias

Type IV hiatal hernias

• Viscera other than the
stomach herniates
into the mediastinum,
most commonly the
colon
Esophageal rings A Ring (muscular)
• Symmetrical band of
hypertrophied muscle
that constricts the
tubular esophageal
lumen
• Located roughly 2 cm
proximal to the
squamocolumnar
junction
• Consist of three
layers: mucosa,
submucosa, and
muscularis propria
• Rare
• Covered by
squamous cell
epithelium
• Dysphagia to solid
and liquid
• Bougienage/dilatation
or botulinium toxin
injection

B Ring - Schatzki Ring

• Common
• Acquired
• Thin membrane that
constricts the
esophageal lumen
located at the
squamocolumnar
junction

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Summarized Notes

• Consist of squamous
epithelium on its
upper surface and
columnar epithelium
on its lower surface
(demarcates the
squamocolumnar
junction)
• Always associated
with Hiatal hernia
• Composed of mucosa
and submucosa
• Mostly asymptomatic
• Intermittent dysphagia
• Steakhouse
syndrome
• Diagnosed by
esophagogram or
endoscopy
• No treatment required
if asymptomatic
• Bougienage/balloon
dilatation
Esophageal diverticula • Outpouchings from
tubular structures.
• True diverticula:
involves the whole
layer of the GIT wall
(congenital lesions)
• False(Pseudo)
diverticula: involves
the mucosa and
submucosa only
through the muscular
wall (acquired lesions)
Zenker’s diverticulum Dysphagia, regurgitation, • Acquired (false Barium swallow • Surgical
choking, aspiration, voice diverticula) diverticulectomy and
changes, • Result from increased cricopharyngeal
halitosis, weight loss intraluminal pressure myotomy for large
associated with distal diverticula (> 5cm)
obstruction • Marsupialization
• Obstruction is a procedure in which an
stenotic endoscopic stapling
cricopharyngeus device is used to
muscle divide the
• Hypopharyngeal cricopharyngeus for
herniation medium sized (2-5
• Most commonly cm)
occurs in an area of
natural weakness
known as Killian's
triangle
Midesophageal • May be caused by
diverticulum traction from adjacent
inflammation
(classically
tuberculosis)
• May be caused by
pulsion associated
with esophageal
motor disorders
• True diverticula
involving all layers of
the esophageal wall
Epiphrenic diverticulum • False diverticula
• Usually associated
with achalasia or a

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Summarized Notes

distal esophageal
stricture
• Small or medium-
sized diverticula,
midesophageal and
epiphrenic diverticula
are usually
asymptomatic
Diffuse intramural • Rare entity that
esophageal results from dilatation
diverticulosis of the excretory ducts
of submucosal
esophageal glands
• Esophageal
candidiasis and
proximal esophageal
strictures are
commonly found in
association with this
disorder
Esophageal cancer • The typical
presentation is
progressive solid food
dysphagia and weight
loss
• Poor survival even if
detected as a small
lesion, because of
• The abundant
esophageal
lymphatics leading to
regional lymph node
metastases
Benign esophageal • Cell types (in
tumors decreasing order of
occurrence):
leiomyomas (most
common),
fibrovascular polyps,
squamous
papillomas, granular
cell, lipomas,
neurofibromas, and
inflammatory fibroid
polyps
• Symptomatic only
when they are
associated with
dysphagia and merit
removal only under
the same
circumstances

Eosinophilic esophagitis Clinical features Pathophysiology Diagnosis Treatment

Eosinophilic Esophagitis Food impaction and Atopic history of food • Peripheral • Characteristic
dysphagia allergy, asthma, eczema, eosinophilia is seen in endoscopic findings
or allergic rhinitis is present >50% of the patients. include loss of
in the majority of patients. • Cytokines such as IL- vascular markings
5, eotaxin, and (edema), multiple
thymus and esophageal rings,
activation-related linear furrows, and
chemokine (TARC) punctate exudates
may be elevated in • Histologic
the serum confirmation is made
with the
demonstration of
increased eosinophils
in the esophagal
mucosa (> 15

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Summarized Notes

eosinophils per high-

power field)
• Fibrosis, narrow
caliber esophagus,
and stricture can
occur with EoE

