DR ABU BAKAR SIDDIQUE

FCPS(Medicine)
Assistant Professor
Dept. of Medicine
SZMC, BOGRA

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 CONTENT
1) DOCTOR- PATIENT RELATIONSHIP
2) Anaemia(IDA)--17
3) Megaloblastic Anaemia—33, HA—54, AA--65
4) JAUNDICE+AVH--73
5) CYANOSIS--97
6) Clubbing--103
7) Oedema--108
8) TEMPERATURE+FEVER--123
9) LYMPHADENOPATHY + HEPATOSPLENOMEGALY--138
10)GERIATRIC PROBLEMS--156
11)WEIGHT GAIN & WEIGHT LOSS—190
12) NUTRIENT & VIT DEFICIENCY– 212.
 DOCTOR- PATIENT RELATIONSHIP

• DR IS AN ANGEL TO ............
• DR IS A SUPERMAN TO .......................
• DR IS AN EVIL TO ..........................
• DPR IS-- ITSELF A THERAPEUTIC;
• A SUCCESSFUL CONSULTATION WITH A
TRUSTED & RESPECTED PRACTITIONER HAVE
BENEFICIAL EFFECTS RATHER THAN ANY
OTHER THERAPY GIVEN.
• Rx IS-- A MULTIDISCIPLINARY TEAM WORK.
• IT IS IMPORTANT TO RECOGNISE A
BREAKDOWN IN RELATIONSHIP QUICKLY &
IF APPROPRIATE AN APOLOGY.
• THE LONGER ONE TAKES TO ADDRESS A
PROBLEM, THE MORE DIFFICULT IT TO
RESOLVE.
 DUTIES OF A DOCTOR
 KNOWLEDGE, SKILLS & PERFORMANCE
 SAFETY & QUALITY
 COMMUNICATION, PARTNERSHIP &
TEAMWORK
 MAINTAINING TRUST
 DIFFICULTIES
ATTITUDE & BELIEFS
 TRUST --- CYNICISM
 RESPECT ---SCORN
 AUTONOMY --- PATERNALISM
 REALISTIC – DISTORTED
 REASONABLE --- NOT AMENABLE TO REASON
BEHAVIOURS & ROLES
BEHAVIOURS & ROLES
 LISTENING/ HEARING –NOT LISTENING /
HEARING
 CLARITY --- JARGON
 CALM – ANGER, IRRITATION
 PRAISE -- CRITICISM
COMMUNICATION & OTHER CLINICAL SKILLS

• COMMUNICATION LIES AT THE HEART OF GOOD

MEDICAL PRACTICE
• COMMUNICATION NOT ONLY WITH PT, BUT ALSO
WITH OTHER DRS & MEMBERS OF THE
MULTIDISCIPLINARY TEAM IS IMPORTANT.
• THE MAIN AIM IS TO ESTABLISH PT’S ACTUAL
ILLNESS
• ALLOW THE PT TO DESCRIBE THE PROBLEM
WITHOUT INTERROGATION.
 BARRIERS TO GOOD COMMUNICATION

 THE CLINICIANS
 AUTHORITARIAN OR DISMISSIVE ATTITUDE
 HURRIED APROACH
 USE OF JARGON
 INABILITY TO SPEAK FIRST LANGUAGE OF PATIENT
 NO EXPERIENCE OF PT’S CULTURAL BACKGROUND
 THE PATIENT
 THE PATIENT
 ANXIETY
 RELACTANCE TO DISCUSS SENSITIVE OR
SEEMINGLY TRIVIAL ISSUES
 MISCONCEPTIONS
 CONFLICTING SOURCES OF INFORMATION
 COGNITIVE IMPAIRMENT
 HEARING/ SPEECH/VISUAL IMPEDIMENT.
• SPECIFIC SCENARIO–
 BREAKING BAD NEWS,
 DEALING WITH AGGRESSION---- REQUIRE
ADDITIONAL TARGETED STRATEGIES.
• NON-VERBAL COMMUNICATION—IS EQUALLY
IMPORTANT ( SMILING, HEAD NODDING).
• SYMPATHY & EMPATHY
• PHYSICAL EXAMINATION & LAB. INVESTIGATIONS
ARE ALSO IMPORTANT CHARACTERISTIC IN DPR.
 DOCTOR- PATIENT RELATIONSHIP

• DR IS AN ANGEL TO ............
• DR IS A SUPERMAN TO .......................
• DR IS AN EVIL TO ..........................
Thanks All
 Anaemia(IDA)
• Def:
• Classification:
• Common causes of anaemia in Bangladesh:
A. Chronic blood loss due to
 PUD
 Ascariasis
 Haemorroids
 Carcinoma
 Menorrhagia
B. Impaired red cell production
 Iron deficiency
 Vit. B12 deficiency
 Folic acid deficiency
 PEM
C. Excessive red cell destruction
 Thalassaemia.
 Sickle cell anaemia
 Autoimmune hemolytic anaemia.
 IDA
• Loss
 PUD
 Gastritis
 GIT malignancy
 IBD
 Diverticulitis
 Polyp
 Angioplasty
 Drugs
• Increased demand / demand exceed absorption
 IDA
• Loss
 Menstrual loss
 Pregnancy
 Breastfeeding
 Chr. Hemoptysis
 Chr. hematuria
• Increased demand / demand exceed
absorption
 IDA

• Increased demand / demand exceed

absorption
 Growth period– Infancy, Puberty
 Pregnancy
 Lactation
 Achlorhydria
 Surgery
• C/F
Non specific symptom
 Tiredness
 Lightheadedness
 Breathlessness
 Leg swelling
Non specific sings
 Pallor
 Tachypnoea
 Tachycardia
 Postural hypotension
 Ankle oedema.
• Features of iron deficiency ( Plummer vinson
syndrome)
 Glossitis
 Dysphagia
 Koilonychia
 Investigation

Confirmation of iron deficiency

 CBC with PBF

 S. Iron profile –Plasma iron, S. ferritin, TIBC.
Hb electrophoresis.
 To diagnosis the cause

 Investigation

 To diagnosis the cause

 Stool OBT,
 Upper & lower GIT endoscopy,
 Stool & urine for parasites
 S. Anti-endomysial or Anti-transglutaminase
antibodies & Duodenal biopsy.
 Treatment

Oral iron suppliment

Parenteral suppliment
Blood transfusion
Treatment of the cause
 Treatment

Oral iron suppliment

Ferrous sulfate 200 mg 8 hrly for 3—6 month.
 If patient is intolerable to ferrous sulfate– Ferrous
gluconate 300mg 12 hrly.

 Parenteral suppliment

 If pt is malabsorptive– parenteral iron sorbitol.

