90. Acute tubular necrosis - ischemic and toxic.

Acute tubular necrosis (ATN) is a medical condition involving the death of

tubular cells that form the tubule that transports urine to the ureters while
reabsorbing 99% of the water.
Classification:
It may be classified as either toxic or ischemic.
Toxic ATN occurs when the tubular cells are exposed to a toxic
substance (nephrotoxic ATN). It can be caused by free hemoglobin or
myoglobin, by medication such as antibiotics ( e.g. aminoglycoside and
cytoxic drugs such as cisplatin), or by intoxication.
Histopathology: Toxic ATN is characterized by proximal tubular
epithelium necrosis (no nuclei, intense eosinophilic homogeneous
cytoplasm) due to a toxic substance (poisons, drugs, heavy metals).
Necrotic cells fall into the tubule lumen, obturating it, and determining
acute renal failure. Basement membrane is intact, so the tubular
epithelium regeneration is possible. Glomeruli are not affected.
Ischemic ATN occurs when the tubular cells do not get enough oxygen,
a condition that they are highly sensitive and susceptible to, due to
their very high metabolism. It can be caused when the kidneys are not
sufficiently perfused for a long period of time (i.e. renal artery
stenosis) or during shock. Hypoperfusion can also be caused by
embolism of the renal arteries. Ischemic ATN specifically causes skip
lesions through the tubules.
91. Nephrolithiasis. Complications.

Renal stones are a solid concretion or crystal aggregation formed in the

kidneys from dietary minerals in the urine. Kidney stones typically leave
the body by passage in the urine stream, and many stones are formed
and passed without causing symptoms. If stones grow to sufficient
size(at least 3 millimeters), they can cause obstruction of the ureter.
Causes: Dietary factors that increase the risk of stone formation include
low fluid intake and high dietary intake of animal protein, sodium,
refined sugars, fructose, etc.

Calcium is one component of the most common type of human kidney

stones, calcium oxalate. Unlike supplemental calcium, high intakes of
dietary calcium do not cause kidney stones and may actually protect
against their development. This is related to the role of calcium in
binding ingested oxalate in the gastrointestinal tract.
Pathophysiology:
supersaturation of the urine: When the urine becomes
supersaturated (when the urine solvent contains more solutes
than it can hold in solution) with one or more calculogenic
substances, a seed crystal may form through the process of
nucleation. Heterogenous nucleation proceeds more rapidly than
homogenous nucleation, because it requires less energy.
Adhering to cells on the surface of a renal papilla, a seed crystal
can grow and aggregate into an organized mass. Depending on
the chemical composition of the crystal, the stone-forming
process may proceed more rapidly when the urine pH is unusually
high or low.
Inhibitors of stone formation: Normal urine contains chelating
agents, such as citrate, that inhibit the nucleation, growth, and
aggregation of calcium-containing crystals. Other endogenous
inhibitors include glycosaminoglycans, prothrombin F1 peptide,
nephrocalcin. When these substances fall below their normal
proportions, stones can form from an aggregation of crystals.
92. Tumors of the kidney and the urinary tract.
Tumors of the kidney: The simplest division of tumors of the kidney is into benign and
malignant. The benign are again, divided into fibroma, lipoma, lymphadenoma,
angionoma, and adenoma. These grow in the cortex of the kidney, forming small nodular
masses, and unless they become very large, an exception, they do not produce any definite
symptoms. They may be congenital or develop later in life.
The malignant tumors are sarcoma and carcinoma, and may be primary or secondary.
While sarcoma may occur in the adult, it is more frequently found in young children, often
being congenital. The most common form is the small-celled variety, while a rare form,
and one generally congenital, is a mixture of sarcoma and striped muscular fiber, the
rhabdomyoma.
Sarcomas develop very rapidly, are vascular, and may attain large size, almost filling the
abdomen.
Carcinoma is not so common as sarcoma, and generally is found in the adult, though it
may occur in children. It is usually soft, encephaloid, and may reach an enormous
2

development. Primary cancer rarely occurs in early life, and is more common in males than
in females. Heredity is a strong predisposing cause.
Secondary carcinoma is found in connection with cancer of the testicle, rectum, uterus,
stomach, or liver.
Symptoms.The characteristic symptoms are pain, hematuria, cancerous cachexia, and
the presence of the tumor mass.
Pain is not always present, and therefore more or less uncertain as a diagnostic aid. When
present, it is located in the affected flank, and extends down the ureter and along the inner
side of the thigh. It may be more or less constant, of a dragging character, or occur at
intervals, and be sharp and lancinating. Hemorrhage occurs in about half the cases, and
though it is usually but small in quantity, it may be severe and exhausting. At times it will
be in clots, there will be casts of the pelvis of the kidney and ureter, and when thus passed
are characteristic of a malignant tumor; often, however, they are mixed with the urine and
perfectly soluble.
Where the hemorrhage is large, anemia rapidly develops. As long as the tumor retains the
position and outline of the kidney it is an important symptom; but as it leaves the flank and
encroaches upon the abdomen, and adhesions form, it may be impossible to distinguish it
from other tumors of the abdomen, though the cancerous cachexia would help in the
differential diagnosis. As the disease advances, the appetite fails, nausea and vomiting are
frequently present, and the emaciation becomes marked.

Treatment.While we have no specifics for malignant growths, there are two remedies
that should be given persistently, with the hope of at least staying somewhat the
destructive character of the disease. They are echinacea and hydrastis. When severe, the
pain will be controlled by morphia. Extirpation may prolong life if resorted to early,
though the diagnosis is usually only made after the system has become so thoroughly
infected with the malignant poison, that successful nephrectomies are very rare.
UT rumors: About 95% of urinary tract tumors are of epithelial origin, the remainder being
mesenchymal tumors. Most epithelial tumors are composed of urothelial (transitional) type
cells and are thus interchangeably called urothelial or transitional tumors, but squamous
and glandular carcinomas also occur. A small number of benign neoplasias of the urinary
tract are represented by small tumors generally of mesenchymal origin. The two most
common are fibroepithelial polyps and leiomyomas. The fibroepithelial polyp is a tumorlike lesion that grossly presents as a small mass projecting into the lumen. The lesion
occurs more commonly in the ureters (left more often than right) but may also appear in
the bladder, renal pelves, and urethra. The polyp presents as a loose, vascularized
connective tissue mass lying beneath the mucosa.

93. Nephrocirrhosis - types. Macroscopic differential diagnosis.

Cirrhosis is a consequence of chronic liver disease characterized by
replacement of liver tissue by fibrosis, scar tissue and regenerative
nodules leading to loss of liver function. Loss of liver function affects the body in
many ways. Cirrhosis, if severe enough, can cause many different complications.
These can be severe, as Hepatorenal syndrome ,for unknown reasons, liver
failure leads to kidney failure in some people.
3

Hepatorenal syndrome (often abbreviated HRS) is a life-threatening medical

condition that consists of rapid deterioration in kidney function in individuals
with cirrhosis or fulminant liver failure.
The classification of hepatorenal syndrome identifies two categories of renal
failure, termed type 1 and type 2 HRS, which both occur in individuals with
either cirrhosis or fulminant liver failure. In both categories, the deterioration in
kidney function is quantified either by an elevation in creatinine level in the blood,
or by decreased clearance of creatinine in the urine.

Type 1 HRS is characterized by rapidly progressive renal failure, with a doubling

of serum creatinine to a level greater than 221 mol/L (2.5 mg/dL) or a halving of
the creatinine clearance to less than 20 mL/min over a period of less than two
weeks. Patients with type 1 HRS are usually ill, may have low blood pressure,
and may require therapy with drugs to improve the strength of heart muscle
contraction (inotropes) or other drugs to maintain blood pressure
In contrast, type 2 HRS is slower in onset and progression. It is defined by an
increase in serum creatinine level to >133 mol/L (1.5 mg/dL) or a creatinine
clearance of less than 40 mL/min, and a urine sodium < 10 mol/L. Most
individuals with type 2 HRS have diuretic-resistant ascites before they develop
deterioration in kidney function.

Diagnosis
The major criteria include liver disease with portal hypertension; renal failure the
absence of shock, infection, recent treatment with medications that affect the function of
the kidney (nephrotoxins), and fluid losses the absence of sustained improvement in
renal function despite treatment with 1.5 litres of intravenous normal saline; the absence
of proteinuria (protein in theurine); and, the absence of renal disease or obstruction of
renal outflow as seen on ultrasound
The minor criteria are the following: a low urine volume (less than 500 mL (18 imp fl oz;
17 US fl oz) per day), low sodium concentration in the urine, a urine osmolality that is
greater than that in the blood, the absence of red blood cells in the urine, and a serum
sodium concentration of less than 130 mmol/L

The renal failure of HRS is a consequence of these changes in blood flow, rather than
direct damage to the kidney; the kidneys themselves appear normal to the naked eye and
tissue is normal when viewed under the microscope, and the kidneys even function
normally when placed in an otherwise healthy environment (such as if transplanted into a
person with a healthy liver). The diagnosis of hepatorenal syndrome is based on
laboratory tests of individuals susceptible to the condition.

94. Acute and chronic renal failure. Pathogenesis. Organs involvement

in uremia, morphology.

Renal failure is a medical condition in which the kidneys fail to adequately

filter waste products from the blood. The two main forms are acute kidney
injury, which is often reversible with adequate treatment, and chronic kidney
disease, which is often not reversible.
Renal failure is mainly determined by a decrease in glomerular filtration rate,
the rate at which blood is filtered in the glomeruli of the kidney. This is
detected by a decrease in or absence of urine production or determination of
waste products (creatinine or urea) in the blood.
Signs: In renal failure, there may be problems with increased fluid in the
body (leading to swelling), increased acid levels, raised levels of potassium,
decreased levels of calcium, increased levels of phosphate, and in later stages
anemia. Bone health may also be affected. Long-term kidney problems are
associated with an increased risk of cardiovascular disease.
Acute failure of the kidneys is a condition in which there is a rapid loss of
the normal function of your kidneys, due to a sudden, acute or chronic insult.
This means that they can not perform their normal functions, resulting in a
range of complications. Some of these include: the build up of waste products
that the kidneys usually excrete, such as urea and creatinine, high or low
concentrations of molecules such as sodium and potassium, low numbers of
red blood cells, inability to concentrate the urine properly and build up of
excess fluid. Acute kidney failure should be treated as a serious condition and
is a potential medical emergency.
Signs: fluid loss, urine changes (presence of blood, pain), etc.
Chronic renal failure (CRF) refers to gradually reduced functioning of the
kidneys that causes eventual kidney atrophy and scarring; it is irreversible and
progressive. Often, symptoms may not occur until more than 70% of kidney
function is lost.
CRF results in the accumulation of fluid and waste products in the blood
(uremia). Healthy kidneys filter the nitrogen end-products of protein and
amino acid metabolism in the blood and change the fluid waste into urine for
excretion. Impaired kidneys, however, will not handle this task efficiently,
and the waste will accumulate in the blood (azotemia).
Treatment: Chronic renal failure is irreversible, but lifelong treatment may
control symptoms and delay progression of the disease. Treatment focuses on
controlling the individual's particular symptoms, minimizing complications,
and slowing disease progression.

