"DiaBeTeS" being the most "trendy disease"

As per the WHO,
Diabetes mellitus (DM) is defined as a hetrogeneous metabolic disorder characterised by common feature of chronic hyperglycaemia with disturbance of carbohydrate, protein metabolism.

At this point, it is also important to understand another related term, metabolic syndrome (also
called syndrome X or insulin resistance syndrome), consisting of a combination of metabolic TYPE 2 DM This type comprises about 80% cases of DM.
It was previously called maturity-onset diabetes, or non-insulin dependent diabetes mellitus (NIDDM) of obese and non-obese type.
Although type 2 DM predominantly affects older individuals, it is now known that it also occurs in obese adolescent children;
Hence the term MOD for it is inappropriate. 
Moreover, many type 2 DM patients also require insulin therapy to control Hyperglycaemia or to prevent ketosis and
Thus are not truly non-insulin dependent contrary to its older nomenclature.

OTHER SPECIFIC ETIOLOGIC TYPES OF DM 
Besides the two main types, about 10% cases of DM have a known specific etiologic defect listed in Table 25.4. One important subtype abnormalities which increase the risk to develop diabetes mellitus and cardiovascular disease.

Major features of metabolic syndrome are-

1.   Central obesity,
2. Hypertriglyceridaemia,
3.  Low LDL cholesterol,
4.  Hyperglycaemia
5.  Hypertension.

DM is a leading cause of morbidity and mortality world over. It is expected to continue as a major health problem owing to its serious complications, especially end-stage renal
disease, IHD, gangrene of the lower extremities, and blindness
in the adults.
 Top 5 countries with highest prevalence of DM are
India, China, US, Indonesia and Japan.
 In India, its incidence is estimated at 7% of adult population (approximately 65 million
affected people), largely due to genetic susceptibility combined with changing life style of low-activity high-calorie diet in the growing Indian middle class. The incidence is somewhat low in
Africa. But prevalence of DM is expected to rise in developing countries of Asia and Africa due to urbanisation and associated obesity and increased body weight.
 The rise in prevalence is more for type 2 diabetes than for type 1. 
It is anticipated that by the year 2030 the number of diabetics globally will double from
the present figure of 250 million.
CLASSIFICATION AND ETIOLOGY
The older classification systems dividing DM into

1.  primary (idiopathic) 
2.  secondary types,
3.  juvenile-onset and 
4. maturity onset types, 
5.  insulin-dependent (IDDM) 
6.  non-insulin dependent (NIDDM)  have become obsolete and

undergone major revision due to extensive understanding of etiology and pathogenesis of DM in recent times.
As outlined in Table 25.4, 
Current Classification of DM based on etiology divides it into two broad categories—
Type 1and Type 2; 
besides there are a few uncommon specific etiologic types, and gestational DM. 
American Diabetes Association (2007) has identified risk factors for type 2 DM listed in
Table 25.5.
Brief comments on etiologic terminologies as contrasted
with former nomenclatures of DM are as under:
TYPE 1 DM It constitutes about 10% cases of DM. It was
previously termed as juvenile-onset diabetes (JOD) due to its
occurrence in younger age, and was called insulin-dependent
DM (IDDM) because it was known that these patients have
absolute requirement for insulin replacement as treatment.
However, in the new classification, neither age nor insulin-
dependence are considered as absolute criteria. Instead, based
on underlying etiology, 
Type 1 DM is further divided into 2 subtypes:

Subtype 1A (immune-mediated)
DM characterised by   " autoimmune destruction of β-cells which usually leads to insulin
deficiency."
Subtype 1B (idiopathic)
DM characterised by   "insulin deficiency with tendency to develop ketosis but these patients
are negative for autoimmune markers."