 Blood transfusion-- if IDA associated with
 Angina
 HF or
 evidence of cerebral hypoxia.
 Treatment of cause.
 Rx responses
• Hb raise 1gm/dl in every 7—10 days
• Reticulocyte count raised within a week

If failure to response—
 Malabsorption,
 Non-compliance,
 Continued loss,
 Incorrect diagnosis.
Thanks All
 Megaloblastic Anaemia
• WHY CALLED
• CAUSE –
• CAUSE – Deficiency or Disturbances in
metabolism of Vit. B12 &/or Folic acid.
• PAHTOPHYSILOGY
 HOMOCYSTEIN + FOLATE -----VIT B12---------
METHIONINE( DNA SYNTHESIS)
 MEGALOBLASTOSIS OF ALL PROLIFERATING
CELLS
 Vit. B12
• Daily requirement– 1ug/ day
• Average daily diet contains – 5 – 30ug
• Sources – Meat, Fish, Egg, Milk.
• Storage - Liver stores enough vit. B12 for 3
years.
• Causes of deficiency –
 Causes of deficiency –

 Dietery deficiency  Small bowel pathology

 Gastric -
hypo/achlorhydria • pancretic exocrine
 Parnicious anaemia– insufficiency,
o Anti-intrinsic factor Ab , • bacterial overgrowth,
o Antiparietal cell Ab. • IBD,
• fish tapeworm
infection,
• surgical resection.
 Folate
• Daily requirement– 50 ug/ day
• Average daily diet contains – more than that but
excess cooking destroyed folates.
• Sources –
 Leafy vegetables ( cabbage, spinach, brocoli, lettuce),
 fruites (bananas, melons) &
 animal proteins ( liver, kidney).
• Storage - Total body stores are minimal & deficiency
can occur in a matter of weeks.
 Causes of deficiency –

 Dietery deficiency  Drugs –

 Malabsoption– • Anticonvulsants( Phenyt
Coeliac disease oin),
 Increased demand – • OCP,
• Pg, • MTX.
• Cell proliferation.
 C/F OF Megaloblastic anaemia

Symptoms
 Malaise  Poor memory
 BreathlessnessParaesth  Depression
esiae  Personality change
 Sore mouth  Hallucination
 Weight loss  Visual disturbance
 Impotence
 Sings

 Pallor  Smooth tongue

 Tachypnoea  Angular cheilosis
 Tachycardia  Vitiligo
 Postural hypotension  Skin
 Ankle oedema pigmentation( Lemon
yellow tint)
 Heart failure
 Pyrexia
 Neurological F/O B12 deficiency
A. Peripheral nerves –Glove & stocking
paraesthesia, Loss of ankle reflexes
B. Spinal cord– SCD–( Post. & Lat Corticospinal)
C. Cerebrum-- Dementia & Optic atrophy
D. Autonomic neuropathy
 Investigations

CBC – Hb, MCV

PBF– Oval macrocytosis, Poikilocytosis,
Red cell fragmentation,
Hypersegmented neutrophil ( >/=6)
RETICULOCYTE COUNT– Low
BONE MARROW STUDY--
 Investigations

BONE MARROW STUDY--

 Increased cellularity,
 Megaloblastic change in erythoid series,
 Giant metamyelocytes,
 Dysplastic megakaryocytes,
 Increased iron in stores,
 Pathological non ring sideroblast.
S. FERRITIN –Insreased
PLASMA LDH –Elevated
VIT B 12 LEVEL IN BLOOD
RED CELL FOLATE LEVEL
S. FOLATE LEVEL
 MANAGEMENT
• Vit B 12 Deficiency --- Inj. Hydroxycobolamine
1000 ugm IM for 6 doses 2 or3 days apart,
followed by maintainance therapy of 1000
ugm every 3 months life long
• Folate deficiency ---
 MANAGEMENT
• Folate deficiency --- Oral folic acid 5 mg daily
for 3 weeks then 5 mg weekly as a
maintainace therapy .
• Supraphysiological dose ( 400 ugm/day)
reduce the risk of IHD & CVD by lowering
plasma homocystein level.( Food fortification)
WHICH ONE FIRST & WHY?
 ?BLOOD TRANSFUSION
• Severe Angina
• Heart failure
Schilling test
 1 PART
st

 1ug radio – labelled B12(58Co) orally + 1mg

ordinary B12 IM
 Measure 58Co excreted in urine over 24 hrs
 If >10% (normal B12 absoption)
 If <10% ( Proceed to 2nd part)
 2 part
nd