Uremia: is the illness accompanying kidney failure (also called renal

failure), in particular the nitrogenous waste products associated with the
failure of this organ
95. Anemias of blood loss - acute and chronic.
Anemia: is a decrease in number of red blood cells (RBCs) or less than the normal
quantity of hemoglobin in the blood.[1][2] However, it can include decreased oxygenbinding ability of each hemoglobin molecule due to deformity or lack in numerical
development as in some other types of hemoglobin deficiency. Because hemoglobin
(found inside RBCs) normally carries oxygen from the lungs to the capillaries, anemia
leads to hypoxia (lack of oxygen) in organs.
Most commonly, people with anemia report feelings of weakness, or fatigue, general
malaise, and sometimes poor concentration. They may also report dyspnea (shortness of
breath) on exertion. In very severe anemia, the body may compensate for the lack of
oxygen-carrying capability of the blood by increasing cardiac output. The patient may have
symptoms related to this, such as palpitations, angina (if pre-existing heart disease is
present), intermittent claudication of the legs, and symptoms of heart failure.
In the morphological approach, anemia is classified by the size of red blood cells; this is
either done automatically or on microscopic examination of a peripheral blood smear. The
size is reflected in the mean corpuscular volume (MCV). If the cells are smaller than
normal (under 80 fl), the anemia is said to be microcytic; if they are normal size (80110
fl), normocytic; and if they are larger than normal (over 100 fl), the anemia is classified as
macrocytic. This scheme quickly exposes some of the most common causes of anemia; for
instance, a microcytic anemia is often the result of iron deficiency.
Anemia usually is grouped into 3 etiologic categories: decreased red blood cell (RBC)
production, increased RBC destruction, and blood loss.
The effects of acute blood loss are mainly due to the loss of intravascular volume, which if
massive can lead to cardiovascular collapse, shock, and death. The clinical features
depend on the rate of hemorrhage and whether the bleeding is external or internal. If the
patient survives, the blood volume is rapidly restored by the intravascular shift of water
from the interstitial fluid compartment.
Acute blood loss anemia is a condition in which a person quickly loses a large volume of
circulating hemoglobin. Acute blood loss is usually associated with an incident of trauma
or a severe injury resulting in a large loss of blood. It can also occur during or after a
surgical procedure.
Chronic blood loss induces anemia only when the rate of loss exceeds the regenerative
capacity of the marrow or when iron reserves are depleted and iron deficiency anemia
appears
96. Hemolytic anemias.
Hemolytic anemia is a form of anemia due to hemolysis, the abnormal breakdown of red
blood cells (RBCs), either in the blood vessels (intravascular hemolysis) or elsewhere in
the human body (extravascular).

Signs and symptoms: In general, signs of anemia (pallor, fatigue, shortness of breath, and
potential for heart failure) are present. Chronic hemolysis leads to an increased excretion
of bilirubin into the biliary tract, which in turn may lead to gallstones. The continuous
release of free hemoglobin has been linked with the development of pulmonary
hypertension (increased pressure over the pulmonary artery); this, in turn, leads to episodes
of syncope (fainting), chest pain, and progressive breathlessness.
Causes:
They may be classified according to the means of hemolysis, being either intrinsic in cases
where the cause is related to the red blood cell (RBC) itself, or extrinsic in cases where
factors external to the RBC dominate. Intrinsic effects may include problems with RBC
proteins or oxidative stress handling, whereas external factors include immune attack and
microvascular angiopathies (RBCs are mechanically damaged in circulation).
Treatment:
Symptomatic treatment can be given by blood transfusion, if there is marked anemia.
In severe immune-related hemolytic anemia, steroid therapy is sometimes necessary.
Sometimes splenectomy can be helpful where extravascular hemolysis, or hereditary
spherocytosis, is predominant
97. Megaloblastic anemias.
Megaloblastic anemia (or megaloblastic anaemia) is an anemia (of macrocytic
classification) that results from inhibition of DNA synthesis during red blood cell
production.[1] When DNA synthesis is impaired, the cell cycle cannot progress from the G2
growth stage to the mitosis (M) stage. This leads to continuing cell growth without
division, which presents as macrocytosis. Megaloblastic anemia has a rather slow onset,
especially when compared to that of other anemias.

Causes: Vitamin B12 deficiency leading to folate deficiency, Inherited DNA Synthesis
Disorders, Toxins and Drugs, erythroleukemia, inherited pyrimidine synthesis disorders.
Hematological findings:
The blood film can point towards vitamin deficiency:

Decreased red blood cell (RBC) count and hemoglobin levels[4]

Normal mean corpuscular hemoglobin concentration (MCHC, 3236 g/dL)
The reticulocyte count is decreased due to destruction of fragile and abnormal
megaloblastic erythroid precursor.
The platelet count may be reduced.
Neutrophil granulocytes may show multisegmented nuclei ("senile neutrophil").
This is thought to be due to decreased production and a compensatory prolonged
lifespan for circulating neutrophils, which increase numbers of nuclear segments
with age.
Anisocytosis (increased variation in RBC size) and poikilocytosis (abnormally
shaped RBCs).
Macrocytes (larger than normal RBCs) are present.
Ovalocytes (oval-shaped RBCs) are present.
Howell-Jolly bodies (chromosomal remnant) also present.

98. Erythrocytosis.
7

Eryhrocytosis is a disease state in which the proportion of blood volume that is occupied
by red blood cells increases. Blood volume proportions can be measured
as hematocrit level.
It can be due to an increase in the mass of red blood cells ("absolute polycythemia") or to
a decrease in the volume of plasma ("relative polycythemia").
Cause: The overproduction of red blood cells may be due to a primary process in the bone
marrow (a so-called myeloproliferative syndrome), or it may be a reaction to
chronically low oxygen levels or, rarely, a malignancy. Alternatively additional red blood
cells may have been received through another process.
99. Thrombocytopenia.
Thrombocytopenia refers to a relative decrease of platelets in blood.
A normal human platelet count ranges from 150,000 to 450,000 platelets per microlitre of
blood. One common definition of thrombocytopenia is a platelet count below 50,000 per
microlitre.
Signs and symptoms: there may be bruising, particularly purpura in the forearms,
petechia (pinpoint hemorrhages on skin and mucous membranes), nosebleeds, and/or
bleeding gums. Painless, round and pinpoint (1 to 3 mm in diameter) petechiae usually
appear and fade, and sometimes group to form ecchymoses. Larger than petechiae,
ecchymoses are purple, blue or yellow-green bruises that vary in size and shape. They can
occur anywhere on the body. There may be also complains about malaise, fatigue and
general weakness.
Causes: decreased platelet counts can be due to Vitamin B12 or folic acid deficiency,
leukemia, decreased production of thrombopoietin by the liver, sepsis, chemotherapy
drugs, antiphospholipid syndrome, etc.
Treatment: Corticosteroids may be used to increase platelet production. Lithium
carbonate or folate may also be used to stimulate the bone marrow production of platelets.
Platelet transfusions may be used to stop episodic abnormal bleeding caused by a low
platelet count.
100. Agranulocytosis. Aplastic anemia.
Agranulocytosis, also known as agranulosis or granulopenia, is an acute condition
involving a severe and dangerous leukopenia (lowered white blood cell count), most
commonly of neutrophils causing a neutropenia in the circulating blood.[1][2] It represents a
severe lack of one major class of infection-fighting white blood cells.
Signs and symptoms: Agranulocytosis may be asymptomatic, or may clinically present
with sudden fever, rigors and sore throat. Infection of any organ may be rapidly
progressive (e.g., pneumonia, urinary tract infection). Septicemia may also progress
rapidly.
Causes: a large number of drugs have been associated with agranulocytosis, including
antiepileptics, antithyroid drugs, antibiotics, NSAIDs.

Treatment: In patients that have no symptoms of infection, management consists of close

monitoring with serial blood counts, withdrawal of the offending agent (e.g., medication),
and general advice on the significance of fever.
Infection in patients with low white blood cell counts is usually treated urgently, and
usually includes a broad-spectrum penicillin (piperacillin-tazobactam or ticarcillin
clavulanate) or cephalosporin (ceftazidime), or meropenem in combination with
gentamicin or amikacin.
Aplastic anemia is a disease in which the bone marrow, and the blood stem cells that
reside there, are damaged. This causes a deficiency of all three blood cell types
(pancytopenia): red blood cells (anemia), white blood cells (leukopenia), and platelets
(thrombocytopenia).[1][2] Aplastic refers to inability of the stem cells to generate the mature
blood cells.

Signs and symptoms: Anemia with malaise, pallor and associated symptoms such as
palpitations, Thrombocytopenia (low platelet counts), leading to increased risk of
hemorrhage, bruising and petechiae, Leukopenia (low white blood cell count), leading to
increased risk of infection, Reticulocytopenia (low counts of reticulocytes, that is,
immature red blood cells).
Causes: Aplastic anemia can be caused by exposure to chemicals, drugs, radiation,
infection, immune disease, and heredity; in about half the cases, the cause is unknown.
Aplastic anemia is also sometimes associated with exposure to toxins such as benzene, or
with the use of certain drugs, such as carbamazepine.
Treatment: Treating immune-mediated aplastic anemia involves suppression of the
immune system, an effect achieved by daily medicine intake, or, in more severe cases, a
bone marrow transplant, a potential cure.
101. Acute leukemias. Types. Morphology.
Leukemia: is a type of cancer of the blood or bone marrow characterized by an abnormal
increase of immature white blood cells called "blasts".
Acute leukemia is characterized by a rapid increase in the number of immature blood
cells. Crowding due to such cells makes the bone marrow unable to produce healthy blood
cells. Immediate treatment is required in acute leukemia due to the rapid progression and
accumulation of the malignant cells, which then spill over into the bloodstream and spread
to other organs of the body. Acute forms of leukemia are the most common forms of
leukemia in children.
Signs and symptoms: generalized weakness and fatigue, anemia, unexplained fever and
infection, weight loss or loss of apetite, bone/ joint pain, breathlessness, etc.

lymphocytic leukemia: is a form of leukemia, or cancer of the white blood cells

characterized by excess lymphoblasts.
Malignant, immature white blood cells continuously multiply and are overproduced
in the bone marrow. ALL causes damage and death by crowding out normal cells in
the bone marrow, and by spreading (infiltrating) to other organs. ALL is most
common in childhood with a peak incidence at 25 years of age, and another peak
in old age.
9

myelogenous leukemia: is a cancer of the myeloid line of blood cells, characterized

by the rapid growth of abnormal white blood cells that accumulate in the bone
marrow and interfere with the production of normal blood cells.
Pathophys: The malignant cell in AML is the myeloblast. In normal hematopoiesis,
the myeloblast is an immature precursor of myeloid white blood cells; a normal
myeloblast will gradually mature into a mature white blood cell. In AML, though, a
single myeloblast accumulates genetic changes which "freeze" the cell in its
immature state and prevent differentiation.[27] Such a mutation alone does not
cause leukemia; however, when such a "differentiation arrest" is combined with
other mutations which disrupt genes controlling proliferation, the result is the
uncontrolled growth of an immature clone of cells, leading to the clinical entity of
AML
causes: A number of risk factors for developing AML have been identified,
including: other blood disorders, chemical exposures, ionizing radiation, and
genetics.

