- Places fingers over the lower ribs on the left side
- Asks patient to take a deep breath
You:
- Percuss over the assistant's fingers
- Dullness indicates splenic enlargement crossing
the midline
Positive Nixon's sign suggests splenomegaly.
Edema is defined and its mechanism explained with reference to the Starling's forces. The causes of localized edema and anasarca discussed.
In history taking, the site and distribution of edema, its duration, association with pain, variability, systemic illness, drug intake, trauma, radiation discussed.
The local and systemic examination described. The approach to investigation including lab tests and imaging explained.
Finally, management is discussed in short.
Edema is defined and its mechanism explained with reference to the Starling's forces. The causes of localized edema and anasarca discussed.
In history taking, the site and distribution of edema, its duration, association with pain, variability, systemic illness, drug intake, trauma, radiation discussed.
The local and systemic examination described. The approach to investigation including lab tests and imaging explained.
Finally, management is discussed in short.
Explanation of what splenomegaly is in relation to its dimension deviation from normal spleen.Classification of splenomegaly according to it's size in adult and pediatric. The causes of splenomegaly along with the symptom that would manifest as a result of this anomaly. Lastly, diagnosis of splenomegaly
Explanation of what splenomegaly is in relation to its dimension deviation from normal spleen.Classification of splenomegaly according to it's size in adult and pediatric. The causes of splenomegaly along with the symptom that would manifest as a result of this anomaly. Lastly, diagnosis of splenomegaly
Hepatomegaly is the condition of having an enlarged liver. It is a non-specific medical sign having many causes, which can broadly be broken down into infection, direct toxicity, hepatic tumors, or metabolic disorder. Often, hepatomegaly will present as an abdominal mass. Depending on the cause, it may sometimes present along with jaundice.
Causes of Splenomegaly By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Assoc...Prof Dr Bashir Ahmed Dar
Dr.Bashir Ahmed Dar Chinkipora Sopore Kashmir India,Associate Prof of medicine presently working in malaysia is a keen teacher, educator and takes pride in his clinical and research accomplishments. His interests include publishing articles related to health issues.Email drbashir123@gmail.com
Massive Splenomegaly By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Associa...Prof Dr Bashir Ahmed Dar
Dr.Bashir Ahmed Dar Chinkipora Sopore Kashmir India,Associate Prof of medicine presently working in malaysia is a keen teacher, educator and takes pride in his clinical and research accomplishments. His interests include publishing articles related to health issues.Email drbashir123@gmail.com
Bile or liver problem causing yellowness
• A yellow discoloration of the skin, mucous membranes, or sclera of the eyes, jaundice indicates excessive levels of conjugated or unconjugated bilirubin in the blood.
• In fair-skinned patients, it’s most noticeable on the face, trunk, and sclera; in dark-skinned patients, on the hard palate, sclera, and conjunctiva.
Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
2. HEPATOMEGALY:
• Enlargement of liver is called hepatomegaly.
• Presence of a palpable liver does not always
represent hepatomegaly .
May be mistaken for
• displacement of the liver by lung pathologies.
• abdominal tumor
• spinal deformity
3. • The normal range for liver span at
–1 week of age - 4.5 to 5 cm.
–At 5 yrs of age- 6 to 8 cms
–12 years, boys - 7 to 9 cm
girls - 6 to 8cm
Procedure:
4. Surface markings :
Upper border:4 th ICS in MCL
Lower border:9 th ICS in MCL
Lateral border:6 th rib in MAL
10. 5, Tenderness:
is seen in acute enlargement of liver due to
stretching of Glisson’s capsule.
in c/o cirrhosis or malignancy it will be tender
when capsule is infiltrated .
localised tenderness is seen in c/o
abscess/infected cyst.
20. Abdomen E/o:
– Firm consistency liver with sharp edge - Cirrhosis,
constrictive pericarditis
– Just palpable soft spleen - Enteric fever, infective
endocarditis, etc.
– Ascites - Suggests cirrhosis with portal hypertension,
malignancy, TB
21. HISTORY:
• Age at onset
• Sex
• Fever, jaundice
• Acute illness, dyspnea, fatigue, diarrhea, vomiting
• Signs of malignancy- proptosis, subcutaneous nodules
• Travel history – endemic diseases
• Developmental milestones
• Nutrition history (neonatal formula)
• Medical history: umbilical catheter, weight loss, failure to
thrive, bleeding, bruising, Pruritis, pallor, heart disease ,
rashes, joint pain.