 Radio –labelled B12 as above + 1mg ordinary

B12 IM + Intrinsic factor
 Measure 58Co excretion as above
 >10% ( PA)
 <10% (Gut disease)
Thanks All
 HA
 SHORTENING OF NORMAL RBC LIFESPAN
 TO COMPENSATE----
 BM INCREASE OUTPUT BY 6 TO 8 FOLDS–
EXPANDING THE VOLUME OF ACTIVE
MARROW &
 REALISING RETICULOCYTE PREMATURELY.
 CAUSES
A)INHERITED
 MEMBRANE DEFECT--- H. SPEROCYTOSIS,
H. ELIPTOCYTOSIS.
 ENZYME DEFECT —G6PD DEFICIENCY
 HB ---
 DEFICIENCY– THALASSAEMIA
 ABNORMALITY—SICKLE-CELL DISEASE
B) ACQUIRED--
B)ACQUIRED---
 IMMUNE— NON-IMMUNE—
 AUTOAb—
o WARM Ab—
 PRIMARY/ IDIOPATHIC
 SECONDERY—SLE, RA, DRUGS(PENICILLIN, METHYLDOPA, L-DOPA),
LYMPHOID MALIGNANCY, OTHER MALIGNANCY (LUNG, COLON,
KIDNEY, OVARY).
o COLD Ab—
 PRIMARY/ IDIOPATHIC
 SECONDARY—INFECTION (MYCOPLASMA, EBV, SYPHILIS), LYMPHOMA.
 ALLOAb– BT REACTION, HAEMOLYTIC DISEASE OF NEWBORN.
 NON-IMMUNE—
 MECHANICAL—PROSTHETIC VALVES,
MICROANGIOPATHIC(DIC, HUS, TTP), MARCH
HBURIA.
 INFECTION—MALARIA, C. perfringens.
 CHEMICAL/PHYSICAL—DRUGS (DAPSONE),
COPPER(WILSON’S) BURNS, DROWNING.
 ACQUIRED MEMBRANE DEFECT--PNH
 FEATURES OF HAEMOLYSIS
• HALLMARK OF HEMOLYSIS-
 REDUCE Hb
 INCREASE RETICULOCYTE
 INCREASE UNCONJUGATED BILIRUBIN
 INCREASE URINARY UROBILINOGEN
 INCREASE LDH
• ADDITIONAL F/O INTRAVASCULAR HEMOLYSIS-
 REDUCE HAPTOGLOBIN
 INCREASE METHAEMALBUIN
 +URINARY HAEMOSIDERIN
 HAEMOGLOBINURIA
 THALASSAMIA
• INHERITED IMPAIRMENT OF Hb PRODUCTION
1) PARTIAL/ COMPLETE FAILURE OF SYNTHESIS OF A SPECIFIC TYPE OF
GLOBIN CHAIN.
• 2 TYPE—
1)ALFA-TH--
 IF 1 IS DELETED---NO C/F
 IF 2 DELETED---MILD HYPOCHROMIC ANAEMIA
 IF 3 DELETED---Hb-H DISEASE
 IF ALL 4DELETED—STILLBORN BABY (HYDROPSFETALIS).
2) BETA TH—
 MAJOR– HbF INCREASE
 MINOR—HbA2 INCREASE
 C/F
SYMPTOMS--
• WEAKNESS, PALPITATION, DIZZINESS
• YELLOW DISCOLORATION OF URINE, EYES
• DARKENING OF SKIN
• FEELING MASS/ HEAVINESS IN LEFT UPPER ABDOMEN
SIGNS—
 SHORT FOR AGE
 MONGOLOID FACIES
 ANAEMIC
 MILD ICTERIC
 G. PIGMENTED SKIN
 HEPATOSPELOMEGALY
 Dx F/O BETA THALASSAEMIA
MAJOR--
• PROFOUND HYPOCHROMIC ANAEMIA
• EVIDENCE OF SEVERE RED CELL DYSPLASIA
• ERYTHROBLASTOSIS
• ABSENCE / GROSS REDUCTION OF Hb A
• RAISED Hb F
• EVIDENCE THAT BOTH PARENTS HAVE THALASSAEMIA MINOR
MINOR---
 MILD ANAEMIA
 MICROCYTIC HYPOCHROMIC RBC
 SOME TARGET CELL
 PUNCTATE BASOPHILIA
 RAISED HbA2.
 Dx CRITERIA OF HA
• TRIAD OF—
1. ANAEMIA
2. JAUNDICE
3. SPLENOMEGALY
 INVESTIGATIONS
 FBC WITH PBF
 RETICULOCYTE COUNT
 Hb ELECTROPHORESIS
 S. BILIRUBIN
 X-RAY SKULL
 CXR
 S. IRON PROFILE.
 Rx
ERYTHROPOIETIC FAILURE---
 CORRECTION OF ANAEMIA– BT TO KEEP Hb% ABOVE 10 g%
 Folic acid 5mg daily
 SPECIFIC Rx—ALLOGENIC BMT FROM HLA COMPATIBLE SIBLING
 IRON OVERLOAD---
 AVOID IRON CONTAINING DRUGS & DIET
 IRON CHELATING AGENTS—DESFERRIOXAMINE( S/C), DEFERIPRONE /
DEFERASIROX( ORAL), ASCORBIC ACID(URINARY EXCRETION).
SPLENECTOMY ( HYPERSPLENISM, HUGE SPEEN WITH PRESSURE
SYMPTOM)
GENETIC COUNSELLING
 APLASTIC ANAEMIA
• APLASIA OF BONEMARROW
• PRESENT WITH –
 F/O ANAEMIA—WEAKNESS, PALPITATION,
DIZZINESS, VERTIGO
 BLEEDING MANIFESTATION
 INFETION
 CAUSES
• PRIMARY/ IDIOPATHIC--
• ACQUIRED/ SECONDARY—
 DRUGS—CYTOTOXIC, ANTIBIOTIC, CARBIMAZOLE,
CARBAMAZEPINE, PENICILLAMINE
 RADIOTHERAPY
 CHEMICALS
 INFECTION– VIRAL HEPATITIS, EBV, HIV,
 OTHERS– PNH, MM, LYMPHOMA, 2ndary deposit in
marrow.
 CAMITTA Dx CRITERIA
• SEVERE AA— MARROW CELLULARITY <25%, PLUS
ATLEAST 2 OF –
1) NEUTROPHIL <500/cmm
2) PLATELETS <20,000/cmm
3) RETICULOCYTE <20,000/cmm
• VERY SEVERE AA— AS FOR SAA BUT NEUTROPHIL
<200/cmm
• NON-SEVERE AA—
 AA NOT FULFILLING THE CRITERIA FOR SAA / VSAA
 INVESTIGATIONS
• CBC WITH PBF—
• BM ASPIRATION & TREPHINE---
 Rx
 SUPPORTIVE---BLOOD PRODUCT SUPPORT &
AGGRESSIVE CONTROL OF INFECTION
 CURATIVE---ALLOGENIC HSCT
 IST– ATG, CICLOSPORIN
 THROMBOPOIETIN RECEPTOR AGONIST--
ELTROMBOPAG
 UNDERLYING CAUSE--- SHOULD BE TREATED /
REMOVED.
• MUST BE F/U FOR LONG TERM BECAUSE MAY
TRANSFORM INTO ANY OF---
 PNH
 MDS
 AML.
Thanks All
 JAUNDICE
• Def:
• Sites of observation:
• Mechanism:
• D/D :
• Classification:
• Cause:
 Haemolytic (Prehepatic)-
 Hepatocellular--
 Obstructive--
 Causes

 Haemolytic (Prehepatic) jaundice-

 HA
 Mismatched blood transfusion
 Malaria
 Congenital hyperbillirubineamia
B. Hepatocellular (Hepatic) jaundice-

 Viral hepatitis
 Drug induced hepatitis
 Alcoholic hepatitis,
 Autoimmune hepatitis
 Pregnancy induced hepatitis
C. Posthepatic/Cholestatic/Obstructive/Surgical
jaundice---
i. Intrahepatic–
 Primary biliary cirrhosis
 Primary sclerosing cholangitis
 Drugs
 Autoimmune hepatitis.
ii. Extrahepatic–
 Choledocholithiasis
 Cholangiocarcinoma
 Carcinoma head of the pancreas
 Biliary stricture
 Parasitic infestation.
 Regarding H/O
 Jaundice– Static/ Increasing/ Fluctuating
 Itching
 Abdominal pain
 Weight loss
 Urine color
 Stool color
 Fever +/- Chills/Rigor
 Recent drug history
 H/O Alcohol
 Exposure to I.V drug or blood transfusion
 H/O TRAVELLING

 F/H/O
 H/O Autoimmune disease
 H/O IBD
 H/O Immunization
 O/E
• Appearance– Hepatic/ Mongoloid facies
• Co-operation
• Pulse
• Temperature
• Anaemia
• JVP
• Oedema
• Lymph node
• Scratch mark
• Nails
• Ascites
• Hepatomegaly
• Splenomegaly
• Palpable gall bladder
• Stigmata of CLD
Features Haemolytic Hepatocellular Obstructive
Jaundice
Conjunctiva Lemon yellow Orange yellow Greenish
tinge yellow
Urine Fresh urine -- Yellowish Deep yellow/
(N) color Dark
Stool High color High color Pale/ Clay
color
Features Haemolytic Hepatocellul Obstructive
Jaundice ar
Prodromal No Yes No
feature
Hepatomegaly +/- + Rare