102. Chronic leukemias. Types. Morphology.

Leukemia: is a type of cancer of the blood or bone marrow characterized by an abnormal
increase of immature white blood cells called "blasts".
Chronic leukemia is characterized by the excessive build up of relatively mature, but still
abnormal, white blood cells. Typically taking months or years to progress, the cells are
produced at a much higher rate than normal, resulting in many abnormal white blood cells.
Whereas acute leukemia must be treated immediately, chronic forms are sometimes
monitored for some time before treatment to ensure maximum effectiveness of therapy.
Chronic leukemia mostly occurs in older people, but can theoretically occur in any age
group.

Chronic lymphocytic leukemia B cells originate in the bone marrow, develop in

the lymph nodes, and normally fight infection by producing antibodies. In CLL, B
cells grow out of control and accumulate in the bone marrow and blood, where
they crowd out healthy blood cells. CLL is a stage of small lymphocytic lymphoma
(SLL), a type of B-cell lymphoma, which presents primarily in the lymph nodes.
most often affects adults over the age of 55. It sometimes occurs in younger
adults, but it almost never affects children. Two-thirds of affected people are men.
It is incurable, but there are many effective treatments. One subtype is B-cell
prolymphocytic leukemia, a more aggressive disease.
Chronic myelogenous leukemia (CML) occurs mainly in adults; a very small
number of children also develop this disease. characterized by the increased and
unregulated growth of predominantly myeloid cells in the bone marrow and the
accumulation of these cells in the blood. CML is a clonal bone marrow stem cell
disorder in which a proliferation of mature granulocytes (neutrophils, eosinophils
and basophils) and their precursors is found. It is a type of myeloproliferative
disease associated with a characteristic chromosomal translocation called the

10

Philadelphia chromosome. Treatment is with imatinib (Gleevec in United States,

Glivec in Europe) or other drugs.
103. Multiple myeloma.
is a cancer of plasma cells, a type of white blood cell normally responsible for producing
antibodies.
In multiple myeloma, collections of abnormal plasma cells accumulate in the bone
marrow, where they interfere with the production of normal blood cells. Most cases of
myeloma also feature the production of a paraproteinan abnormal antibody which can
cause kidney problems. Bone lesions and hypercalcemia (high calcium levels) are also
often encountered.
Pathophys: B lymphocytes start in the bone marrow and move to the lymph nodes. As
they progress, they mature and display different proteins on their cell surface. When they
are activated to secrete antibodies, they are known as plasma cells.
Multiple myeloma develops in B lymphocytes after they have left the part of the lymph
node known as the germinal center. The normal cell line most closely associated with MM
cells is generally taken to be either an activated memory B cell or the precursor to plasma
cells, the plasmablast.
Myeloma is generally thought to be incurable but highly treatable. Remissions may be
induced with steroids, chemotherapy, proteasome inhibitors, immunomodulatory drugs
(IMiDs) such as thalidomide or lenalidomide, and stem cell transplants. Radiation therapy
is sometimes used to reduce pain from bone lesions
Signs and symptoms: bone pain, anemia, renal failure, infection, neurological symptoms
like weakness, confusion and fatigue.
104. Hodgkin disease - types.
is a type of lymphoma, which is a cancer originating from white blood cells called
lymphocytes.
Hodgkin's lymphoma is characterised by the orderly spread of disease from one lymph
node group to another and by the development of systemic symptoms with advanced
disease. When Hodgkins cells are examined microscopically, multinucleated Reed
Sternberg cells (RS cells) are the characteristic histopathologic finding.
Hodgkin's lymphoma may be treated with radiation therapy, chemotherapy, or
hematopoietic stem cell transplantation, with the choice of treatment depending on the age
and sex of the patient and the stage, bulk, and histological subtype of the disease. The
disease occurrence shows two peaks: the first in young adulthood (age 1535) and the
second in those over 55 years old.
Pathology
Macroscopy
Affected lymph nodes (most often, laterocervical lymph nodes) are enlarged, but their
shape is preserved because the capsule is not invaded. Usually, the cut surface is white-

11

grey and uniform; in some histological subtypes (e.g. nodular sclerosis) a nodular aspect
may appear.
A fibrin ring granuloma may be seen.
Microscopic examination of the lymph node biopsy reveals complete or partial effacement
of the lymph node architecture by scattered large malignant cells known as Reed
Sternberg cells (RSC) (typical and variants) admixed within a reactive cell infiltrate
composed of variable proportions of lymphocytes, histiocytes, eosinophils, and plasma
cells.
105. Non - Hodgkin lymphomas.
are diverse group of blood cancers that include any kind of lymphoma except Hodgkin's
lymphomas.[1] Types of NHL vary significantly in their severity, from indolent to very
aggressive.

The many different forms of lymphoma likely have different causes. These possible causes
and associations with at least some forms of NHL include:

Infectious agents like Epstein-Barr virus, Human T-cell leukemia virus,

Helicobacter pylori, HHV-8, and HIV infection.
Chemicals, like diphenylhydantoin, dioxin, and phenoxyherbicides.
Medical treatments like radiation therapy and chemotherapy
Genetic diseases, like Klinefelter's syndrome, Chdiak-Higashi syndrome, ataxia
telangiectasia syndrome
Autoimmune diseases, like Sjgrens syndrome, celiac sprue, rheumatoid arthritis,
and systemic lupus erythematosus.[

treated by combinations of chemotherapy, monoclonal antibodies (CD20), immunotherapy,

radiation, and hematopoietic stem cell transplantation.
CLASSIFICATION
Classified based on cell of origin and stage of differentiationMost common types in
children are acute lymphoblastic leukemias and lymphomas, which are derived from Band T-cell precursors.
Highly aggressive tumors that present with symptoms of bone marrow failure, or as
rapidly growing massesTumor cells contain genetic lesions that block differentiation,
leading to the accumulation of immature blasts that cannot function as immune cells.
Most common types in adults are non-Hodgkin lymphomas derived from germinal
center B cells.
May be indolent (e.g., follicular lymphoma) or aggressive (e.g., diffuse large B-cell
lymphoma)Sometimes interfere with the immune system by dysregulating the function of
normal B and T cells (e.g., chronic lymphocytic leukemia, multiple myeloma)Often contain
chromosomal translocations or mutations involving genes (such as BCL2 and BCL6) that
regulate normal mature B-cell development and survival
12

106. Lymphadenitis acute, chronic.

Lymphadenitis: Lymphadenitis is an infection of the lymph nodes (also called lymph
glands). It is a common complication of certain bacterial infections.
Causes: Lymphadenitis occurs when the glands become enlarged by swelling
(inflammation), often in response to bacteria, viruses, or fungi. The swollen glands are
usually found near the site of an infection, tumor, or inflammation.
Lymphadenitis may occur after skin infections or other infections caused by bacteria such
as Streptococcus or Staphylococcus. Sometimes it is caused by rare infections such as
tuberculosis or cat scratch disease (Bartonella).
Symptoms

Red, tender skin over lymph node

Swollen, tender, or hard lymph nodes

Lymph nodes may feel rubbery if an abscess has formed or they have become inflamed.
Treatment
Lymphadenitis may spread within hours. Treatment should begin promptly.
Treatment may include:

Antibiotics to treat any infection

Analgesics (painkillers) to control pain
Anti-inflammatory medications to reduce inflammation
Cool compresses to reduce inflammation and pain

Surgery may be needed to drain an abscess.

Possible Complications

Abscess formation
Cellulitis (a skin infection)
Fistulas (seen in lymphadenitis that is due to tuberculosis)
Sepsis (bloodstream infection)

107. Thymus - hyperplasia, tumors.

THYMIC HYPERPLASIA: Thymic hyperplasia is a disorder whereby there is
hyperplasia of the thymus gland.
Pathology
It can be subdivided into two forms:

true thymic hyperplasia

lymphoid hyperplasia

13

Both true thymic hyperplasia and lymphoid hyperplasia manifest as diffuse symmetric
enlargement of the thymus, so that it is difficult to distinguish between the two types on
the basis of imaging findings alone.
It is important that radiologists be able to distinguish thymic hyperplasia from neoplasm.
True thymic hyperplasia
True thymic hyperplasia associations include:

rebound hyperplasia to chemotherapy - thymic rebound hyperplasia

radiation therapy
burns
other severe systemic stresses

Lymphoid hyperplasia
This is also known as lymphoid follicular hyperplasia of the thymus or autoimmune
thymitis.
Lymphoid hyperplasia associations include :

myaesthenia gravis
systemic lupus erythematosus (SLE)
rheumatoid arthritis
scleroderma
Graves disease 4

108. Benign prostate hypertrophy or hyperplasia.

Benign prostate hypertrophy is an increase in size of the prostate.
BPH involves hyperplasia of prostatic stromal and epithelial cells, resulting in the
formation of large, fairly discrete nodules in the periurethral region of the prostate. When
sufficiently large, the nodules compress the urethral canal to cause partial, or sometimes
virtually complete, obstruction of the urethra, which interferes with the normal flow of
urine.
It leads to symptoms of urinary hesitancy, frequent urination, increased risk of urinary tract
infections, urinary retention, or contribute to or cause insomnia. Although prostate specific
antigen levels may be elevated in these patients because of increased organ volume and
inflammation due to urinary tract infections, BPH does not lead to cancer or increase the
risk of cancer.

Symptoms: Benign prostatic hyperplasia symptoms are classified as storage or voiding.

Storage symptoms include urinary frequency, urgency (compelling need to void that
cannot be deferred), urgency incontinence, and voiding at night (nocturia).