Infectious esophagitis Clinical features Pathophysiology Diagnosis Treatment

Esophageal candidiasis • Candida albicans Atopic history of food • Histologic (PAS or • Oral fluconazole (200
st
• Can occur with allergy, asthma, eczema, Gomori silver stains) mg 1 day then 100
esophageal stasis or allergic rhinitis is present • KOH smear mg daily for 7-14
secondary to in the majority of patients. • Upper endoscopy days)
esophageal motor findings • Others: itraconazole,
disorders and ü Mild diseases: IV anti-fungal
diverticula endoscopically (echinocandin,
• Oral thrush shows small, Amphotericin B)
yellow-white
raised plaques
with surrounding
erythema
ü Extensive
disease:
confluent linear
and nodular
plaques
Herpetic esophagitis Self-limited after 1-2 week • HSV 1 and 2: vesicles • Endoscopy: vesicles 1. Immunocompletent:
period on the nose and lips and small, discrete, Acyclovir (200 mg orally 5
• VZV: children and punch-out (volcano- times a day for 7
adults like) days10 days)
ü Early stage:
superficial 2. Immunocompromised
ulceration with or patients: Acyclovir (400mg
without a fibrous orally 5 x day for
exudate 14-21 days), Famciclovir
ü Late stage: (SOOmg OD TID),
enlargement and Valacvcolvir (1 gm TID)
coalescence of
ulcers 3. Severe odynophagia:
• Biopsy: ground-glass Acyclovir IV, 5mg/kg q8 -7-
nuclei, eosinophilic 14 days
Cowdry’s type A
inclusion bodies and
giant cells
• PCR
Cytomegalovirus Latent stage or may be • Endoscopy: • Ganciclovir, 5 mg/kg
acquired from transfusions serpiginous ulcers in every 12 h IV
the distal esophagus • Valaciclovir
• Biopsy: large nuclear
or cytoplasmic
inclusion bodies
• Immunohistology:
early diagnosis
Bacterial Occurs in
immunocompromised
patients: B-hemolytic
streptococci, Lactobacillus,
Mycobacterium
tuberculosis

Mechanical tear Clinical features Pathophysiology Diagnosis Treatment

Mallory-Weiss tear • Upper GI bleed • Caused by vomiting, • Endoscopy • Surgery is rarely
retching or vigorous needed
retching
• Involves the Z-line
Esophageal rupture • Severe retrosternal • Iatrogenic damage • CT scan • Esophageal and
chest pain • Tumors gastric suction and
• Subcutaneous chest • Boerhave’s syndrome parenteral antibiotics
pain • Surgical repair

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Summarized Notes

• Tactile and • Endoscopic clipping

auscultatory crepitus
• Pneumothorax
Radiation esophagitis • Dysphagia • Complication in • • Esophageal dilatation
• Odynophagia treatment of thoracic
• Esophageal mucosa cancers
becomes
erythematous,
edematous, and
triable
• Submucosal fibrosis
and degenerative
tissue and stricturing
Corrosive esophagitis Acid • Stricture requires
• HCl (toilet bowl esophageal dilatation
cleaner, metal • Extensive corrosive
cleaner, pool cleaner, damage requires
(antirust) sulfuric acid esophageal diversion
(battery fluids) and excision of
• Causes immediate damage portion
pain hence expelled
rapidly
• Coagulation
necrosis
• Limited penetration
and injury to
esophagus

Alkali
• Lye (strong alkali)
• Bleaching products,
button batteries, drain
cleaners, dish
washing detergents
• Usually odorless and
tasteless hence may
be swallowed
• Before protective
reactions are invoked
• Liquefaction
necrosis
• Can penetrate the
whole thickness of the
esophageal wall
Pill-induced esophagitis • Sudden chest pain • Doxycycline, • Anti-secretory agents
• Odynophagia tetracycline, quinidine,
• Most common site: phenytoin, potassium
mid-esophagus chloride, ferrous
sulfate, NSAIDs,
biphosphonates
Esophageal ring body • Chest pain • Food impaction may • Can be removed
be due to stricture, endoscopically
carcinoma, Schatzki
ring, eosinophilic
esophagitis, or eating

Esophageal Clinical features Pathophysiology Diagnosis Treatment

manifestation of
systemic disease
Scleroderma esophagus • Reflux symptom • Atrophy and fibrosis • Barium swallow • Dietary adjustments
• Dysphagia of smooth muscle • Manometry:
region of the aperistalsis of the
esophagus smooth muscle region
• CREST syndrome: and hypotension of
calcinosis, Raynaud’s LES
phenomenon,
esophageal
dysfunction,

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Summarized Notes

sclerodactyly,
telangiectasia)
• End results is
hypomotility
Dermatologic diseases • Blisters • Pemphigus vulgaris • • Glucocorticoid
• Bullae • Bullous pemphigoid • Esophageal
• Webs • Cicatricial pemphigoid dilatation: treat
• Strictures • Behçet's syndrome strictures
• Epidermolysis bullosa

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Summarized Notes

HEMATOLOGY

Starting here, I will only include the type of disorder and its management based on the CPG. Haba ng hema actually at mahirap intindihin so
magrely na lang sa guidelines since doon umiikot mga tanong nina doc. I added some notes din sa TopNotch para madaling intindihin.

I. Approach to Anemia

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MODULE B (Endo, Pulmo, Neuro, Gastro, Hema)
Summarized Notes

II. Hypoproliferative anemia

III. Functional Impairment Anemia

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Summarized Notes

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Summarized Notes

III. Coagulation Disorders

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Summarized Notes

IV. Hematologic Malignancy

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