Splenomegaly Characteris +/ _ Rare

tic
Anaemia + _ _
Features Haemolytic Hepatocellul Obstructive
Jaundice ar
Pruritus No No Yes
Sinus No No Yes
bradycardia

Xanthelasma No No Yes
Bleeding No No Yes
Gall bladder Not palpable Not palpable Palpable
 Investigations

 LFT
 Viral marker
 USG of HBS
 CBC with PBF
 Other tests according to suspicion

 Investigations

 LFT
 S. Bilirubin
 Direct/ Conjugated
 Indirect/ Unconjugated
 S. Transaminase (ALT, AST)
 Alkaline phosphatase
 S. Total protein, Albumin & A : G
 Prothrombin time
 Gamma - GT
 Viral marker
o Anti HAV Antibody (Ig M)
o HBs Ag
o HBe Ag
o Anti HBc Antibody( Ig M)
o Anti HEV Antibody(IgM)
Mx
Thanks All
 AVH
• Viruses causing hepatitis
Common – Hepatitis A, B, D, E.
Others--- CMV, EBV, HSV.
 All hepatotrophic viruses cause acute hepatitis
except C.
• C/F
 Anorexia, Nausea, Vomiting.
 Myalgia, Arthralgia.
 Abdominal discomfort, Diarrhoea.
 Dark urine, Pale stool.
 Jaundice
 Enlarged tender liver.
• Investigation
 LFT
 S. Bilirubin
 S. Transaminase (ALT, AST)
 Alkaline phosphatase
 S. Total protein, Albumin & A : G
 Prothrombin time
 USG of HBS
 Viral marker
o HBs Ag
o HBe Ag
o Anti HBc Antibody( Ig M)
o Anti HAV Antibody (Ig M)
o Anti HEV Antibody(IgM)
 CBC
• Treatment
 Symptomatic & supportive
 Bed rest
 Normal diet
 Avoid Alcohol, Sedative & Hypnotics.
 Lactulose
 Domperidone
 Vitamins (specially vit. K)
 CYANOSIS
• Def: Blue discoloration of skin & mucus
membrane due to increased concentration of
deoxygenated Hb in blood (> 5gm/dl).
• Type:
1) Central
2) Peripheral
• Sites of observation:
 Tip of tongue
 Tip of nose
 Lips
 Ear lobule
 Tip of fingers & toes.
• Cause:
Central-
 Congenital cyanotic heart disease
 Severe acute br. Asthma
 Acute exacerbation of COPD
 Severe pneumonia
 Massive pulmonary embolism
 Tension pneumothorax
Peripheral-
 Cold exposure
 Peripheral venous obstruction
 Shock
 Difference between
Central cyanosis Peripheral
cyanosis
Sites Commonly Peripheral parts
tongue only , no tongue
involvement.
Application of No change Cyanosis
heat decrease
Application of O2 May improve No response
Dyspnoea Usually present Usually absent
Clubbing May present Absent
Pulse volume May be high Usually low
 Clubbing
• Def– Thickening of soft tissue at the nail base
and nail become convex from above
downwards & side to side is called clubbing.
Clubbing
• Causes-
A. Respiratory
 Bronchogenic carcinoma
 Lung abscess
 Bronchiectasis
 Empyema thorasis
 ILD
B. CVS

Congenital cyanotic heart disease

Sub acute bacterial endocarditis
C. Alimentary
IBD
PBC
CLD

D. Others
Thyrotoxicisis
Idiopathic
DR ABU BAKAR SIDDIQUE
FCPS(Medicine)
Assistant Professor
Dept. of Medicine
SZMC, BOGRA

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 Oedema
• DEF: ---- Accumulation of
 abnormal &
 excessive
 free fluid in
 interstitial space or
 body cavity is called oedema.
 Classification:

A. Localized oedema
B. Generalized oedema

a. Pitting oedema
b. Non-pitting oedema
• Causes:

Localized--
 Soft tissue infection &/or inflammation–
 Cellulitis,
 Gout,
 Snake bite etc.
 Trauma
 Venous obstruction--
 Lymphatic obstruction--
 Causes:

Localized--

 Venous obstruction---  Lymphatic obstruction--

 Deep vein thrombosis,  Filariasis,
 pregnancy,  Ca breast,
 SVC obstruction,  post operative
 IVC obstruction lymphatic destruction,
congenital
Generalized—
 CCF  Hypothyroidism
 NS  Hypoproteinemia
 AGN  Drugs
 CLD  Nutritional
 Idiopathic
• Causes of non-pitting oedema—
 Hypothyroidism/Myxoedema
 Filariasis
 Lymphatic obstruction
 approach to
• H/O---
 First site & time of appearnce--
 Whether localized / generalized
 If localized--- local phenomena that my
responsible should be consider---
 If generalized--- first consider hypolbuminemia
 approach to
• H/O---

 If generalized--- first consider hypolbuminemia

 If hypoalbuminemia not present--- any
evidence of HF
 associated symptoms—
 Finally consider urine output adequate or not
• O/E---
 Site—
 Pitting / non-pitting
 Pulse—
 BP—
 JVP—
 CYANOSIS
 JAUNDICE
 ASCITIS
 hepatomegally
 INVESTIGTION--

• Cardiac FT---
• Renal FT—
• LFT---
• THYROID FT--
Thanks All
 TEMPERATURE
 BODY TEMPERATURE IS CONTROLLED IN THE
HYPOTHALAMUS, WHICH IS DIRECTLY SENSITIVE TO
CHANGE IN BODY CORE TEMP.
 THE NORMAL ‘SET-POINT’ OF CORE TEMP IS
TIGHTLY REGULATED WITHIN 37+/- 0.5 DEGREE C,
WHICH IS NECESSARY FOR NORMAL FUNCTION OF
MANY ENZYMES & METABOLIC PROCESSES.
 THIS ‘SET-POINT’ IS INCREASED IN RESPONSE TO
INFECTION.
 MEASUREMENT
• INSTRUMENT
• UNIT/SCALE
• SITE
• TIME
 TEMPERATURE
Hypothermia <95 Degree F
Subnormal <98 Degree F
Normal 98—99 Degree F
Fever >99 Degree F
Hyperpyrexia >107 Degree F
 HYPOTHERMIA
 WHEN THE BODY’S NORMAL THERMAL
REGULATORY MECHANISM ARE UNABLE TO
MAINTAIN HEAT IN A COLD ENVIRONMENT.
 CAUSES– HYPOTHYROIDISM, ALCOHOLISM,
DRUGS, CORTISOL DEFICIENCY, STROKE,
HYPOGLYCEMIA, HEPATIC FAILURE.
 C/F–
CONFUSION, DEHYDRATION, ATAXIA,
BRADYCARDIA, HYPOTENSION, COMA,
MUSCLE STIFFNESS, MIMIC DEAD(ABSENT
PUPIL & CORNEAL REFLEXES).