Though type 1 DM occurs commonly in patients under 30
years of age, autoimmune destruction of β-cells can occur at
any age. In fact, 5-10% patients who develop DM above 30 years
of age are of type 1A DM and hence the term JOD has becomeTYPE 2 DM This type comprises about 80% cases of DM. It was previously called maturity-onset diabetes, or non-insulin
dependent diabetes mellitus (NIDDM) of obese and non-
obese type.
Although type 2 DM predominantly affects older individuals,
it is now known that it also occurs in obese adolescent children;
hence the term MOD for it is inappropriate. Moreover, many
type 2 DM patients also require insulin therapy to control
hyperglycaemia or to prevent ketosis and thus are not truly
non-insulin dependent contrary to its older nomenclature.
OTHER SPECIFIC ETIOLOGIC TYPES OF DM
 Besides the two main types, about 10% cases of DM have a known specific
etiologic defect listed in Table 25.4. One important subtype

"ALCOHOL" AS A HUMAN FRIENDLY POISION

LEMME START WITH THE FAMOUS DIALOUGE FROM THE FILM
"DEVDAAS"
"Kon  Kmbkth bardasht krne k liye peeta 🍺hai "
I think now u can guess what im talking about
yeah yeah ....
its

ALCOHOL:-

INTRODUCTION:-
IT IS A HYDROCYLATED HYDROCARBON

Absorbtion:-
Alcohol is absorbed 20% through the empty stomach & 80% through the small intestine to the blood.
Liver where it’s metabolized by a specific enzyme at a constant rate.
It interferes with the normal brain functions such as judgment an coordination of muscle movements by acting of cerebellum & frontal lobe of brain.


1. Absorption is slower in the stomach than intestine.
2. Absorption is faster in empty stomach than when it contains food.
3. Food affects the absorption by delaying the emptying time of the stomach:
(i) Fatty foods, proteins and starch delay the absorption
(ii ) Milk has similar effect i.e., it delays absorption
(iii) Food prevents 10-20% of the ingested alcohol from being absorbed.
4. Diluted form of alcohol is absorbed slowly than the concentrated form
5. The type of beverage also affects the rate of absorption
.6. The absorption of alcohol depends on habituation and tolerance of the individual.
7. Emotional state of the person affects the contraction of the stomach resulting in rapid emptying time and the rate of absorption.
8. Drugs like Benzedrine and atropine slows the absorption and retards the emptying time.
9. The age of the person also has an effect on the absorption as it occurs less rapidly in younger (<35years) individuals.
10. Inhalation: Concentration in the blood is proportional to the concentration in the inspired air.
11. Weight of the subject: The same amount when taken by subjects of different weight has different blood levels depending upon the amount of bone, fat and muscles

• Excretion of the Alcohol:-
• Excreted 5% in urine,

5% in breath and very little through the sweat, feces and saliva.
In hot climates, significant amount is lost through the sweat

METABOLISM:-
??About 90% of the alcohol absorbed & oxidized in liver and rest 10% excreted.
??Alcohol from blood disappear at a rate of
10-15 ml/hour (15 mg % / hour) .
v Due to an increase in liver enzymes, chronic alcoholic can metabolize alcohol faster at the rate of 40-50 mg%/hour.
vMetabolized alcohol 10% get deposited in the tissues in the form of cholesterol and fats.

ALCOHOLIC BEVERAGES:-
Any fermented liquor, such as wine, beer, or distilled liquor, that contains ethyl alcohol, or ethanol, as an intoxicating agent.y fermented liquor, such as wine, beer, or distilled liquor, that contains ethyl alcohol, or ethanol, as an intoxicating agent. fermented liquor, such as wine, beer, or distilled liquor, that contains ethyl alcohol, or ethanol, as an intoxicating agent.

ALCOHOLIC %IN DIFFERENT BEVERAGES

1. Rum 50-60
2. Whisky / Gin / Brandy 40-45%
3. Sherry & Port Wine 15-20%
4. Wine 10-15
5. Beer 04-08%
6. Liquor 35-60
7. Alcohol Varies

General measuring terms used
One unit of alcohol is the amount of alcohol metabolized by the liver in one hour.
One pint of beer is one unit of alcohol.
One glass of wine or sherry or single whisky each provides 8 grams of pure alcohol,which is one unit.

ALCOHOL POISONING:-Ethyl alcohol depresses the central nervous system irregularly in descending order from cortex to medulla.
—ACUTE POISONING OR ALCOHOLIC INTOXICATION
—It results from consumption of alcohol either in small does at shorter intervals or in one big dose.
MC EVANS SIGNS
—Pinching the skin of the neck or face
—The constricted pupil will get dilated.