14

Voiding symptoms include urinary stream hesitancy (needing to wait for the stream to
begin), intermittency (when the stream starts and stops intermittently), straining to void,
and dribbling. Pain and dysuria are usually not present.
Treatment:
Lifestyle changes: decreasing fluid intake before bedtime, moderating the consumption of
alcohol and caffeine-containing products, and following a timed voiding schedule.
medications:The two main medications for management of BPH are alpha blockers and
5-reductase inhibitors.
109. Prostate carcinoma. Complications.
Prostate cancer is a form of cancer that develops in the prostate, a gland in the male
reproductive system.
The cancer cells may metastasize from the prostate to other parts of the body, particularly
the bones and lymph nodes.
Signs and symptoms: Early prostate cancer usually causes no symptoms. Sometimes,
however, prostate cancer does cause symptoms, often similar to those of diseases such as
benign prostatic hyperplasia. These include frequent urination, nocturia (increased
urination at night), difficulty starting and maintaining a steady stream of urine, hematuria
(blood in the urine), and dysuria (painful urination).
Complications:
Cancer that spreads. Prostate cancer can spread to nearby organs or travel through your
bloodstream or lymphatic system to your bones or other organs. Advanced prostate cancer
can cause fatigue, weakness and weight loss. Prostate cancer can grow to block the tubes
(ureters) that carry urine from the kidneys to the bladder, causing kidney problems.
Prostate cancer that spreads to the bones can cause pain and broken bones. Once prostate
cancer has spread to other areas of the body, it may still respond to treatment and may be
controlled, but it can no longer be cured.
Incontinence. Both prostate cancer and its treatment can cause urinary incontinence.
Treatment for incontinence depends on the type you have, how severe it is and the
likelihood it will improve over time. Treatment options may include medications, catheters
and surgery.
Erectile dysfunction. Erectile dysfunction can be a result of prostate cancer or its
treatment, including surgery, radiation or hormone treatments. Medications, vacuum
devices that assist in achieving erection and surgery are available to treat erectile
dysfunction.
110. Testis - inflammation, tumors.
Testicular cancer is cancer that develops in the testicles, a part of the male reproductive
system
Testicular cancer has one of the highest cure rates of all cancers
Not all lumps on the testicles are tumors, and not all tumors are malignant (cancerous).
There are many other conditions, such as testicular microlithiasis, epididymal cysts,
and appendix testis (hydatid of Morgagni), which may be painful but are non-cancerous.

15

Signs and symptoms : One of the first signs of testicular cancer is often a lump or
swelling in the testes.
a lump in one testis which may or may not be painful

sharp pain or a dull ache in the lower abdomen or scrotum

a feeling often described as "heaviness" in the scrotum
breast enlargement (gynecomastia) from hormonal effects of -hCG
low back pain (lumbago) tumor spread to the lymph nodes along the back

It is not very common for testicular cancer to spread to other organs, apart from the lungs.
However, if it has, the following symptoms may be present:

shortness of breath (dyspnea), cough or coughing up blood (hemoptysis) from

metastatic spread to the lungs
a lump in the neck due to metastases to the lymph nodes

Motphology:
Cryptorchidism involves the right testis somewhat more commonly than the
left. In approximately 10% of cases, the condition is bilateral. The cryptorchid
testis may be of normal size early in life, although some degree of atrophy is
usually present by the time of puberty. Microscopic evidence of tubular
atrophy is evident by 5 to 6 years of age, and hyalinization is present by the
time of puberty. Loss of tubules is usually accompanied by hyperplasia of
Leydig cells. Foci of intratubular germ cell neoplasia (discussed later) may
be present in cryptorchid testes and may be the source of subsequent tumors
developing in these organs. Atrophic changes similar to those seen in
cryptorchid testes may be caused by several other conditions, including chronic
ischemia, trauma, radiation, antineoplastic chemotherapy, and conditions
associated with chronic elevation in estrogen levels (e.g., cirrhosis).
Intratubular germ cell neoplasia is not a feature of these latter conditions,
however.
treatment:
The three basic types of treatment are surgery, radiation therapy, and chemotherapy.

111. Female genital infection. Oophoritis.

A large variety of organisms can infect the female genital tract. Infections with some
microorganisms, such as Candida, Trichomonas, and Gardnerella, are extremely common
and may cause significant discomfort with no serious sequelae. Others, such as Neisseria
gonorrhoeae and Chlamydia infections, are major causes of female infertility, and others
still, such as Ureaplasma urealyticum and Mycoplasma hominis infections, are implicated
in preterm deliveries.

Oophoritis: Inflammation of one or both ovaries. The inflammation usually occurs with
salpingitis (infection of the fallopian tube), pelvic inflammatory disease or other infections.
The ovaries are a pair of internal reproductive organs that produce eggs and hence
oophoritis may affect fertility.
Symptoms: Pelvic pain , Lower back pain , Fever , Side tenderness , Tenderness on
internal examination.

16

Treatment with antibiotics.

112. Endometrial hyperplasia.
Endometrial hyperplasia is a condition of excessive proliferation of the cells of
the endometrium, or inner lining of the uterus.
Most cases of endometrial hyperplasia result from high levels ofestrogens, combined with
insufficient levels of the progesterone-likehormones which ordinarily counteract estrogen's
proliferative effects on this tissue
Like other hyperplastic disorders, endometrial hyperplasia initially represents
a physiological response of endometrial tissue to the growth-promoting actions
of estrogen. However, the gland-forming cells of a hyperplastic endometrium may also
undergo changes over time which predispose them to cancerous transformation.
Severalhistopathology subtypes of endometrial hyperplasia are recognisable to
the pathologist, with different therapeutic and prognostic implications.
Morphology:
Based on architectural and cytologic features, endometrial hyperplasia is divided into four major
categories:
Simple hyperplasia without atypia, also known as cystic or mild hyperplasia, is characterized by
glands of various sizes and irregular shapes with cystic dilatation. There is a mild increase in the
gland-to-stroma ratio. The epithelial growth pattern and cytology are similar to those of
proliferative endometrium, although mitoses are not as prominent. These lesions uncommonly
progress to adenocarcinoma and largely reflect a response to persistent estrogen stimulation.
Simple hyperplasia may evolve into cystic atrophy when the estrogen stimulation is withdrawn.
Simple hyperplasia with atypia is uncommon. Architecturally it has the appearance of simple
hyperplasia, but there is cytologic atypia within the glandular epithelial cells, as defined by loss of
polarity, vesicular nuclei, and prominent nucleoli. Morphologically the cells become rounded and
lose the normal perpendicular orientation to the basement membrane. In addition, the nuclei have
an open chromatin pattern and conspicuous nucleoli. Approximately 8% of such lesions progress to
carcinoma.
Complex hyperplasia without atypia shows an increase in the number and size of endometrial
glands, marked gland crowding, and branching of glands. As a result, the glands may be crowded
back-to-back with little intervening stroma and abundant mitotic. However, the glands remain
distinct and nonconfluent, and the epithelial cells remain cytologically normal. This class of lesions
has about a 3% progression to carcinoma, lower than that of simple hyperplasia with atypia.
Complex hyperplasia with atypia has considerable morphologic overlap with well-differentiated
endometrioid adenocarcinoma , and an accurate distinction between complex hyperplasia with
atypia and cancer may not be possible without hysterectomy

Treatment :
Treatment of endometrial hyperplasia is individualized, and may include hormonal
therapy, such as cyclic or continuous progestin therapy, or hysterectomy.

113. Precancerous conditions in uterine cervix. Dysplasia. Cervical intraepithelial

neoplasia. The importance of an early morphologic diagnosis.

Premalignant lesion is a morphologically altered tissue in which cancer is more likely to

occur than its apparently normal counterpart.

17

Cervical intraepithelial neoplasia (CIN), also known as cervical dysplasia and cervical
interstitial neoplasia, is the potentially premalignant transformation and abnormal growth
(dysplasia) of squamous cells on the surface of the cervix.[1] CIN is not cancer, and is usually
curable.[2] Most cases of CIN remain stable, or are eliminated by the host's immune system without
intervention. However a small percentage of cases progress to become cervical cancer, usually
cervical squamous cell carcinoma (SCC), if left untreated.[3]
Cause :
The major cause of CIN is chronic infection of the cervix with the sexually transmitted human
papillomavirus (HPV), especially the high-risk HPV types 16 or 18.
Treatment
Treatment for higher grade CIN involves removal or destruction of the neoplastic cervical cells by
cryocautery, electrocautery, laser cautery, loop electrical excision procedure (LEEP), or cervical
conization

114. Carcinoma of the body of uterus.

Most endometrial cancers are carcinomas (usually adenocarcinomas), meaning that they
originate from the single layer of epithelial cells that line the endometrium and form the
endometrial glands. There are many microscopic subtypes of endometrial carcinoma, but
they are broadly organized into two categories, type I and type II, based on clinical
features and pathogenesis.[3]
The first type, type I endometrial cancers occur most commonly in pre- and perimenopausal women, are more common in white women, often with a history of excessive
thickening of the inner lining of the uterus (endometrial hyperplasia) and exposure to
elevated levels of estrogen that are not counterbalanced by progesterone
(unopposed estrogen exposure). Type I endometrial cancers are often low-grade,
minimally invasive into the underlying uterine wall (myometrium), and are of
the endometrioid type, and carry a good prognosis.[3] In endometrioid cancer, the cancer
cells grow in patterns reminiscent of normal endometrium.
The second type, type II endometrial cancers usually occur in older, post-menopausal
women, are more common in African-Americans, and are not associated with increased
exposure to estrogen. Type II endometrial cancers are often high-grade, with deep
invasion into the underlying uterine wall (myometrium), and are of the serous or clear
cell type, and carry a poorer prognosis.[3]
Sarcoma
In contrast to endometrial carcinomas, the uncommon endometrial stromal sarcomas are
cancers that originate in the non-glandular connective tissue of the endometrium.
Uterinecarcinosarcoma, formerly called Malignant mixed mllerian tumor, is a rare uterine
cancer that contains cancerous cells of both glandular and sarcomatous appearance - in
this case, the cell of origin is unknown.
Signs and symptoms :

Vaginal bleeding and/or spotting in postmenopausal women.

Abnormal uterine bleeding, abnormal menstrual periods.
Bleeding between normal periods in premenopausal women in women older than 40:
extremely long, heavy, or frequent episodes of bleeding (may indicate premalignant
changes).

18

Anemia, caused by chronic loss of blood. (This may occur if the woman has had
symptoms of prolonged or frequent abnormal menstrual bleeding.)
Lower abdominal pain or pelvic cramping.
Thin white or clear vaginal discharge in postmenopausal women.
Unexplained weight gain.
Swollen glands/lymph nodes in the neck, under chin, back of head and top of
clavicles.
Incontinence.