 INV --- ABG, CBC, ELECTROLYTES, ECG, CXR.

 Mx–
 Mx–
o RESUSCITATE & PREVENT CONTINUED HEAT
LOSS
o REWARMING
o CORRECTION OF ELECTROLYTES IMBALANCE &
CARDIAC ARRHYTHMIAS
 COLD INJURY—
• FROSTBITE
• TRENCH/ IMMERSION FOOT
• CHILBLAINS
FEVER/PYREXIA
 Types of fever
1. Continued fever--
2. Remittent fever
3. Intermittent fever
Types of fever Definition Causes
Continued Temp. does not Typhoid
fever fluctuate >1.5 Miliary TB
degree F Lobar
during 24 pneumonia
hours & never
touches the
baseline
Types of fever Definition Causes
Remittent Temp. Liver abscess
fever fluctuates >3 Lung abscess
degree F Pus in any
during 24 body cavity
hours but
never touches
the baseline
Types of fever Definition Causes
Intermittent Fever is present only for a few
fever hours of the day during 24
hours .
a)Quotidian Fever comes Kala azar
everyday
b)Tertian Fever comes Vivax & ovale
on alternate malaria
day
c)Quartan Fever comes p. malariae
on every 3rd malaria
day
 HYPERPYREXIA
• Causes of hyperpyrexia
1. Heat stroke
2. Pontine haemorrhage
3. Cerebral malaria
4. Pneumonia
5. Meningitis
6. Atropine poisoning
7. Thyroid storm
 HEAT RELATED ILLNESS
 HEAT CRAMPS
 HEAT SYNCOPE
 HEAT EXHAUSTION– HOT & SWEATING,
DEHYDREATED, TACHYCARDIA, IRRITABLE,
FATIGUE, HEADACHE, WEAKNESS.
 HEAT STROKE– HOT & NOT SWEATING, MOF,
SHOCK, CONFUSION, AGRESSION.
 LYMPHADENOPATHY
• ABNORMAL ENLARGEMENT OF LYMPH NODE
IS LYMPHADENOPATHY
• ONCE LYMPH NODE IS PALPABLE, FOLLOWING
POINTS TO BE NOTED----
 ONCE LYMPH NODE IS PALPABLE, FOLLOWING POINTS TO BE
NOTED----

1) SITE— GENERALISED / LOCALISED

2) NUMBER—
3) SIZE
4) CONSISTENCY----FIRM & MATTED, RUBBERY, HARD, STONY
HARD, SOFT/CYSTIC.

5) TENDERNESS
6) DISCRETE / MATTED
7) FIXATION
8) DISCHARGING SINUS
 CAUSES
A) LOCALISED LYMPHADENOPATHY—
 LYMPH NODE DRAINING AN INFLAMMED
AREA
 INFECTION OF LYMPH NODE ITSELF
 METASTASIS
 REACTIVE HYPERPLASIA
B) GENERALISED LYMPHADENOPATHY
 HAEMATOLOGICAL MALIGNANCY–
 INFECTION—
 SARCOIDOSIS
 SLE
 DRUGS
B) GENERALISED LYMPHADENOPATHY
 HAEMATOLOGICAL MALIGNANCY–
 LYMPHOMA
 ALL
 CLL

 INFECTION—
 INFECTION—
 DISSEMINATED TB,
 HIV
 CMV
 INFECTIOUS MONONUCLEOSIS
 DRUGS--- PHENYTOIN
 HEPATOMEGALY

 ENLARGEMENT OF LIVER—
 POINTS TO BE NOTED—
 SIZE
 MARZIN
 SURFACE
 TENDERNESS
 CONSISTENCY
 UPPER BORDER OF—
 HEPATIC BRIUT / RUB
 CAUSES OF ISOLATED HEPATOMEGALY
 AVH
 LIVER ABSCESS
 HEPATOMA
 SECONDARIES IN LIVER
 CLD( ALCOHOLIC, PBC)
 CCF
 HYDATID CYST
 AMYLOIDOSIS
 POLYCYSTIC LIVER
 SPLENOMEGALY
 ENLARGEMENT OF SPLEEN
 POINTS TO BE NOTED—
 SIZE
 DIRECTION
 CONSISTENCY
 NOTCH
 INSINUATION
 MOVEMENT WITH RESPIRATION
 PERCUTION NOTE
 CAUSES OF ISOLATED SPLENOMEGALY

 MALARIA
 KALA-AZAR
 CML
 MYELOFIBROSIS
 LYMPHOMA
 CLD WITH PORTAL HTN
 CLL
 CAUSES OF ISOLATED SPLENOMEGALY

 TROPICAL SPLENOMEGALY SYNDROME

 HHA
 ENTERIC FEVER
 SLE
 SBE
 PRV
 VIRAL INFECTION( INFECTIOUS MONONUCLEOSIS,
CMV)
 HOW YOU WILL DIFFERENTIATE BET. SPLEEN
& LT KIDNEY
POINTS SPLEEN LEFT KIDNEY
SITE IN THE LT IN LT LUMBER REGION /
HYPOCHONDRIUM LOIN
ENLARGED TOWARDS RT ILLIAC FOSSA TO DOWNWARD
NOTCH PRESENT ABSENT
INSINUATION – NOT POSSIBLE POSSIBLE
MEDIAL BORDER WELL DEFINED ROUND IN SHAPE
BIMANUALLY PALPATION & NOT POSSIBLE BIMANUALLY PAALPABLE &
BALLOTMENT BALLOTABLE
MOVEMENT WITH MOVES NOT MOVES
RESPIRATION
PERRCUTION NOTE DULL TYMPANIC
CAUSES OF HEPATOSPLENOMEGALY
1) CHRONIC KALA-AZAR
2) CHRONIC MALARIA
3) CML
4) LYMPHOMA
5) HEREDITERY HAEMOLYTIC ANAEMIA
6) MYELOFIBROSIS
7) CLD WITH PORTAL HYPERTENTION
 GERIATRIC PROBLEMS
WHAT?
AGEING- Chronological age & Biological
age.
WORKING AG  20 –64 YRS
LIFE EXPECTANCY
FRAIL
DIFFICULTIES
CHANGES & CLINICAL CONSEQUENCES
 Biology of ageing
Ageing  A progressive accumulation through life
of random molecular defects that build up within
cells & tissues.
Despite multiple repair & maintenance mechanism,
these result in age-related functional impairment of
tissues & organs.

Factors of ageingMany genes contribute to

ageing(25%).
Others 
 Biology of ageing
Others Nutritional & environmental factors
determine the rest.
Production of reactive oxygen species play a major
role in ageing.