SYMPTOMS:
—The symptoms are entirely due to its narcotic action on central nervous system-
—It produces 3 stages viz. (from medicolegal angle)
1) Excitement (0.05-0.01%)
2) Incoordination (0.2-0.5%)
3) Narcosis (0.5% & Above)

SOBER STAGE:-
??Person looks absolutely normal
—Blood concentration:
—10-50 mg %

STAGE OF EUPHORIA:-
??Person is delighted
A feeling well being
—Increased self confidence
—Blood con: 50-100 mg %

STAGE OF EXCITEMENT:-
??Person is delighted
??A feeling well being
??Increased self confidence
??Blood con: 50-100 mg %

STAGE OF CONFUSION:-

1. Blood Con. 150-200 mg %
2. —Mental confusion
3. —Disorientation
4. —Vertigo
5. —Visual disturbances
6. —Increased muscular incoordiantion
7. —Staggering gait
8. —Slurred speech

STAGE OF STUPOR

??Blood Con. 150-200 mg %

??Mental confusion

??Disorientation

??Vertigo

??Visual disturbances

??Increased muscular incoordiantion

??Staggering gait

??Slurred speech 

STAGE OF COMA:-

—Dead drunk

—Blood con: 300-500 mg %

—Deeply unconscious

—Hypothermia 

Difficulty in breathing 

DEATH

—Blood Con: > 500 mg%
—Respiratory Failure  

• Hangover- as death is rare in alcohol poisoning, person recovers after prolonged sleep but may suffer from headache, irritability, nausea and abdominal discomfort.
  Most of the hangover symptoms are due to congeners and hypoglycemia induced by alcohol.
   

GET A HEAD ATTACK BY READING ABOUT "HEART ATTACK"

MYOCARDIAL INFARCTION

INTRODUCTION:-

•  Myocardial infarction (MI) is the most important and feared consequence of coronary artery disease.
• Many patients may die within the first few hours of the onset, while remainder suffer from effects of impaired cardiac function.
•  A significant factor that may prevent or diminish the myocardial damage is the development of collateral circulation through anastomotic channels over a period of time.
•  A regular and well-planned exercise programme encourages good collateral circulation and improved cardiac performance.

INCIDENCE:-
 In developed countries, acute MI accounts for
10-25% of all deaths. Due to the dominant etiologic role of
coronary atherosclerosis in acute MI, the incidence of acute
MI correlates well with the incidence of atherosclerosis in a
geographic area.

Age:-
 Acute MI may virtually occur at all ages, though the
incidence is higher in the elderly. About 5% of heart attacks
occur in young people under the age of 40 years, particularly
in those with major risk factors to develop atherosclerosis
like hypertension, diabetes mellitus, cigarette smoking and
dyslipidaemia including familial hypercholesterolaemia.

Sex:-
 Males throughout their life are at a significantly higher
risk of developing acute MI as compared to females. Women
during reproductive period have remarkably low incidence of
acute MI, probably due to the protective influence of oestrogen.
The use of oral contraceptives is associated with high risk of
developing acute MI. After menopause, this gender difference
gradually declines but the incidence of disease among women
never reaches that among men of the same age.