Pathology
The histopathology of endometrial cancers is highly diverse. The most common finding is
a well-differentiated endometrioid adenocarcinoma, which is composed of numerous,
small, crowded glands with varying degrees of nuclear atypia, mitotic activity, and
stratification. This often appears on a background of endometrial hyperplasia. Frank
adenocarcinoma may be distinguished from atypical hyperplasia by the finding of clear
stromal invasion, or "back-to-back" glands which represent nondestructive replacement of
the endometrial stroma by the cancer. With progression of the disease, the myometrium is
infiltrated.[4]However, other subtypes of endometrial cancer exist and carry a less
favorable diagnosis such as the uterine papillary serous carcinoma and the clear cell
carcinoma.
Treatment : The primary treatment is surgical. Surgical treatment should consist of, at
least, cytologic sampling of the peritoneal fluid, abdominal exploration, palpation and
biopsy of suspicious lymph nodes, abdominal hysterectomy, and removal of
both ovaries (bilateral salpingo-oophorectomy). Lymphadenectomy, or removal of pelvic
and para-aortic lymph nodes, is sometimes performed for tumors that have high risk
features, such as pathologic grade 3 serous or clear-cell tumors, invasion of more than
1/2 the myometrium, or extension to the cervix or adnexa. Sometimes, removal of
the omentum is also performed .

115. Tumors of myometrium. Adenomyosis.

Tumors of the Myometrium
LEIOMYOMAS
Uterine leiomyomas (commonly called fibroids) are perhaps the most common tumor in women.
They are benign smooth muscle neoplasms that may occur singly, but most often are multiple.
Morphology. Leiomyomas are sharply circumscribed, discrete, round, firm, gray-white tumors
varying in size from small, barely visible nodules to massive tumors that fill the pelvis. Except in
rare instances, they are found within the myometrium of the corpus. They can occur within the
myometrium (intramural), just beneath the endometrium (submucosal) or beneath the serosa
(subserosal).
Whatever their size, the characteristic whorled pattern of smooth muscle bundles on cut section
usually makes these lesions readily identifiable on gross inspection. Large tumors may develop
areas of yellow-brown to red softening (red degeneration).
Benign variants of leiomyoma include atypical or bizarre (symplastic) tumors with nuclear atypia
and giant cells, and cellular leiomyomas. Importantly, both have a low mitotic index. An
extremely rare variant, benign metastasizing leiomyoma, consists of a uterine tumor that
extends into vessels and migrates to other sites, most commonly the lung. Another variant,

19

disseminated peritoneal leiomyomatosis, presents as multiple small nodules on the peritoneum.

Both are considered benign despite their unusual behavior.
Leiomyomas of the uterus, even when they are extensive, may be asymptomatic. The most
important symptoms are abnormal bleeding, compression of the bladder (urinary frequency),
sudden pain if disruption of blood supply occurs, and impaired fertility.
LEIOMYOSARCOMAS
Malignant neoplasms. Leiomyosarcomas have complex, highly variable karyotypes that frequently
include deletions.[68]
Morphology. Leiomyosarcomas grow within the uterus in two somewhat distinctive patterns:
bulky, fleshy masses that invade the uterine wall, or polypoid masses that project into the uterine
lumen. The distinction from leiomyomas is based on nuclear atypia, mitotic index, and zonal
necrosis. With few exceptions, the presence of 10 or more mitoses per 10 high-power (400)
fields indicates malignancy, particularly if accompanied by cytologic atypia and/or necrosis.
ADENOMYOSIS
is a medical condition characterized by the presence of ectopic glandular tissue found in
muscle .
Adenomyosis refers to the growth of the basal layer of the endometrium down into the
myometrium. Nests of endometrial stroma, glands, or both, are found well down in the
myometrium between the muscle bundles. The uterine wall often becomes thickened and the uterus
is enlarged and globular as a result of the presence of endometrial tissue and a reactive hypertrophy
of the myometrium. Because these glands derive from the stratum basalis of the endometrium, they
do not undergo cyclical bleeding. Nevertheless, marked adenomyosis may produce menorrhagia,
dysmenorrhea, and pelvic pain before the onset of menstruation

117. Ovarian tumors - tumors of the surface epithelium, germ cell tumors and sexcord stromal tumors.
Ovarian Tumors
There are numerous types of ovarian tumors, and overall they fall into benign, borderline, and
malignant categories these occur mostly in young women between the ages of 20 and 45 years.
Borderline tumors occur at slightly older ages. Malignant tumors are more common in older
women, between the ages of 45 and 65 years. Among cancers of the female genital tract, the
incidence of ovarian cancer ranks below only carcinoma of the cervix and the endometrium. In
addition, because most ovarian cancers are detected when they have spread beyond the ovary, they
account for a disproportionate number of deaths from cancer of the female genital tract.
Classification.
Ovarian cancer is a cancerous growth arising from the ovary. Symptoms are frequently
very subtle early on and may include: bloating, pelvic pain, difficulty eating and frequent
urination, and are easily confused with other illnesses.
Signs and symptoms :
Signs and symptoms of ovarian cancer are frequently absent early on and when they
exist they may be subtle.[4] In most cases, the symptoms persist for several months before
being recognized and diagnosed. Most typical symptoms include: bloating, abdominal or
pelvic pain, difficulty eating, and possibly urinary symptoms.[5] If these symptoms recently
started and occur more than 12 times per month the diagnosis should be considered.[5]
Other findings include an abdominal mass, back pain, constipation, tiredness and a range
of other non-specific symptoms, as well as more specific symptoms such as

20

abnormal vaginal bleedingor involuntary weight loss.[6] There can be a build-up of fluid
(ascites) in the abdominal cavity.

tumors of the ovary arise ultimately from one of three ovarian components:
(1) surface epithelium derived from the coelomic epithelium; (2) the germ cells, which migrate to
the ovary from the yolk sac and are pluripotent; and (3) the stroma of the ovary, including the sex
cords, which are forerunners of the endocrine apparatus of the postnatal ovary. There is also a
group of tumors that defy classification, and finally there are secondary or metastatic tumors to the
ovary.

SURFACE EPITHELIAL-STROMAL TUMORS

Serous tumors
Benign (cystadenoma)
Borderline tumors (serous borderline tumor)
Malignant (serous adenocarcinoma)
Mucinous tumors, endocervical-like and intestinal type
Benign (cystadenoma)
Borderline tumors (mucinous borderline tumor)
Malignant (mucinous adenocarcinoma)
Endometrioid tumors
Benign (cystadenoma)
Borderline tumors (endometrioid borderline tumor)
Malignant (endometrioid adenocarcinoma)
Clear cell tumors
Benign
Borderline tumors
Malignant (clear cell adenocarcinoma)
Transitional cell tumors
Brenner tumor
Brenner tumor of borderline malignancy
Malignant Brenner tumor
Transitional cell carcinoma (non-Brenner type)
Epithelial-stromal
Adenosarcoma
Malignant mixed mllerian tumor
SEX CORDSTROMAL TUMORS
Granulosa tumors

21

Fibromas
Fibrothecomas
Thecomas
Sertoli cell tumors
Leydig cell tumors
Sex cord tumor with annular tubules
Gynandroblastoma
Steroid (lipid) cell tumors
GERM CELL TUMORS
Teratoma
Immature
Mature
Solid
Cystic (dermoid cyst)
Monodermal (e.g., struma ovarii, carcinoid)
Dysgerminoma
Yolk sac tumor (endodermal sinus tumor)
Mixed germ cell tumors

TUMORS OF SURFACE EPITHELIUM

Most primary neoplasms in the ovary fall within this category. The classification of epithelial
tumors of the ovary is based on both differentiation and extent of proliferation of the epithelium.
There are three major histologic types based on the differentiation of the neoplastic epithelium:
serous, mucinous, and endometrioid tumors. The extent of epithelial proliferation is associated
with the biologic behavior of the tumor and is classified as benign (minimal epithelial
proliferation), borderline (moderate epithelial proliferation), and malignant (marked epithelial
proliferation with stromal invasion). The benign tumors are often further classified based on the
components of the tumors, which may include cystic areas (cystadenomas), cystic and fibrous areas
(cystadenofibromas), and predominantly fibrous areas (adenofibromas). The borderline tumors and
the malignant tumors can also have a cystic component, and when malignant they are sometimes
referred to as cystadenocarcinomas. The tumors can be relatively small, or they can grow to fill the
entire pelvis before they are detected.
The origin of ovarian epithelial tumors is, at present, unresolved. This is in large part because most
tumors are detected relatively late, interfering with the identification of a precursor lesion. The
most widely accepted theory for the derivation of epithelial tumors is the transformation of
coelomic epithelium. This view is based on the embryologic pathway by which the mllerian ducts
are formed from the coelomic epithelium and evolve into serous (tubal), endometrioid
(endometrial), and mucinous (cervical) epithelia present in the normal female genital tract. Such
tumors are thought to occur predominantly in the ovary, because coelomic epithelium is
incorporated into the ovarian cortex to form epithelial inclusion cysts (also known as mesothelial,
cortical, or germinal inclusion cysts) The exact mechanism by which the cysts develop is not
known, but they are thought to result from invaginations of the surface epithelium that
subsequently loses its connection to the surface. The cysts are most often lined by either
mesothelial or tubal-type epithelium. The close association of ovarian carcinomas with either the

22

ovarian surface epithelium or inclusion cysts may explain the development of extra-ovarian
carcinomas of similar histology from coelomic epithelial rests (so-called endosalpingiosis) in the
mesentery. However, this is clearly an oversimplification of the pathogenesis of ovarian cancer.

118. Non- neoplastic functional cysts or ovary. Ovarian tumors - classification.

Non-Neoplastic and Functional Cysts
FOLLICLE AND LUTEAL CYSTS
Cystic follicles in the ovary are so common that they are considered virtually normal. They
originate in unruptured graafian follicles or in follicles that have ruptured and immediately sealed.
Morphology. These cysts are usually multiple. They range in size up to 2 cm in diameter, are
filled with a clear serous fluid, and are lined by a gray, glistening membrane. The outer theca
cells may be conspicuous due to increased amounts of pale cytoplasm. when this alteration is
pronounced, it may be associated with increased estrogen production and endometrial
abnormalities.
Granulosa luteal cysts are normally present in the ovary. These cysts are lined by a rim of bright
yellow tissue containing luteinized granulosa cells. They occasionally rupture and cause a
peritoneal reaction
POLYCYSTIC OVARIES AND STROMAL HYPERTHECOSIS: The central pathologic
abnormality is numerous cystic follicles or follicle cysts, often associated with oligomenorrhea.
Morphology. The ovaries are usually twice normal size and have a smooth, gray-white outer
cortex studded with subcortical cysts. On histologic examination, there is a thickened, fibrotic
superficial cortex beneath which are innumerable follicle cysts associated with hyperplasia of the
theca interna (follicular hyperthecosis).