Heterogeneity is the hallmark of ageing, meaning

that each person must be assessed individually &
the same management cannot be applied
unthinkingly to all people of a certain age.
 CHANGES & CLINICAL CONSEQUENCES

Changes with ageing Clinical consequences

CNS –
 Neuronal loss  Increased risk of delirium
 Cochlear degeneration  Presbyacusis
 Increased lens rigidity  Presbyopsia
 Lens opacity  Cataract
 Anterior horn cell loss  Reduced position &
 Dorsal column loss vibration sense
 Increased risk of fall
Changes with ageing
• RESPIRATORY
 Reduced lung elasticity
 Increased chest wall rigidity
 Increased V/Q mismatch
Clinical consequences
 Reduced vital capacity &
PEF
 Increased RV
 Increased risk of infection
Changes with ageing Clinical consequences

CVS  Reduced exercise tolerance

 Reduced maximum heart  Widened pulse pressure
rate  Postural hypotension
 Reduced elasticity of  Risk of AF
capacitance vessel
Changes with ageing Clinical consequences

• Renal  Impaired fluid balance

 Loss of neurons  Impaired drug metabolism
 Reduced GFR & excretion

• Endocrine
 Deterioration of pancreatic  Risk of IGT &/ OR DM
beta cells
Changes with ageing Clinical consequences

• GIT
 Reduced GI motility  Constipation

Bones
 Reduced BMD  Increased risk of
osteoporosis
 CHARACTERISTICS OF PRESENTING
PROBLEMS
o Late presentation
o Atypical presentation
o Acute illness & changes in function
o Multiple pathology
 Approach to a geriatric patient
 Obtain a collateral history
 Check all medication
 Search for & treat any acute illness
 Identify & reverse predisposing risk factors
 FRAILTY

• DEF: The loss of an individual’s ability to withstand minor

stresses
• because the reserves in function of several organ system
are so severely reduced that even a trivial illness or
adverse drug reaction may result in organ failure or death.
• Frailty indicates increased vulnerability to loss of function.
• DISABILITY– Established loss of function
• CO-(MULTI)-MORBIDITY– The number of diagnoses
present.
HOW TO ASSESS A FRIED FRAILTY SCORE
1) Hand grip strength in bottom 20% of healthy
elderly distribution
2) Walking speed in bottom 20% of healthy elderly
distribution
3) Self- reported exhaustion
4) Physically inactive
5) At least 6 kg wt loss within 1 yr
A pt is defined as frail if 3 or more factors are present
 GERIATRIC GIANTS

FALLS
DIZZINESS
CONFUSION
URINARY INCONTINENCE
 FALLS

• Around 30% of those >65 yrs of age fall each

yr & >40% in >80.
• Only 10– 15% of falls results serious injury.
• Causes :
 Acute illness
 Blackouts
 Mechanical
 Risk factors
 Muscle weakness  Impaired activities of
 Gait or balance daily living
abnormality  Depression
 Use of a walking aid  Cognitive impairment
 Visual impairment  Age over 80 yrs
 Arthritis  Psychotropic
medication
 Intervention to prevent falls
 Individual or group exercise training
 Ca & vit-D suplementaion
 Rationalization of medication/ medication review
 Correction of visual impairment( cataract surgery)
 Home environment hazard assessment & safety
education
 Anti-slip shoes
 Correction of cardiovascular disorder
( pacemaker).
 DIZZINESS
• Difficult to describe
 Lightheadedness
 Vertigo
 Unsteadiness/ Poor balance

o Common causes—
 Hypotension--- due to arrhythmia, MI, GI bleeding,
pulmonary embolism
 Posterior fossa stroke
 Vestibular neuronitis.
 CONFUSION/ DELIRIUM

• Def: A syndrome of transient, reversible

cognitive dysfunction.
• Clinical assesment :
Two main goals ---
1) To Establish the diagnosis
2) To identify the reversible precipitating factors
 Risk factors
Predisposing factors
 Old age
 Dementia
 Frailty
 Sensory impairment
 Polypharmacy
 Renal impairment
 Precipitating factors

 Intercurrent illness  Pain

 Surgery  Constipation
 Change of  Urinary retention
environment  Urinary catheterization
 Sensory deprivation  Hypoxia
(darkness) or overload  Fever
(noise)
 Alcohol withdrawal
 Medication
 Dehydration
 Common causes
o Infections – Pneumonia, UTI, SSTI, Sepsis
o Metabolic disturbances -- AKI, Electrolytes
imbalance, Hypoglycemia, Hypothyroidism
Hepatic encephalopathy,
o Toxic insult--- Any drug or toxin
o Acute neurological..............
 Common causes

o Acute neurological conditions – CVD, Head

injury, Meningitis / encephalitis, ICSOL,
Seizure.
o Hypoxia – Pul. Embolism, Pul. eodema,
Pneumonia, COPD exacerbation, AMI
 Investigations
 CBC  RBS
 Urinalysis & C/S  LFT
 CXR  TFT
 ECG  Imaging of head
 CRP  LP
 Urea & Electrolytes  ABG
 URINARY INCONTINENCE

• The involuntary loss of urine &

• comes to medical attention when sufficiently
severe to cause a social or hygienic problem.
 Contributory factors
 UTI
 Severe constipation
 Drugs
 Hyperglycemia
 Hypercalcaemia
 Restricted mobility
 Acute confusion
 If still incontinent
 Establish pattern of urinary loss
 Measure RUV
 Assess genital prolapse & atrophic vaginitis in
women
 Assess prostate in men.
 Management
• Urge incontinence :
 Bladder retraining,
 Antimuscarinic drugs (Solifenacin, Tolterodine)

• Stress incontinence :
 Pelvic floor muscle training,
 Surgical intervention .

• Overflow incontinence :
 Management
• Overflow incontinence :
 Surgical relief of obstruction,
 Intermittent catheterization if no obstruction.
• If pt with severe stroke disease or dementia,
treatment may be ineffective, as frontal
inhibitory signals to bladder emptying are lost.
 Prescribing & deprescribing
 Polypharmacy  define as the use of four or
more drugs
 Associated with several adverse effects
including
 Falls
 Hospitalisation
 Increased risk of death.
Factors leading to polypharmacy in old age

1) Multiple pathology
2) Poor pt education
3) Lack of routine review of all medications
4) Pt’s expectations of prescribing
5) Over-use of drug interventions by doctors
6) Attendance at multiple specialist clinics
7) Poor communication between specialists.
 The clinical presentation of ADRs are diverse, so for any
presenting problem in old age the possibility that the
pt’s medication is a contributing factor should always be
considered
 Failure to recognise this may lead to the use of a further
drug to treat the problem, making matter worse
 When the better---
 course would be to stop or
 reduce the dose of the offending drug or
 to find an alternative.
Appropriate prescribing & deprescribing