ETIOPATHOGENESIS:-
 The etiologic role of severe coronary
atherosclerosis (more than 75% compromise of lumen)
of one or more of the three major coronary arterial
trunks
in the pathogenesis of about 90% cases of acute MI is well
documented by autopsy studies as well as by coronary angiographic
studies. A few notable features in the development of
acute MI are as under:
1. Myocardial ischaemia Myocardial ischaemia is brought
about by one or more of the following mechanisms:
i) Diminished coronary blood flow e.g. in coronary artery
disease, shock.
ii) Increased myocardial demand e.g. in exercise, emotions.
iii) Hypertrophy of the heart without simultaneous increase
of coronary blood flow e.g. in hypertension, valvular heart
disease.
2. Role of platelets Rupture of an atherosclerotic plaque
exposes the subendothelial collagen to platelets which
undergo aggregation, activation and release reaction. These
events contribute to the build-up of the platelet mass that may
give rise to emboli or initiate thrombosis.
3. Acute plaque rupture In general, slowly-developing
coronary ischaemia from stenosing coronary atherosclerosis of
high-grade may not cause acute MI but continue to produce
episodes of angina pectoris. But acute complications in
coronary atherosclerotic plaques in the form of superimposed
coronary thrombosis due to plaque rupture and plaque
haemorrhage is frequently encountered in cases of acute MI:
i) Superimposed coronary thrombosis due to disruption of
plaque is seen in about half the cases of acute MI. Infusion
of intracoronary fibrinolysins
in the first half an hour of
development of acute MI in such cases restores blood flow in
the blocked vessel in majority of cases.
ii) Intramural haemorrhage is found in about one-third cases
of acute MI.
Plaque haemorrhage and thrombosis may occur together
in some cases.
4. Non-atherosclerotic causes About 10% cases of acute
MI are caused by non-atherosclerotic factors such as coronary
vasospasm, arteritis, coronary ostial stenosis,
embolism,
thrombotic
diseases, trauma and outside compression as
already described.
5. Transmural versus subendocardial infarcts There
are some differences in the pathogenesis of the transmural
infarcts involving the full thickness of ventricular wall and the
subendocardial (laminar) infarcts affecting the inner subendocardial
one-third to half
i) Transmural (full thickness) infarcts are the most common
type seen in 95% cases. Critical coronary narrowing
(more than 75% compromised lumen) is of great significance in
the causation of such infarcts. Atherosclerotic plaques with
superimposed thrombosis and intramural haemorrhage are
significant in about 90% cases, and non-atherosclerotic causes
in the remaining 10% cases.
ii) Subendocardial (laminar) infarcts have their genesis in
reduced coronary perfusion due to coronary atherosclerosis
but without critical stenosis (not necessarily 75% compromised
lumen), aortic stenosis or haemorrhagic shock. This is because
subendocardial myocardium is normally least well perfused
by coronaries and thus is more vulnerable to any reduction
in the coronary flow. Superimposed coronary thrombosis
is frequently encountered in these cases too, and hence the
beneficial role of fibrinolytic treatment in such patients.

TYPES OF INFARCTS :-
Infarcts have been classified in a
number of ways by the physicians and the pathologists:
1. According to the anatomic region of the left ventricle involved,
they are called anterior, posterior (inferior), lateral,
septal and circumferential, and their combinations
like anterolateral,
posterolateral (or inferolateral) and anteroseptal.

2. According to the degree of thickness of the ventricular wall
involved, infarcts are of two types 
i) Full-thickness or transmural, when they involve the entire
thickness of the ventricular wall.
ii) Subendocardial or laminar, when they occupy the inner
subendocardial half of the myocardium.

3. According to, the age of infarcts they are of two types:
i) Newly-formed infarcts called as acute, recent or fresh.
ii) Advanced infarcts called as old, healed or organised.

LOCATION OF INFARCTS:-


Infarcts are most frequently located in the left ventricle. Right ventricle is less susceptible
to infarction due to its thin wall, having less metabolic requirements  and is thus adequately nourished by the thebesian vessels. 
Atrial infarcts, whenever present, are more often in the right atrium, usually accompanying the infarct
of the left ventricle.
Left atrium is relatively protected from infarction because it is supplied by the oxygenated blood in the left atrial chamber.
The region of infarction depends upon the area of obstructed blood supply by one or more of the three coronary arterial trunks.

Accordingly, there are three regions of myocardial infarction:-

1. Stenosis of the left anterior descending coronary artery is the
most common (40-50%). The region of infarction is the anterior
part of the left ventricle including the apex and the anterior
two-thirds of the interventricular septum.
2. Stenosis of the right coronary artery is the next most frequent
(30-40%). It involves the posterior part of the left ventricle
and the posterior one-third of the interventricular septum.
3. Stenosis of the left circumflex coronary artery is seen least
frequently (15-20%). Its area of involvement is the lateral wall
of the left ventricle.