• Family history: Early cholecystectomy, gallstones, anemias,
ethnic heritage, liver disease, maternal HBV, HCV
22. Age
• Neonates and first few months of life - e.g.
Haemolytic anaemias (Thalassaemia major),
storage disorders
• Any age - Malaria, kala azar, sepsis, enteric
fever, etc.
29. TREATMENT STRATEGIES
• Therapy is directed at treatment of underlying disease
• Infections
–Consider interferon for hepatitis B
–Consider interferon and ribavarin for hepatitis C
• Metabolic disease
–Metabolism consultation
–Often requires specific restricted formulas
• Cholestasis
–Ursodeoxycholic acid
–Supplemental fat soluble vitamins A, D, E, K
30. •Immune suppression for autoimmune hepatitis
•Chemotherapy – Histiocytosis, leukemia, lymphoma
•Surgical treatment
•Kasai portoenterostomy for biliary atresia has better
outcome if done before 60 days of age
31. CASE HISTORY
• A three years old first order female
child
• Born out of 2nd degree consanguineous
marriage
32. presented with chief complaint of
• Distension of abdomen since 4months of age.
• No h/o:
– Jaundice, edema
– Change in bowel pattern , weight loss
• Past h/o:at 4 months of age child developed
convulsions-
fever
34. • Development history :
–Sat without support at the age of 1 year
–Walked unassisted at the age of 2 years
• On examination:
–Weight : 14 kg; Height: 84 cm (< 3rd
percentile)
–Doll like face, protuberant abdomen
–No pallor, cyanosis, clubbing,
lymphadenopathy, icterus
35. –P/A: huge hepatomegaly almost reaching
right lower quadrant; no splenomegaly
–CNS: Normal muscle tone and power,
normal deep tendon reflexes
–Other systems: NAD
–Fundus : NAD
36. • Attending paediatrician may have following
questions:
• Differential diagnosis?
• Is this is a routine chronic liver disease?
• Am I dealing with GSD or fatty oxidation
disorder where we get hypoglycaemia,
Hepatomegaly, and metabolic acidosis
37. • How will I explain acidosis?
• What is my diagnosis here?
• How should I investigate this case further?
38. APPROACH TO A CHILD WITH
HEPATOMEGALY
Let me examine him fully before I can say
that this person is dead !!
39. First be sure it is
hepatomegaly and
not a pushed down
liver !!!!
Always assess
Liver span
Consistency
Surface
40. APPROACH TO A CHILD WITH
HEPATOMEGALY
In this particular case one may just
consider SIZE of the liver which was
huge.
• Very limited causes of huge
hepatomegaly at this age.
• Most likely is some kind of storage
disorder; GSD, LSD or stretching a little
bit FAOD.
41. APPROACH TO A CHILD WITH
HEPATOMEGALY
• Presence of hypoglycemia and severe
metabolic acidosis will further reduce
the differential diagnosis to GSD and
FAOD
42. APPROACH TO A CHILD WITH
HEPATOMEGALY
• On the other hand, if size of the liver is
moderate or mild, differential diagnoses
could be altogether different.
• Since there could be many causes to
consider; good history and physical
examinaton are very essential
43. –Keep in mind that Wilson’s disease
could have an acute presentation.
–Chronic liver disease may have acute
decompensation
44. RULE OF THUMB ???
• Huge hepatomegaly with preserved liver
functions suggests
–storage disorder; at any age; or
–Reticuloendothelial hyperplasia
45. INVESTIGATIONS
• Remember!!
• Good history, aided by meticulous
examination will give clue to the
underlying cause, more than any single
investigation
Let me see if I can
find out what is
wrong with you!!
46. Liver biopsy showing mosaic
pattern, prominent cell
membranes and nuclear
hyperglycogenation (HE stain);
Distended hepatocytes without
fibrosis
49. SPLEENOMEGALY
• It refers to enlargement of spleen beyond its normal
size.
• A spleen is said to be significantly enlarged if it is
palpable atleast 1cm below costal margin in a child
more than 6months of age.
• In 30% of newborns & 15% of infants <6months
palpable spleen is a normal variant.
50. Anatomy
• It lies within the left upper quadrant of the
peritoneal cavity.
• Abuts ribs 9-11, the stomach, the left kidney, the
splenic flexure of the colon, and the tail of the
pancreas.
51. Anatomy
• Normal Spleen
• Autopsy: <250g.
• Radioisotope Scintiscan: 12cm long x 7cm wide.
• Ultrasound: 11cm cephalocaudad diameter.