Ovarian Tumors
There are numerous types of ovarian tumors, and overall they fall into benign, borderline, and
malignant categories. About 80% are benign.
Classification.
Classification, which separates ovarian neoplasms according to the most probable tissue of origin.
tumors of the ovary arise ultimately from one of three ovarian components: (1) surface epithelium
derived from the coelomic epithelium; (2) the germ cells, which migrate to the ovary from the yolk
sac and are pluripotent; and (3) the stroma of the ovary, including the sex cords, which are
forerunners of the endocrine apparatus of the postnatal ovary
SURFACE EPITHELIAL-STROMAL TUMORS
Serous tumors
Benign (cystadenoma)
Borderline tumors (serous borderline tumor)
Malignant (serous adenocarcinoma)
Mucinous tumors, endocervical-like and intestinal type
Benign (cystadenoma)
Borderline tumors (mucinous borderline tumor)

23

Malignant (mucinous adenocarcinoma)

Endometrioid tumors
Benign (cystadenoma)
Borderline tumors (endometrioid borderline tumor)
Malignant (endometrioid adenocarcinoma)
Clear cell tumors
Benign
Borderline tumors
Malignant (clear cell adenocarcinoma)
Transitional cell tumors
Brenner tumor
Brenner tumor of borderline malignancy
Malignant Brenner tumor
Transitional cell carcinoma (non-Brenner type)
Epithelial-stromal
Adenosarcoma
Malignant mixed mllerian tumor
SEX CORDSTROMAL TUMORS
Granulosa tumors
Fibromas
Fibrothecomas
Thecomas
Sertoli cell tumors
Leydig cell tumors
Sex cord tumor with annular tubules
Gynandroblastoma
Steroid (lipid) cell tumors
GERM CELL TUMORS
Teratoma
Immature
Mature
Solid
Cystic (dermoid cyst)
Monodermal (e.g., struma ovarii, carcinoid)
Dysgerminoma
Yolk sac tumor (endodermal sinus tumor)

24

Mixed germ cell tumors

MALIGNANT, NOT OTHERWISE SPECIFIED
METASTATIC CANCER FROM NONOVARIAN PRIMARY
Colonic, appendiceal
Gastric
Breast

119. Fibro-cystic changes in breast. Fibroadenoma.

characterized by noncancerous breast lumps in the breast which can sometimes cause
discomfort, often periodically related to hormonal influences from the menstrual cycle.
Symptoms: The changes in fibrocystic breast disease are characterised by the appearance
of fibrous tissue and a lumpy, cobblestone texture in the breasts. These lumps are smooth
with defined edges, and are usually free-moving in regard to adjacent structures. The
bumps can sometimes be obscured by irregularities in the breast that are associated with
the condition. The lumps are most often found in the upper, outer sections of the breast
(nearest to the armpit). Women with fibrocystic changes may experience a persistent or
intermittent breast aching or breast tenderness related to periodic swelling. Breasts and
nipples may be tender or itchy.
Usually treated by Progesterone ointments and supplements.
Fibroadenomas of the breast are lumps composed of fibrous and glandular tissue. Unlike
typical lumps from breast cancer, fibroadenomas are easy to move, with clearly defined
edges.[
Fibroadenoma of the breast is a benign tumor composed of two elements : epithelium and
stroma. It is nodular and encapsulated, included in breast. A) Intracanalicular
fibroadenoma : stromal proliferation predominates and compresses the ducts, which are
irregular, reduced to slits. B) Pericanalicular fibroadenoma : fibrous stroma proliferates
around the ductal spaces, so that they remain round or oval, on cross section. The basement
membrane is intact.
120. Carcinoma or the breast: classification, spreading of metastasis.
Breast cancer is a type of cancer originating from breast tissue, most commonly from the
inner lining of milk ducts or the lobules that supply the ducts with milk.
Cancers originating from ducts are known as ductal carcinomas, while those originating
from lobules are known as lobular carcinomas. The most common type of breast cancer is
ductal adenocarcinoma, which arises in the milk ducts, but lumps may appear anywhere in
the breast tissue or in the nearby lymph nodes.
Causes: the most important genes involved are BRCA1 and BRCA2.
Signs and symptoms: The first noticeable symptom of breast cancer is typically a lump that
feels different from the rest of the breast tissue. Other symptoms are skin changes, inverted
nipples, nipple discharge.

25

Occasionally, breast cancer presents as metastatic diseasethat is, cancer that has spread
beyond the original organ. The symptoms caused by metastatic breast cancer will depend
on the location of metastasis. Common sites of metastasis include bone, liver, lung and
brain.Unexplained weight loss can occasionally herald an occult breast cancer, as can
symptoms of fevers or chills. Bone or joint pains can sometimes be manifestations of
metastatic breast cancer, as can jaundice or neurological symptoms.
121. Toxemia of pregnancy.
An abnormal condition of pregnancy characterized by hypertension and edema and protein in the
urine.
Pre-eclampsia or preeclampsia is a medical condition in which hypertension arises in pregnancy
(pregnancy-induced hypertension) in association with significant amounts of protein in the urine.
It is the most common of the dangerous pregnancy complications; it may affect both the mother
and the unborn child.
Causes
The pre-eclampsia syndrome is thought in many cases to be caused by a shallowly implanted
placenta which becomes hypoxic, leading to an immune reaction characterized by secretion of
upregulated inflammatory mediators from the placenta, and acting on the vascular endothelium.
The shallow implantation is thought to stem from the maternal immune system's response to the
placenta. In some cases of pre-eclampsia it is thought that the mother lacks the receptors for the
proteins the placenta is using to downregulate the maternal immune system's response to it.
Signs and symptoms :

endothelial cell injury

immune rejection of the placenta
compromised placental perfusion
altered vascular reactivity
imbalance between prostacyclin and thromboxane
decreased glomerular filtration rate with retention of salt and water
decreased intravascular volume
increased central nervous system irritability
disseminated intravascular coagulation
uterine muscle stretch (ischemia)
dietary factors, including vitamin deficiency
Hughes syndrome
genetic factors[15]
air pollution[16]
obesity [17]
unfamiliar sperm theory [18]
Thyroid dysfunction: Subclinical hypothyroidism in early pregnancy, compared with
normal thyroid function, has been estimated to increase the risk of pre-eclampsia with an
odds ratio of 1.7.[19]

The current understanding of the syndrome is as a two-stage process, with a highly variable first
stage which predisposes the placenta to hypoxia, followed by the release of soluble factors which
result in many of the other observed phenomena.
treatment :
The only known treatments for eclampsia or advancing pre-eclampsia are abortion or delivery,
either by labor induction or Caesarean section. However, post-partum pre-eclampsia may occur up

26

to six weeks following delivery even if symptoms were not present during the pregnancy. Postpartum pre-eclampsia is dangerous to the health of the mother since she may ignore or dismiss
symptoms as simple post-delivery headaches and edema. Hypertension can sometimes be
controlled with anti-hypertensive medication.

122. Morphology of pregnancy disorders. Gestational trophoblastic disease.

Gestational trophoblastic disease
Gestational trophoblastic disease (GTD) is a term used for a group of pregnancy-related tumours.
These tumours are rare, and they appear when cells in the womb start to grow out of control. The
cells that form gestational trophoblastic tumours are called trophoblasts and come from tissue that
grows to form the placenta during pregnancy.
There are several different types of GTD. Some, such as molar pregnancy are nearly always
curable. Others, such as choriocarcinoma, are more likely to spread and can be difficult to treat.[1][2]
Gestational trophoblasts are of particular interest to cell biologists because, like cancer, these cells
invade tissue (the uterus), but unlike cancer, sometimes "know" when to stop.[citation needed]
GTD can simulate pregnancy, because the uterus may contain fetal tissue, albeit abnormal. This
tissue may grow at the same rate as a normal pregnancy, and produces chorionic gonadotropin, a
hormone which is measured to monitor fetal well-being.[3]
While GTD overwhelmingly affects women of child-bearing age, it may rarely occur in
postmenopausal women.[
Diagnosis
Cases of GTD can be diagnosed through routine tests given during pregnancy, such as blood tests
and ultrasound, or through tests done after miscarriage or abortion.[17] Vaginal bleeding, enlarged
uterus, pelvic pain or discomfort, and vomiting too much (hyperemesis) are the commonest
symptoms of GTD.
Treatment
Treatment is always necessary.
The treatment for hydatidiform mole consists of the evacuation of pregnancy. Evacuation will lead
to the relief of symptoms, and also prevent later complications. Suction curettage is the preferred
method of evacuation.
The treatment for invasive mole or choriocarcinoma generally is the same. Both are usually treated
with chemotherapy .

123. Postpartum uterine infection. Postpartum sepsis.

Postpartum infections comprise a wide range of entities that can occur after vaginal and
cesarean delivery or during breastfeeding. In addition to trauma sustained during the birth
process or cesarean procedure, physiologic changes during pregnancy contribute to the
development of postpartum infections.[1] The typical pain that many women feel in the
immediate postpartum period also makes it difficult to discern postpartum infection from
postpartum pain.
Postpartum patients are frequently discharged within a couple days following delivery. The
short period of observation may not afford enough time to exclude evidence of infection

27

prior to discharge from the hospital. In one study, 94% of postpartum infection cases were
diagnosed after discharge from the hospital.[2] Postpartum fever is defined as a temperature
greater than 38.0C on any 2 of the first 10 days following delivery exclusive of the first
24 hours.[3] The presence of postpartum fever is generally accepted among clinicians as a
sign of infection that must be determined and managed.
124. Pituitary gland pathology - Acromegaly. Icenko - Kusching disease. Simonds
disease. Diabetes insipidus.
ACROMEGALY
is a syndrome that results when the anterior pituitary gland produces excess growth
hormone (GH) after epiphyseal plate closure at puberty. A number of disorders may
increase the pituitary's GH output, although most commonly it involves a GH-producing
tumor called pituitary adenoma, derived from a distinct type of cell (somatotrophs).
Acromegaly most commonly affects adults in middle age,[1] and can result in severe
disfigurement, serious complicating conditions, and premature death if unchecked.
Because of its insidious pathogenesis and slow progression, the disease is hard to diagnose
in the early stages and is frequently missed for many years, until changes in external
features, especially of the face, become noticeable.
Itsenko- Cushing's disease: Excessive pituitary function may be caused by a tumor
(basophilic adenoma) or by injury to the hypothalamic region of the brain, the site of
production of a special substance (corticotropin releasing factor) that intensifies the
synthesis and liberation of adrenocorticotropic hormone (ACTH). The symptom complex
of Itsenko-Cushings disease is brought about by the elevated level of secretion of
adrenocortical hormones (glucocorticoids, mineralocorticoids, and ketosteroids);
manifestations include adiposis (mainly in the region of the pectoral girdle, trunk,
abdomen, and face), hypertension, hirsutism (in females), osteoporosis, diabetes mellitus,
lowered sexual function, and dryness of the cutaneous integuments. Treatment involves Xirradiation of the pituitary region. Symptomatic treatment includes the administration of
agents that lower blood pressure, antidiabetic preparations, and substances that inhibit
adrenal function (amphenone, metopyrone). Subtotal or total adrenalectomy may be
performed and followed by the administration of adrenal hormones.
Simmonds disease, also known as anterior pituitary hypofunction, is lack secretion of
pituitary hormones, lesions of pituitary or hypothalamus involve the endocrine function in
pituitary gland. when the pituitary had destroyed, may produce the performance of
endocrine gland hypofunction, the mainly involvement of the gland is sex gland, thyroid
and adrenal cortex.
Symptoms and signs: lack of gonadotropin, growth hormone, prolactin, thyroxin
stimulating hormone, adrenocorticotropic hormone, pituitary crisis.