EVERY MEDICO SHOULD KNOW ABOUT "CHRONIC MYELOID LEUKAEMIA"

Definition and Pathophysiology

By WHO definition,

1. CML is  identification of the clone of haematopoietic stem cell that possesses the balanced reciprocal translocation between chromosomes 9 and 22, forming Philadelphia chromosome.
2. The t(9;22) involves fusion of BCR (breakpoint cluster region) gene onThe Philadelphia (Ph) chromosome. 
3. There is reciprocal translocation of the part of the long arms of chromosome 22 to the long arms of chromosome 9 written as t(9;22). gene located on chromosome 9q34. 
4. The fusion product so formed is termed “Ph chromosome t(9;22)(q34;11), BCR/ABL” which should be positive for making the diagnosis of CML. 

This identification may be done by PCR or by FISH. 


Pathophysiology

includes the mechanism of human CML is based on observing the
BCR/ABL fusion product proteins are capable of transforming haematopoietic progenitor cells in vitro and form malignant clone. BCR/ABL fusion product brings about following functional changes:
i) ABL protein is activated to function as a tyrosine kinase enzyme
that in turn activates other kinases which inhibits apoptosis.
ii) Ability of ABL to act as DNA-binding protein is altered.
iii) Binding of ABL to actin microfilaments of the cytoskeleton
is increased.
Exact mechanism of progression of CML to the blastic
phase is unclear but following mechanisms may be involved:
i) Structural alterations in tumour suppressor p53 gene.
ii) Structural alterations in tumour suppressor RB gene.
iii) Alterations in RAS oncogene.
iv) Alterations in MYC oncogene.
v) Release of cytokine IL-1b.
vi) Functional inactivation of tumour suppressor protein,
phosphatase A2.
Clinical Features
Chronic myeloid (myelogenous, granulocytic) leukaemia
comprises about 
20% of all leukaemias
 its peak incidence is seen in 3rd and 4th decades of life.
 A distinctive variant of CML seen in children is called juvenile CML. 
Both sexes are affected equally. 
The onset generally insidious.
 Some of the common presenting manifestations are :-
1. Features of anaemia such as weakness, pallor, dyspnoea and tachycardia.
2. Symptoms due to hypermetabolism such as weight loss, lassitude, anorexia, night sweats.
3. Splenomegaly is almost always present .In some patients, it may be associated with acute pain due to splenic infarction.
4. Bleeding tendencies such as easy bruising, epistaxis, menorrhagia and haematomas may occur.
5. Less common features include gout, visual disturbance, neurologic manifestations and priapism.
6. Juvenile CML is more often associated with lymph node enlargement than splenomegaly. Other features are frequent infections, haemorrhagic manifestations and facial rash.

Laboratory Findings
The diagnosis of CML
blood picture alone... but bone marrow, cytochemical stains can be used

I. BLOOD PICTURE 
1. Anaemia:-  
moderate degree
normocytic normochromic
Occasional normoblasts may be present.

2. White blood cells 
 marked leucocytosis 
(approximately 200,000/μl or more at the time of presentation). 

The natural history of CML consists of 3 phases—

1. Chronic
2. accelerated 
3. blastic.

””Chronic phase of CML 
myeloproliferative disorder
proliferation of 

1. myeloid cells  (i.e. myelocytes and metamyelocytes) 
2. mature segmented neutrophils.

Myeloblasts usually do not exceed 10% of cells in
the peripheral blood and bone marrow
An increase in the proportion of basophils up to 10% is a characteristic feature of CML.
A rising basophilia is indicative of impending blastic transformation.
An accelerated phase of CML is also rising leucocytosis
associated with thrombocytosis or thrombocytopenia and
splenomegaly.

Accelerated phase has increasing degree of anaemia, blast count in blood or marrow between 10-20%,
marrow basophils 20% or more, and platelet count falling
below 1,00,000/μl.
””Blastic phase or blast crisis in CML fulfills the definition
of acute leukaemia in having blood or marrow blasts >20%.
These blast cells may be myeloid, lymphoid, erythroid
or undifferentiated and are established by morphology,
cytochemistry, or immunophenotyping. 
Myeloid blast crisis
in CML is more common and resembles AML. However,
unlike AML, Auer rods are not seen in myeloblasts of CML
in blast crisis.
3. Platelets Platelet count may be normal but is raised in
about half the cases.