 Deprescribing is as important as prescribing in

older people
 Regular review of medications should be
undertaken---
 To ensure that medications are still required
 To establish that they are still working
 To check that they are not causing side effects
 To ascertain whether the pt is taking them.
 This should be done in a controlled manner,
with dose reduction to ensure that rebound
symptoms or withdrawal effects do not occur
 The pt or carer should therefore be asked to
bring all medications for review rather than
relying on previous records.
 Rehabilitation
 Aims to improve the ability of people of all ages to
perform day to day activities & to optimise their
physical, mental & social capabilities
 This is a multidisciplinary team work
 Rehabilitation process includes---
 Assessment
 Goal setting
 Intervention
 Re-assessment
 WEIGHT LOSS & WEIGHT GAIN
• DR ABU BAKAR SIDDIQUE
FCPS(Medicine)
Assistant Professor, Dept. of Medicine
SZMC, BOGRA
w
e
l
c
o
m
 WEIGHT LOSS
• LOSS OF TOTAL BODY FAT &/ OR MUSCLE BULK
(EMACIATION)
• CACHEXIA– EMACIATION+ANOREXIA+ ANAEMIA.
• CAUSES OF WEIGHT LOSS---
WEIGHT LOSS
 CAUSES OF WEIGHT LOSS

1)MALNUTRITION
2)MALABSORPTION
3)DM
4)THYROTOXOCOSIS
5)ADDISON’S DISEASE
6)TB
7)ANOREXIA NERVOSA
8)DISSEMINATED MALIGNANCY
9)AIDS
 INDICATORS OF WEIGHT LOSS
 % OF WEIGHT LOSS
 MID ARM CIRCUMFERENCE
 TRICEPS SKINFOLD THIKNESS
 WEIGHT GAIN
• WEIGHT GAIN IS PANDEMIC
• ALMOST 2/3 OF UK ADULT & 1/4 OF URBAN
INDIAN WOMEN ARE OVERWEIGHT
• OBESITY AT 40 YRS OF AGE REDUCE LIFE
EXPECTANCY BY UPTO 7 YRS FOR NON-
SMOKER & BY 13 YRS FOR SMOKERS.
WEIGHT GAIN
 PATHOPHYSIOLOGY
• WT GAIN IS USUALLY DUE TO FAT, FLUID &/OR
MUSCLE.
• WT GAIN DUE TO EXCESS FAT IS OBESITY.
• OBESOGENIC ENVIRONMENT—
A. INCREASEING ENERGY INTAKE
B. DECREASING ENERGY EXPENDITURE
 A. INCREASEING ENERGY INTAKE

 INCREASE PORTION SIZE

 CONSUMTION OF ENERGY DENSE FOOD
 SNACKING & LOSS OF REGULAR MEALS
 AFFLUENCY
 B. DECREASING ENERGY EXPENDITURE

 INCREASE CAR OWNERSHIP

 AUTOMATION –REDUCES MANUAL LABOUR
 TIME SPEND IN COMPUTER GAME & TV
WATCHING
 REDUCE WALKING & SPORTS IN SCHOOL
 POTENTIALLY REVERSIBLE CAUSES OF WT
GAIN
• ENDOCRINE
 HYPOTHYROIDISM
 CUSHING’S SYNDROME
 INSULINOMA
 HYPOTHALAMIC TUMOUR/ INJURY
 DRUGS—
DRUGS—
 ATYPICAL ANTIPSYCHOTIC --OLANZAPINE, MIRTAZAPINE
 SU
 INSULIN
 PIZOTIFEN
 STEROIDS
 SODIUM VALPROATE
 BETA BLOCKER
 CLINICAL ASSESMENT
• AIMS ARE TO—
 QUANTIFY THE PROBLEM
 EXCLUDE AN UNDERLINE CAUSE
 IDENTIFY COMPLICATIONS
 REACH A Mx PLAN
 QUANTIFYING WITH BMI
BMI CLASSIFICATION
18.5 ---- 24.9 NORMAL
25 ---- 29.9 OVERWEIGHT
>30 OBESE
 COMPLICATIONS
RISK FACTOR OUTCOMES
METABOLIC CORONARY HEART
SYNDROME DISEASE
STROKE
DM COMPLICATIONS

LIVER FAT NASH

ACCUMULATION CIRRHOSIS
 COMPLICATIONS
RISK FACTOR OUTCOMES

RESTRICTED SOB(E)
VENTILATION OBSTRUCTIVE SLEEP
APNOEA
PICKWICKIAN
SYNDROME
 COMPLICATIONS
RISK FACTOR OUTCOMES
MECHANICAL EFFECT URINARY
INCONTINENCE
OA
VARICOSE VEINS
INCREASED HORMONE
PERIPHERAL STEROID DEPENDENT CANCER
INTERCOVERSION IN ( BREAST, UTERUS)
ADIPOSE TISSUE PCOS
 COMPLICATIONS
RISK FACTOR OUTCOMES
OTHERS PSYCHOLOGICAL
MORBIDITY
SOCIOECONOMIC
DISADVANTAGES
GALLSTONE
Ca COLON
SSTI
 SCRENING INVESTIGATION
• CBC
• CXR
• ECG
• B. GLUCOSE & HbA1c
• F. LIPID PROFILE
• LFT
• THYROID FUNCTION TEST
 Mx
• LIFE STYLE ADVICE
• WT LOSS DIET
• DRUGS—ORLISTAT
• SURGERY—
 Mx

• SURGERY—
 GASTRIC BANDING,
 SLEEVE GASTRECTOMY,
 ROUX-EN-Y GASTRIC BYPASS,
 DUODENAL SWITCH
 COSMETIC SURGERY (APRONENTOMY)
Thanks All
 NUTRIENT & VIT. DEFICIENCY
 IMPORTANT ELEMENT OF DIETERY H/O—
ASK ABOUTH WT
ABOUT CURRENT FOOD INTAKE
ABOUT SYMPTOMS THAT INTERFERE
WITHEATING
ABOUT ACTIVITY LEVELS/ PERFORMANCE
STATUS
 NUTRIENT & VIT. DEFICIENCY
 IMPORTANT ELEMENT OF DIETERY H/O—
ASK ABOUTH WT—
 CURRENT WT
 WT 2 WKS, 1 MON & 6 MON AGO
 ASSESMENT OF DEGREE OF CHANGE
ABOUT CURRENT FOOD INTAKE—
 QUANTITY OF FOOD & IF ANY CHANGE
 QUALITY OF FOOD
 AVOIDANCE OF SPECIFIC FOOD TYPE
 ANY NUTRITIONAL SUPPLIMENT
 ANY CHANGE IN APPETITE / INTEREST IN
FOOD
 ANY TASTE DISTURBANCE
ABOUT SYMPTOMS THAT INTERFERE WITHEATING—
 ORAL ULCER / PAIN
 DIFFICULTIES IN SWALLOWING
 NAUSEA / VOMITING
 EARLY SATIETY
 ALTERATION IN BOWEL HABIT
 ABDOMINAL / OTHER PAIN
ABOUT ACTIVITY LEVELS/ PERFORMANCE STATUS
ABOUT ACTIVITY LEVELS/ PERFORMANCE
STATUS—
 NORMAL ACTIVITY
 SLIGHTLY REDUCED ACTIVITY
 INACTIVE <50% OF THE TIME
 INACTIVE MOST OF THE TIME
 CLINICALLY IMPORTANT VITAMINS & THEIR
DEFICIENCIES
VITAMINS DEFICIENCY EXCESS
DISEASES
FAT SOLUBLOE VIT A
D
E
K
WATER SOLUBLE B
VIT C
VITAMINS DEFICIENCY VIT. EXCESS
DISEASES
FAT SOLUBLOE VIT A NIGHT BLINDNESS LIVER DAMAGE
XEROPHPHALMIA HYPEROSTOSIS
KERATOMALACIA TERATOGENECITY
CORNEAL HYPERCAROTENO
ULCERATION, SIS
SCARING ACUTE OVERDOSE
IRREVERSIBLE CAUSES—
BLINDNESS •NAUSEA
•HAEDACHE
•RAISED ICP
•SKIN
DESQUAAMATION
D
E
K
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS DEFICIENCY EXCESS
DISEASES
FAT SOLUBLOE VIT A