Diabetes insipidus is a condition in which the ability to control the balance of water
within the body is not working properly. The kidneys are not able to retain water and this
causes the passage of large amounts of urine.
There are 2 different types of diabetes insipidus: cranial (when the brain produces or
releases a reduced amount of ADH) and nephrogenic (ADH is still being released by your
brain but the kidneys become resistant to the effects of it).

28

Classification:

Neurogenic
Neurogenic diabetes insipidus, more commonly known as central diabetes insipidus, is due
to a lack of vasopressin production in the brain.

Nephrogenic
Nephrogenic diabetes insipidus is due to the inability of the kidney to respond normally to
vasopressin.

Dipsogenic
Dipsogenic DI is due to a defect or damage to the thirst mechanism, which is located in the
hypothalamus. This defect results in an abnormal increase in thirst and fluid intake that
suppresses vasopressin secretion and increases urine output. Desmopressin is ineffective,
and can lead to fluid overload as the thirst remains.

Gestational
Gestational DI only occurs during pregnancy. During pregnancy, all women produce
vasopressinase in the placenta, which breaks down ADH. Gestational DI is thought to
occur with excessive vasopressinase production.
125. Tumors of the anterior pituitary. Morphology. Diseases.
Pituitary Adenomas and Hyperpituitarism
The most common cause of hyperpituitarism is an adenoma arising in the anterior lobe. Pituitary
adenomas are classified on the basis of hormone(s) produced by the neoplastic cells, which are
detected by immunohistochemical stains Some pituitary adenomas can secrete two hormones (GH
and prolactin being the most common combination), and rarely, pituitary adenomas are
plurihormonal. Pituitary adenomas can be
functional ( associated with hormone excess and clinical manifestations thereof)
or nonfunctioning ( immunohistochemical and/or ultrastructural demonstration of hormone
production at the tissue level, without clinical symptoms of hormone excess).
Less common causes of hyperpituitarism include pituitary carcinomas and some hypothalamic
disorders. Large pituitary adenomas, and particularly nonfunctioning ones, may cause
hypopituitarism as they encroach on and destroy adjacent anterior pituitary parenchyma.

Classification of Pituitary Adenomas

Pituitary Cell Type Hormone

Tumor Type

Corticotroph

ACTH cell (corticotroph)

adenoma

ACTH and other

POMC-derived
peptides

Associated Syndrome[*]
Cushing syndrome
Nelson syndrome

29

Pituitary Cell Type Hormone

Tumor Type

Somatotroph

GH cell (somatotroph)
adenoma

GH

Associated Syndrome[*]
Gigantism (children)
Acromegaly (adults)

Lactotroph

Prolactin

Prolactin cell (lactotroph)

adenoma

Galactorrhea and
amenorrhea (in
females)
Sexual dysfunction,
infertility

Mammosomatotroph Prolactin, GH

Mammosomatotroph

Combined features of GH
and prolactin excess

Thyrotroph

TSH

TSH cell (thyrotroph)

adenoma

Hyperthyroidism

Gonadotroph

FSH, LH

Gonadotroph, null cell,

oncocytic adenomas

Hypogonadism, mass
effects, and
hypopituitarism

Morphology. The typical pituitary adenoma is a soft, well-circumscribed lesion that may be
confined to the sella turcica. Larger lesions typically extend superiorly through the diaphragm sella
into the suprasellar region, where they often compress the optic chiasm and adjacent structures,
such as some of the cranial nerves . As these adenomas expand, they frequently erode the sella
turcica and anterior clinoid processes. In as many as 30% of cases, the adenomas are not grossly
encapsulated and infiltrate neighboring tissues such as the cavernous and sphenoid sinuses, dura,
and on occasion, the brain itself. Such lesions are termed invasive adenomas. Not unexpectedly,
macroadenomas tend to be invasive more frequently than smaller tumors. Foci of hemorrhage and
necrosis are also more common in these larger adenomas.

126. Thyroid epithelial hyperplasia. Hypothyroidism.

Hypothyroidism is a state in which the thyroid gland does not make enough thyroid
hormone.
Hypothyroidism upsets the normal balance of chemical reactions in the body. It seldom
causes symptoms in the early stages, but, over time, untreated hypothyroidism can cause
a number of health problems, such as obesity, joint pain, infertility, fatigue, memory loss,
dry skin, menstrual changes and heart disease.
Causes: Iodine deficiency is the most common cause of hypothyroidism worldwide.
Exposure to iodine-131 from nuclear fallout, which is chemically indistinguishable from
non-radioactive isotopes and taken up by the thyroid gland with them, destroys thyroid
cells and increases the risk of hypothyroidism.
Pathophysiology: The genes that code triiodothyronine receptors are differentially
expressed in various tissues, and the effects of triiodothyronine (bind to regulatory
regions of genes and modify their expression) depend on the specific isoform of the
receptor. The receptors are expressed in a developmentally specific pattern, especially in
the brain. Many of the specific genes regulated by triiodothyronine in various tissues have
not been identified, but the general metabolic effects of thyroid hormones are to
stimulate oxygen consumption in almost all metabolically active tissues, increase
absorption of carbohydrates from the intestine, and modulate lipid metabolism. Thyroid
30

hormones mobilize mucopolysaccharides and prevent their deposition in skin and

connective tissues. Thyroid hormones also interact with catecholamines. A variety of
factors may be involved, including reduced responsiveness of the reticular activating
system to catecholamines, impaired fluid and electrolyte regulation and altered blood
flow.
Treatment: Hypothyroidism is treated with replacement doses of thyroid hormones.

127. Hyperthyroidism.
Hyperthyroidism is a condition in which the thyroid gland produces and secretes
excessive amounts of the free (not protein bound, and circulating in the blood) thyroid
hormones.
Causes: There are several causes of hyperthyroidism. Most often, the entire gland is
overproducing thyroid hormone. Less commonly, a single nodule is responsible for the
excess hormone secretion, called a "hot" nodule. Thyroiditis (inflammation of the thyroid)
can also cause hyperthyroidism.
Hyperthyroidism may be asymptomatic, but when it is not, symptoms are due to an
excess of thyroid hormone. If there is too much thyroid hormone, every function of the
body tends to speed up. Therefore, some of the symptoms of hyperthyroidism may be
nervousness, irritability, increased perspiration, heart racing, hand tremors, anxiety,
difficulty sleeping, etc.
Pathophysiology: The thyroid is a hormone that controls the metabolism of the body. The
hypothalamus and the pituitary gland control the secretion of TSH which stimulates the
secretion of the thyroid hormones, triiodothyronine, or T3 and thyroxine, or T4. When
the body secretes an over abundance of these hormones it is referred to as
hyperthyroidism. Hyper-secretion may be due to certain tumor or any other
defects.Goiter that is enlargement of thyroid gland may be present.
Management: antithyroid drugs, beta- blockers, food and diet, surgery, radioiodine.
128. Tumors of the thyroid gland. Morphology.
The thyroid gland gives rise to a variety of neoplasms, ranging from circumscribed,
benign adenomas to highly aggressive, anaplastic carcinomas. The overwhelming
majority of solitary nodules of the thyroid prove to be benign lesions, either
follicular adenomas or localized, non-neoplastic conditions.
Follicular adenomas and carcinomas are both composed of well-differentiated
follicular epithelial cells, and are distinguished by evidence of capsular and/or
vascular invasion in the latter.Papillary carcinomas are recognized based on
nuclear features (ground-glass nuclei, pseudo-inclusions) even in the absence of
papillae.
Adenomas
Adenomas of the thyroid are benign neoplasms derived from follicular epithelium. As in
the case of all thyroid neoplasms, follicular adenomas are usually solitary. Clinically and
morphologically, they may be difficult to distinguish, on the one hand, from hyperplastic

31

nodules or, on the other hand, from the less common follicular carcinomas. Although the
vast majority of adenomas are nonfunctional, a small proportion produces thyroid
hormones ("toxic adenomas") and causes clinically apparent thyrotoxicosis.
Morphology
The typical thyroid adenoma is a solitary, spherical lesion that
compresses the adjacent non-neoplastic thyroid. The neoplastic cells are
demarcated from the adjacent parenchyma by a well-defined, intact
capsule. Multinodular goiters, which contain multiple nodules on their
cut surface, do not demonstrate compression of the adjacent thyroid
parenchyma, and lack a well-formed capsule. Microscopically, the
constituent cells are arranged in uniform follicles that contain colloi. The
neoplastic cells are uniform, with well-defined cell borders
Most thyroid carcinomas are derived from the follicular epithelium, except for medullary
carcinomas; the latter are derived from the parafollicular, or C, cells. Because of the unique
clinical and biologic features associated with each variant of thyroid carcinoma, these
subtypes will be described separately, after discussion of pathogenesis
Papillary Carcinoma
As mentioned above, papillary carcinomas represent the most common form of thyroid
cancer. They may occur at any age, and they account for the vast majority of thyroid
carcinomas associated with previous exposure to ionizing radiation.
Morphology
Papillary carcinomas may present as solitary or multifocal lesions within
the thyroid. In some cases, they may be well circumscribed and even
encapsulated; in other instances, they infiltrate the adjacent parenchyma
with ill-defined margins. The lesions may contain areas of fibrosis and
calcification and are often cystic. On the cut surface, they may appear
granular and may sometimes contain grossly discernible papillary foci
.The definitive diagnosis of papillary carcinoma can be made only after
microscopic examination. The nuclei of papillary carcinoma cells
contain very finely dispersed chromatin. When present, the papillae of
papillary carcinoma differ from those seen in areas of hyperplasia.
Metastases to adjacent cervical lymph nodes are estimated to occur in
about half of cases.
129. Thyroiditis. Classitication. Morphology.
Thyroiditis is the inflammation of the thyroid gland.
Classification: Thyroiditis is a group of disorders that all cause thyroidal inflammation.
Forms of the disease are Hashimoto's thyroiditis, the most common cause of
hypothyroidism in the US, postpartum thyroiditis, subacute thyroiditis, silent thyroiditis,
drug-induced thyroiditis, radiation-induced thyroiditis, acute thyroiditis, and Riedel's
thyroiditis.
Morphology: The thyroid usually is diffusely and symmetrically enlarged, although more
localized enlargement may be seen in some cases. The cut surface is pale and gray-tan in
appearance, and the tissue is firm and somewhat friable. Microscopic examination reveals
widespread infiltration of the parenchyma by a mononuclear inflammatory infiltrate
containing small lymphocytes, plasma cells, and well-developed germinal centers. The
thyroid follicles are atrophic and are lined in many areas by epithelial cells distinguished