 BONE MARROW EXAMINATION
 Examination of marrow aspiration yields the following results:
1. Cellularity Generally, there is hypercellularity with
total or partial replacement of fat spaces by proliferating
myeloid cells.
2. Myeloid cells The myeloid cells predominate in the
bone marrow with increased myeloid-erythroid ratio.
The differential counts of myeloid cells in the marrow
show similar findings as seen in the peripheral blood with
predominance of myelocytes.
3. Erythropoiesis Erythropoiesis is normoblastic but
there is reduction in erythropoietic cells.
4. Megakaryocytes Megakaryocytes are conspicuous but
are usually smaller in size than normal.
5. Cytogenetics Cytogenetic studies on blood and
bone marrow cells show the characteristic chromosomal
abnormality called Philadelphia (Ph) chromosome seen
in 90-95% cases of CML. Ph chromosome is formed by
reciprocal balanced translocation between part of long arm
of chromosome 22 and part of long arm of chromosome
9{(t(9;22) (q34;11)} forming product of fusion gene, BCR/
ABL (see Fig. 12.11).
III. CYTOCHEMISTRY 
The only significant finding on
cytochemical stains is reduced scores of neutrophil alkaline
phosphatase (NAP) which helps to distinguish CML from
myeloid leukaemoid reaction in which case NAP scores are
elevated (see Fig. 12.10,B, and Table 12.3). However, NAP
scores in CML return to normal with successful therapy,
corticosteroid administration and in infections.
IV. OTHER INVESTIGATIONS A few other accompanying
findings are seen in CML:
1. Elevated serum B12 and vitamin B12 binding capacity.
2. Elevated serum uric acid (hyperuricaemia).

WHO CLASSIFICATION OF MYELOID NEOPLASM
MYELOPROLIFERATIVE DISEASES
1. Chronic myeloid leukaemia (CML), {Ph chromosome t(9;22)
(q34;11), BCR/ABL-positive}
2. Chronic neutrophilic leukaemia
3. Chronic eosinophilic leukaemia/ hypereosinophilic
syndrome
4. Chronic idiopathic myelofibrosis
5. Polycythaemia vera (PV)
6. Essential thrombocythaemia (ET)
7. Chronic myeloproliferative disease, unclassifiable
II. MYELODYSPLASTIC/MYELOPROLIFERATIVE DISEASES
1. Chronic myelomonocytic leukaemia (CMML)
III. MYELODYSPLASTIC SYNDROME (MDS)
1. Refractory anaemia (RA)
2. Refractory anaemia with ring sideroblasts (RARS)
3. Refractory cytopenia with multilineage dysplasia (RCMD)
4. RCMD with ringed sideroblasts (RCMD-RS)
5. Refractory anaemia with excess blasts (RAEB-1)
6. RAEB-2
7. Myelodysplastic syndrome unclassified (MDS-U)
8. MDS with isolated del 5q
IV. ACUTE MYELOID LEUKAEMIA (AML)
1. Acute myeloid leukaemias with recurrent genetic
abnormalities
i. AML with t(8;21)(q22;q22); RUNX1-RUNX1T1
ii. AML with inv(16)(p13.1;q22) or t(16;16)(p13.1;q22); CBF
& b-MYH11
iii. Acute promyelocytic leukaemia (M3) with t(15;17)
(q22;q12); PML/RAR-a and variants
iv. AML with t(9;11)(p22;q23); MLLT3-MLL
v. AML with t(6;9)(p23;q34); DEK-NUP214
vi. AML with inv(3)(q21q26.2) or t(3;3)(q21;q26.2); RPN1-
EVI1
vii. AML (megakaryoblastic) with t(1;22)(p13;q13); RBM15-
MKL1
viii. AML with mutated NPM1
ix. AML with mutated CEBPA
2. Acute myeloid leukaemia with myelodysplasia related
changes
3. Therapy related acute myeloid leukaemia
i. Alkylating agent related
ii. Topoisomerase II inhibitor related (some may be
lymphoid)
4. Acute myeloid leukaemia, not otherwise categorised
i. AML minimally differentiated (M0)
ii. AML without maturation (M1)
iii. AML with maturation (M2)*
iv. Acute myelomonocytic leukaemia (M4)
v. Acute monoblastic and monocytic leukaemia (M5a,
M5b)
vi. Acute erythroid leukaemia (M6)
vii. Acute megakaryoblastic leukaemia (M7)
viii. Acute basophilic leukaemia
ix. Acute panmyelosis with myelofibrosis
5. Myeloid sarcoma
6. Myeloid proliferations related to Down’s syndrome
i. Transient abnormal myelopoiesis
ii. Myeloid leukaemia associated with Down’s syndrome
7. Blastic plasmacytoid dentritic cell neoplasm
V. ACUTE BIPHENOTYPIC LEUKEMIA