D USUALLY HYPERCALCAEMIA
ASYMPTOMATIC
OSTEOMALACIA
RICKETS
HAVE BEEN
ASSOCIATED WTH—
oMOST TYPE OF
CANCER
oDM
oMULTIPLE
SCLEROSIS
E
K
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS DEFICIENCY EXCESS
DISEASES
FAT SOLUBLOE VIT A
D
E HUMAN 1000 FOLD
DEFICIENCY IS RARE GREATER THAN
DEFICIENCY ONLY NORMAL
IN PREMATURE RECOMMENDED
INFANTS & IN DOSE ARE
MALABSOPTION CONSIDERED SAFE
CAUESES—
oHA
oATAXIA
oVISUAL
SCOTOMAS
K
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS DEFICIENCY EXCESS
DISEASES
FAT SOLUBLOE VIT A
D
E
K DELAYED SYMPTOMS OF
COAGULATION & EXCESS ONLY IN
BLEEDING INFANTS
oHAEMOLYSIS
oLIVER DISEASE
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS SUB DIVISION DEFICIENCY EXCESS
DISEASES
WATER B B1(THIAMINE)
SOLUBLE VIT B2(RIBOFLAVIN
)
B3(NIACIN,NIC
OTINIC
ACID,NOCOTIN
AMIDE)
B6(PYRIDOXINE
)
FOLATE
B12(COBALAMI
N)
BIOTIN
C
 S

VITAMINS DEFICIENCY DISEASES

EXCESS
WATER B COMPLEX B1 MAINLY IN CHRONIC
SOLUBLE VIT ALCOHOLISM BUT POOR DIET,
IMPAIRED ABSORBSORPTION &
STORAGE ,INRCEASED DEMAND
MAY CONTRIBUTE
BERI-BERI
oDRY (NEUROLOGICAL) BERI-
BERI
CHRONIC PERIPHERAL
NEUROPATHY WITH WRIST
&/OR FOOT DROP
KORSAKOFF’S PSYCHOSIS
WERNICKE’S
ENCEPHALOPATHY
oWET (CARDIAC) BERI-BERI–
BIVENTRICULAR FAILURE WITH
PULMONARY CONGESTION
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS SUB DIVISION DEFICIENCY EXCESS
DISEASES
WATER B B1(THIAMINE) GLOSSITIS
SOLUBLE VIT B2(RIBOFLAVIN ANGULAR
) STOMATITIS
CHEILOSIS
FACIAL
DYSSEBACEA

C
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS SUB DIVISION DEFICIENCY EXCESS
DISEASES
WATER B PELLAGRA– REVERSIBLE
SOLUBLE VIT DISEASE OF 3 HEPATITIS
Ds;-- FLUSHING
B3(NIACIN,NIC oDERMATITIS HYPOTENSIO
OTINIC oDIARRHOEA N
ACID,NOCOTIN oDEMENTIA
AMIDE)

C
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS SUB DIVISION DEFICIENCY EXCESS
DISEASES
WATER B PERIPHERAL SENSORY
SOLUBLE VIT NEUROPATHY POLYNEUROPAT
SIDEROBLAST HY
IC ANAEMIA
B6(PYRIDOXINE
)

C
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS SUB DIVISION DEFICIENCY EXCESS
DISEASES
WATER B 3 MAJOR COLON
SOLUBLE VIT BIRTH DEFECT CANCER
— THROUGH
SPINA BIFIDA GROWTH OF
ANENCEPHAL POLYPS
FOLATE Y
ENCEPHALOC
ELE
HEART
DISEASE
DEMENTIA
CANCER
C
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS SUB DIVISION DEFICIENCY DISEASES EXC
ESS
WATER B MEGALOBLASTIC ANAEMIA
SOLUBLE VIT
NEUROLOGICAL –

PERIPHERAL NERVE—
oGLOVES & STOCKING PARAESTHESIA
B12(COBALAMIN) oLOSS OF ANKLE JERK

SPINAL CORD—
oSCD

CEREBRUM
oDEMENTIA
oOPTIC ATROPHY

AUTONOMIC NEUROPATHY
C
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS SUB DIVISION DEFICIENCY EXCESS
DISEASES
WATER B SCALY
SOLUBLE VIT DERMATITIS
ALOPECIA
PARAESTHESI
A

BIOTIN
C
 CLINICALLY IMPORTANT VITAMINS &
THEIR DEFICIENCIES
VITAMINS DEFICIENCY EXCESS
DISEASES
WATER C SCURVY— DIARRHOEA
SOLUBLE VIT MENIFEST AS RENAL
 SWOLLEN OXALATE
GUMS THAT STONE
BLEED EASILY
PERIFOLLICUL
AR &
PETECHIAL HGE
ECHIMOSES
HAEMARTHR
OSIS
GI BLEEDING
ANAEMIA
POOR
WOUND
HEALING
 INORGANIC MICRONUTRIENTS
MINERALS DEFICIENCY DISEASES EXCESS
Ca & PHOSPHORUS Ca DEFICIENCY CAUSES— CONSTIPATION
 IMPAIRED BONE MILK ALKALY SYNDROME
MINERALISATION &
OSTEOMALACIAIN ADULT

PHOSPHATE DEFICIENCY
CAUSES MUSCLE
WEAKNESS
IRON IDA ACCUMULATION IN LIVER
& RARELY CIRRHOSIS
HAEMOCROMATOSIS
 INORGANIC MICRONUTRIENTS
MINERALS DEFICIENCY DISEASES EXCESS

IODINE ENDEMIC GOITRE

CRETINSM
ZINC DWARFISM
HYPOGONADISM
THYMIC ATROPHY
SELENIUM oHYPOTHYROIDISM HEART DISEASE
oCARDIOMYOPATHY IN
CHILD
oMYOPATHY IN ADULT
FLUORIDE DENTAL CARIES PITTING OF TEETH
Thanks All