• ~3% of healthy people have splenomegaly.
52. Splenomegaly
Poulin et al defined splenomegaly on the
basis of size of spleen
• Moderate; if the largest dimension is 11-20 cm.
• severe; if the largest dimension is greater than
20 cm.
53. Splenomegaly
Splenomegaly definition by weight
• MILD; Spleens weighing 400-500 g.
Moderate; Spleen weighing 750-1000g.
Massive; More than 1000 g to indicate massive
splenomegaly.
54. Functions of spleen:
• Reservior for platelets,monocytes,FVIII etc.
• Haematopoiesis in fetus.
• Repairs and destruction of RBC’s by culling &
pitting.
PITTINGremoval of inclusion bodies (heinz
bodies,howell jolly bodies) without destroying
RBC’s.
CULLINGremoval of damaged/old RBC’s from
circulation.
55. • Immune function: IgM ,properidin,tuftsin are
produced by spleen.
prevention of inf. By capsulated org.(H.influ etc)
role in phagocytosis.
56. Grading of spleenomegaly:
Grade 1-normal,not palpable even on deep inspiration.
Grade 2-palpable just below costal margin usually on
deep inspiration.
Grade 3-palpable below costal margin but not projected
beyond a horizontal line half way b/w costal margin and
umblicus.the projection need to be ascertained along a
line dropped vertically from the left nipple.
57. Grade 4- lowest palpable point approaching the
umblical level but not below a line drawn
horizontally through umblicus.
Grade 5-lowest palpable point below umblical level
but not projected beyond a horizontal line situated
halfway b/w umblicus and symphysis pubis.
Grade 6-lowest palpable point beyond lower limit of
grade 5.
58.
59.
60. Grading according to size of spleen below LCM:
MILD palpable <3cms below LCM
MODERATE 4-7 below LCM
SEVERE >7cms below LCM.
61. Clinical E/o :
Size & Degree:
• it usually enlarges towards RIF.
• it is measured as child takes a deep breath from a
point on LCM in MCL to the tip of the enlarged
spleen.
Margin:
• Splenic notch is felt on the Ant. border & has a
sharp margin.
• Diff from kidney where there is absence of notch &
margin is round
62. Spleen vs. Kidney
Spleen
• Splenic notch.
• Can cross midline.
• Can’t get above.
• Moves down on
inspiration.
• Not ballotable.
• Splenic rub.
Kidney
• No notch.
• Never cross the
midline.
• May get above.
• Doesn’t move with
respiration.
• Ballotable.
• No rub.
64. Percussion of spleen
Normal
• Left midaxillary line 9th –11th intercostal space
width 4-7cm.
• Enlargement of splenic dullness: splenomegaly.
65. Percussion (3 methods):
• Percussion of Traube's Space boundaries –
Left anterior axillary line
6th rib
costal margin .
• This area should be resonant on percussion.
• Dullness indicates possible splenic enlargement
66.
67. Percussion by Castell’s method :
• percuss in the lowest Left intercostal space in the
anterior axillary line (usually the 8th or 9th IC
space)
• this space should remain resonant during full
inspiration .
• dullness on full inspiration indicates possible
splenic enlargement (a positive Castell’s sign)
68. Percussion by Nixon’s method:
• place the patient in Right lateral decubitus
• begin percussion midway along the Left costal
margin proceed in a line perpendicular to the Left
costal margin
• if the upper limit of dullness extends >8 cm above
the Left costal margin, this indicates possible
splenomegaly
69.
70. Palpation of spleen
• To palpate the spleen, the patient is in the supine
position with the knees flexed to decrease
abdominal muscle tone.
• Begin the examination by palpating the right lower
quadrant and move upward across the abdomen as
the patient.
71. Palpation (3 methods)
Method #1:
• begin palpation in the RLQ.
• direct the patient's breathing by telling them when
to take a deep breath and when to exhale while
proceeding diagonally towards the Left Upper
Quadrant (LUQ), try to palpate the spleen edge
during each inspiratory phase
72. Method #2:
• place the patient’s Left fist under their Left
posterior chest.
• With your Right hand, begin palpation in the RLQ.
• Direct the patient's breathing by telling them when
to take a deep breath and when to exhale while
proceeding diagonally towards the LUQ, try to
palpate the spleen edge during each inspiratory
phase
73. Method #3 –The Hooking maneuver of Middleton
(optional):
• Place the patient’s Left fist under their Left
posterior chest position yourself on the patient’s
Left side, facing the patient’s feet.