A BRIEF about GANGRENE

CHANGES AFTER CELL DEATH
Two types of pathologic changes may superimpose following
cell injury: gangrene (after necrosis) and pathologic calcifi -
cation (after degenerations as well as necrosis).

GANGRENE
Gangrene is necrosis of tissue associated with superadded
putrefaction, most often following coagulative necrosis due to
ischaemia (e.g. in gangrene of the bowel, gangrene of limb).
On the other hand, gangrenous or necrotising infl ammation is
characterised primarily by inflammation provoked by virulent
bacteria resulting in massive tissue necrosis. Thus, the endresult
of necrotising infl ammation and gangrene is the same
but the way the two are produced, is diff erent. The examples
of necrotising infl ammation are: gangre nous appendicitis,
gangrenous stomatitis (noma, cancrum oris).
There are 2 main types of gangrene—dry and wet, and
a variant of wet gangrene called gas gangrene. In all types of
gangrene, necrosis undergoes liquefaction by the action of
putrefactive bacteria.

Dry Gangrene
Th is form of gangrene begins in the distal part of a limb due
to ischaemia. Th e typical example is the dry gangrene in the toes and feet of an old patient due to severe atherossclerosis.

Other causes of dry gangrene foot include thromboangiitis

obliterans (Buerger’s disease), Raynaud’s disease, trauma,

ergot poisoning. It is usually initiated in one of the toes which

is farthest from the blood supply, containing so little blood that

even the invading bacteria fi nd it hard to grow in the necrosed

tissue. Th e gangrene spreads slowly upwards until it reaches

a point where the blood supply is adequate to keep the tissue

viable. A line of separation is formed at this point between the

gangrenous part and the viable part.

MORPHOLOGIC FEATURES Grossly, the aff ec ted part

is dry, shrunken and dark black, resemb ling the foot of

a mummy. It is black due to liberation of haemoglobin

from haemolysed red blood cells which is acted upon by

hydrogen disulfi de (H2S) produced by bacteria resulting in

formation of black iron sulfi de. Th e line of separation usually

brings about complete separation with eventual falling off

of the gangrenous tissue if it is not removed surgi cally (i.e.

spontaneous amputation) (Fig. 2.29).

Histologically, there is necrosis with smudging of the tissue.

Th e line of separation consists of infl am matory granulation

tissue (Fig. 2.30).

Wet Gangrene

Wet gangrene occurs in naturally moist tissues and organs such

as the bowel, lung, mouth, cervix, vulva etc. To other examples

of wet gangrene having clinical signifi cance are as follows:

 Diabetic foot which is due to high glucose content in the

necrosed tissue which favours growth of bacteria.

 Bed sores occurring in a bed-ridden patient due to pressure

on sites like the sacrum, buttocks and heel.

Wet gangrene usually develops due to blockage of both

venous as well as arterial blood fl ow and is more rapid.

Th e aff ected part is stuff ed with blood which favours the

rapid growth of putrefactive bacteria. Th e toxic products

formed by bacteria are absorbed causing profound systemic

manifestations of septicaemia, and fi nally death. Th e spreading

wet gangrene generally lacks clear-cut line of demarcation and

may spread to peritoneal cavity causing peritonitis.

MORPHOLOGIC FEATURES Grossly, the aff ected part is

soft, swollen, putrid, rotten and dark. Th e classic example

is gangrene of the bowel, commonly due to strangulated

hernia, volvulus or intussuscep tion. Th e part is stained

dark black due to the same mecha nism as in dry gangrene

Histologically, there is coagulative necrosis with stuffi ng

of aff ected part with blood. Th e mucosa is ulcerated

and sloughed. Lumen of the bowel contains mucus and

blood. Th ere is intense acute infl ammatory exudates and

thrombosed vessels. Th e line of demarcation between

gangrenous segment and viable bowel is generally not clearcut

GAS GANGRENE 

It is a special form of wet gangrene caused

by gas-forming clostridia (gram-positive anaerobic bacteria)

which gain entry into the tissues through open contaminated

wounds, especially in the muscles, or as a complication

of operation on colon which normally contains clostridia.

Clostridia produce various toxins which produce necrosis and

oedema locally and are also absorbed producing profound

systemic manifes tations.

MORPHOLOGIC FEATURES Grossly, the aff ected

area is swollen, oedematous, painful and crepitant due to

accumulation of gas bubbles of carbon dioxide within the

tissues formed by fermentation of sugars by bacterial toxins

Subsequently, the aff ected tissue becomes dark black and is

foul smelling.

Microscopically, the muscle fi bres undergo coagu lative

necrosis with liquefaction. Large number of gram-positive

bacilli can be identifi ed. At the peri phery, a zone of

leucocytic infi ltration, oedema and conges tion are found.

Capillary and venous thrombi are common.

You MUST GET EVERTHING IN YOUR HEAD ABOUT " HEAD INJURY"

                 HEAD INJURY CLASSIFICATION

Depending on the state of dura:
—Closed head injury- dura intact, irrespective of skull fracture
—Open head injury - dura open, torn by penetrating injury, bone fragment or due to skull fracture
Contents:—Scalp injury.——Injury to face.——skull fracture.——Injury to meninges.——Injury to brain.
Head injury: It is defined as a morbid state resulting from gross or subtle structural changes in the scalp , skull and/or the contents of the skull produced by mechanical force.SCALP INJURIESScalp is covering of head extending from eyebrows superiorly to posterior nuchal line and laterally bounded by temporal lines  
Layers are:—
Skin—
Connective tissue
—Aponeurosis—
Loose areolar tissue—
Periosteum


Following injuries may occur on  scalp:
1.Abrasion
2.Contusion
3.Laceration ( linear y- shaped, stellate , cruciate, penetration, crescent.etc)
4.Incise wound
5.Avulsion
6.Puncture wounds—
Contusion of scalp:Ectopic bruises:
Mobile contusion of ant. scalp may shift downwards producing black eye or spectacle haematoma/racoon eyeContusion in temporal scalp shifting downwards behind ear is similar to battle sign.Hematoma below the aponeurotica is commonly called under scalp hematoma.

—Under scalp haematoma: Beneath aponeurotica—INJURY TO FACE-
  —Abrasion
—Contusion
—Laceration—Incised wound—Chop—Penetrating wound—Fracture of bone.
— INJURY TO TEETH-—of tooth/teeth.—Dislocation of tooth/ teeth—Contusion of gums—Laceration of gums—Fracture of alveolar margins.SKULL FRACTURE- General deformation:    Skull behaves like an elastic sphere. Fracture may be due to :—Impact on one plane—Compression between two objectsFracture seen at distal site.  Combination of focal and general deformation produces spider web pattern
Puppe’s rule:  When 2 or more separate fractures occur from successive impacts and meet each other , the second fracture will terminate in the first fracture.FORCE APPLIED TO CHIN-

Types of skull fracture

1.VAULT FRACTURE

1.Linear/fissured
2.Depressed
3.Comminuted/spider web
4.Pond orindented
5.Gutter
6.Sutural
7.Perforating
8.Cut 

2.BASILAR  FRACTURES
1.Linear/fissured
2.Ring
3.Hinge
4.Longitudinal
5.Secondary
——