• Using both hands, curl your fingers under the
patient’s Left costal margin ask the patient to take a
long, deep breath à attempt to palpate the spleen
with your fingertips
74. Percussion of spleen
• Percussion is also used to delineate the size of
the spleen.
• Percussion is only approximately 60%
accurate in most studies, with palpation about
50% accurate.
77. • Spleen moves downwards and medially during
inspiration.
• Fingers cannot be insinuated btw enlarged spleen
and LCM
• Spleenic rub is palpable in spleenitis
78. Mechanism of splenomegaly:
• Reactive Reticulo-endothelial hyperplasia
• Lymphoid hyperplasia
• Proliferation of lymphoma cells
• Infiltration by abnormal cells
• Extramedullary hemopoeisis
• Proliferation of macrophages d/t RBC
destruction
• Vascular congestion
79. Symptoms and signs
• Abdominal pain/tiredness.
• Early satiety due to splenic encroachment.
• Symptoms of anemia due to accompanying cytopenia.
• Febrile illness (infectious).
• Pallor, dyspnea, bruising, and/or petechiae (hemolytic
process).
80. Symptoms and signs
• History of liver disease (congestive).
• Weight loss, constitutional symptoms (neoplastic).
• Pancreatitis (splenic vein thrombosis).
• Alcoholism, hepatitis (cirrhosis).
99. Hypersplenism
Criteria for a diagnosis of hypersplenism:
• anemia.
• Leukopenia.
• Thrombocytopenia.
• combinations thereof, plus cellular bone marrow,
splenomegaly, and improvement after splenectomy.
100. Approach to Splenomegaly
Depends on Pretest Probability
• Clinical Suspicion of Splenomegaly (>10%).
• Percuss first and if positive palpate.
• If percussion is negative and suspicious,
order an ultrasound.
• If percussion positive but palpation is
negative, order an ultrasound.
• Both percussion and palpation
positive = SPLENOMEGALY.
101. Diagnostic Approach
• CBC provides information about hematological,
infectious, and inflammatory processes.
• Finding of pancytopenia, Anemia, Leukopenia,
Thrombocytopenia may indicate bone marrow
dysfunction or portal hypertension with
hypersplenism.
102. Laboratory tests
Routine tests :
• CBC, platelet count, sedimentation rate.
• chemistry panel, febrile agglutinins, serum
haptoglobins, ANA test, Monospot test, serum protein
electrophoresis, tuberculin test.
• chest x-ray, EKG, and flat plate of the abdomen.
103. Diagnostic Approach
• Increased sedimentation rate suggests infectious,
inflammatory, or neoplastic process.
• Bacterial, fungal, and other cultures may be
performed with suspected infection.
104. Diagnostic Approach
• Bone marrow exam is useful in diagnosis of
histiocytoses, lysosomal storage disorders,
and some infections(e.g., disseminated
histoplasmosis).
105. Diagnostic Approach
• Liver function tests and abdominalU/S with Doppler
methods should be performed with suspected portal
hypertension.
• Abdominal U/S and CT locate and define extent of
splenic masses
106. If there is jaundice
• A hepatitis profile, red cell fragility test, and blood
smear for parasites should be done.
If there is fever.
• Serial blood cultures, leptospirosis antibody titer,
and smear for malarial parasites should be done.
Laboratory tests
107. Laboratory tests
If there is a petechial rash
• A coagulation profile should be done.
To rule out malignancies
• Lymph node biopsies and bone marrow
examinations may be necessary.
109. imaging
• MRI scan- liver hemangiomas
hemochromatosis
erlenmeyer flask sign(Gaucher)
• PET scan - Dx & staging of lymphomas
- determine metabolic cells in spleen
110. Imaging Studies
Splenoportography
o This modality is used to evaluate portal vein patency
and the distribution of collateral vessels before shunt
operations for cirrhosis.
o Findings can help identify the cause of idiopathic
splenomegaly, especially in children.
• Angiography: Angiographic findings are used to
differentiate splenic cysts from other splenic tumors.
111. Imaging Studies
• Liver-spleen colloid scanning
o Erythrocytes are labeled with chromium-51 (51 Cr) ,
mercury-197 (197 Hg), rubidium-81 (81 Rb), or
technetium-99m (99m Tc), and the cells are altered by
treatment with heat, antibody, chemicals, or metal
ions so that the spleen sequesters them after
infusion.
o A spleen length >14 cm is consider enlarged on liver-
spleen scan