32

by the presence of abundant eosinophilic, granular cytoplasm, termed Hrthle, or oxyphil,

cells. This is a metaplastic response of the normally low cuboidal follicular epithelium to
ongoing injury; on ultrastructural examination, the Hrthle cells are characterized by
numerous prominent mitochondria. Interstitial connective tissue is increased and may be
abundant. Less commonly, the thyroid is small and atrophic as a result of more extensive
fibrosis (fibrosing variant). Unlike in Reidel thyroiditis, the fibrosis does not extend
beyond the capsule of the gland.
130. Hypo- and hyperparathyreoidism. Organs involvement. Tumors of the
parathyroid gland.
Hypoparathyroidism is decreased function of the parathyroid glands with
underproduction of parathyroid hormone. This can lead to low levels of calcium in the
blood, often causing cramping and twitching of muscles or involuntary muscle
contraction, etc. The condition can be inherited, but it is also encountered after thyroid
or parathyroid gland surgery, immune system-related damage, absence or dysfunction of
the parathyroid glands is one of the components of chromosome 22q11 microdeletion
syndrome, magnesium deficiency, etc.
Pathophysiology: PTH is released from the parathyroid gland when a calcium-sensing
receptor perceives decreased ionised calcium. PTH acts to increase serum calcium by
liberating calcium from bone, increasing intestinal calcium absorption by promoting
vitamin D synthesis and conversion to active form, and promoting calcium resorption in
the kidneys. Inadequate PTH secretion in response to low calcium levels results in
hypocalcaemia, with symptoms of hypersensitivity of nerve and muscle, paraesthesias,
twitching, anxiety, and ECG abnormality (QT prolongation). If calcium levels are not
corrected, this will progress to seizures, cardiac arrhythmia, and death.
The diagnosis is made with blood tests, and other investigations such as genetic testing
depending on the results.
The treatment of hypoparathyroidism is limited by the fact that there is no artificial form
of the hormone that can be administered as replacement. Calcium replacement or
vitamin D can ameliorate the symptoms but can increase the risk of kidney stones and
chronic kidney disease.
Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess
production of parathyroid hormone. The parathyroid hormone regulates calcium and
phosphate levels and helps to maintain these levels.
Primary: results from a hyperfunction of the parathyroid glands themselves. Causes
hypercalcemia (elevated blood calcium levels) through the excessive secretion of
parathyroid hormone , usually by an adenoma (benign tumors) of the parathyroid glands.
Secondary: is due to excessive secretion of parathyroid hormone by the parathyroid
glands in response to hypocalcemia (low blood calcium levels)and associated hypertrophy
of the glands. The most common causes are vitamin D deficiency and chronic renal
failure.
Bone and joint pain are common, as are limb deformities. The elevated PTH has also
pleiotropic effects on blood, immune system and neurological system.

33

Familial hypocalciuric hypercalcemia: a condition that can cause hypercalcemia, a serum

calcium level typically above 10.2 mg/dL.
Most cases are associated with loss of function mutations in the CASR gene, which
encodes a calcium-sensing receptor, expressed in parathyroid and kidney tissue. The
perceived lack of calcium levels by the parathyroid leads to constitutively high levels of
parathyroid hormone, and hypercalcemia. Functionally, parathyroid hormone increases
calcium resorption from the bone and increases phosphate excretion from the kidney
which increases serum calcium and decreases serum phosphate.
131. Diabetes mellitus. Morphology and complications.
Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar,
either because the pancreas does not produce enough insulin, or because cells do not
respond to the insulin that is produced.
There are three main types:
Type 1 DM results from the body's failure to produce insulin, and currently
requires the person to inject insulin or wear an insulin pump. Insulitis
(inflammatory infiltrate of T cells and macrophages) -cell depletion, islet atrophy.
Type 2 DM results from insulin resistance, a condition in which cells fail to use
insulin properly, sometimes combined with an absolute insulin deficiency. No
insulitis; amyloid deposition in islets. Mild -cell depletion.
The third form, gestational diabetes occurs when pregnant women without a
previous diagnosis of diabetes develop a high blood glucose level. It may precede
development of type 2 DM.
Amyloid deposition within islets in type 2 diabetes begins in and around capillaries and
between cells.
In most patients, however, morphologic changes are likely to be found in arteries
(macrovascular disease), basement membranes of small vessels (microangiopathy),
kidneys (diabetic nephropathy), retina (retinopathy), nerves (neuropathy), and other
tissues.
Pancreas. Lesions in the pancreas are inconstant and rarely of diagnostic value.
Diabetic Macrovascular Disease. Diabetes exacts a heavy toll on the vascular system.
Endothelial dysfunction, which predisposes to atherosclerosis and other cardiovascular
morbidities, is widespread in diabetes, as a consequence of the deleterious effects of
persistent hyperglycemia and insulin resistance on the vascular compartment. The hallmark
of diabetic macrovascular disease is accelerated atherosclerosis involving the aorta and
large- and medium-sized arteries.
Myocardial infarction, caused by atherosclerosis of the coronary arteries, is the most
common cause of death in diabetics, and an elevated risk for cardiovascular disease is
even observed in pre-diabetics. Significantly, myocardial infarction is almost as common
in diabetic women as in diabetic men. In contrast, myocardial infarction is uncommon in
nondiabetic women of reproductive age.

34

Diabetic Microangiopathy. One of the most consistent morphologic features of diabetes

is diffuse thickening of basement membranes. The thickening is most evident in the
capillaries of the skin, skeletal muscle, retina, renal glomeruli, and renal medulla
Diabetic Nephropathy. The kidneys are prime targets of diabetes. Renal failure is second
only to myocardial infarction as a cause of death from this disease. Three lesions are
encountered: (1) glomerular lesions; (2) renal vascular lesions, principally
arteriolosclerosis; and (3) pyelonephritis, including necrotizing papillitis.
Capillary Basement Membrane Thickening. Widespread thickening of the glomerular
capillary basement membrane (GBM) occurs in virtually all cases of diabetic
nephropathy and is part and parcel of the diabetic microangiopathy.

Renal atherosclerosis and arteriolosclerosis constitute part of the macrovascular disease

in diabetics. The kidney is one of the most frequently and severely affected organs;
however, the changes in the arteries and arterioles are similar to those found throughout the
body.
Pyelonephritis is an acute or chronic inflammation of the kidneys that usually begins in
the interstitial tissue and then spreads to affect the tubules. One special pattern of acute
pyelonephritis, necrotizing papillitis (or papillary necrosis), is much more prevalent in
diabetics than in nondiabetics.
Diabetic Ocular Complications: The ocular involvement may take the form of
retinopathy, cataract formation, or glaucoma.
132. Islet cell tumors of pancreas. Zollinger - Ellison Syndrome.
Islet cell tumors of the pancreas are different from adenocarcinoma of the pancreas. These
tumors are derived from neuroendocrine cells and tend to be slow growing tumors that are
treatable even after they have metastasized. Islet cell tumors can produce dramatic
symptoms since up to half of these tumors may secrete hormones that produce side effects
due to excessive secretion of the hormones.
The following types of islet cell tumors are recognized:

Non-functioning islet cell tumors. These are the majority of the islet cell tumors of
the pancreas and may account for up to 60% of all neuroendocrine tumors of the
pancreas. Patients with non-functioning tumors do not have any symptoms from
excessive hormone secretion by the tumor since the tumor does not release any
hormones into the blood. These tumors are often diagnosed because of non-specific
abdominal symptoms that lead the physician to get a CT scan of the abdomen.
Functional islet cell tumors. These tumors produce dramatic symptoms because of
excess release of various different hormones by the tumor into the blood.

The following types of functional islet cell tumors are recognized: Insulinoma: a tumor
that produces excessive amounts of insulin. Gastrinoma: a tumor that produces excessive
amounts of gastrin. Glucagonoma: an extremely rare tumor that produces excessive
amounts of glucagon. VIPoma: an extremely rare islet cell tumor the produces excessive
amounts of VIP. Somatostatinoma: an extremely rare tumor that produces excessive
amounts of somatostatin.

35

Non-functioning islet cell tumors

Non-functioning islet cell tumors are being identified more frequently because of
widespread availability of CT scan imaging. These tumors have a histological appearance
of islet cell tumors but do not produce any symptoms since they do not release excessive
amounts of hormones in the blood.
More than 50% of all non-functioning islet cell tumors are malignant (cancerous) and at
the time of diagnosis the tumors are typically large and easily localized by CT scanning or
MRI.
Treatment: Surgical removal of non-functioning islet cell tumors is often curative. These
tumors typically tend to be large and therefore enucleation of the tumor is usually not
possible.
Functioning islet cell tumors
Functional islet cell tumors often present in a dramatic fashion due to secretion of
excessive amounts of hormones such as insulin, gastrin, or glucagon. These tumors tend to
present at a very early stage when the tumor is tiny and is often not readily detectable.
Localization of these tumors is an important consideration since the tumors may be very
small, only a few millimeters in size, when the patient presents with major symptoms
related to over secretion of the hormones.
ZollingerEllison syndrome is a triad of gastric acid hypersecretion, severe peptic
ulceration, and non-beta cell islet tumor of pancreas (gastrinoma). In this syndrome
increased levels of the hormone gastrin are produced, causing the stomach to produce
excess hydrochloric acid. Often the cause is a tumor (gastrinoma) of the duodenum or
pancreas producing the hormone gastrin.
Symptoms: Chronic Diarrhea, Pain in the Esophagus, Nausea, Wheezing, Vomiting Blood
(digested Blood), Malnourishment, loss of weight due to loss of appettite.
133. Acute and chronic adrenocortical insufficiency.

Adrenal insufficiency is a condition in which the adrenal glands, located above the
kidneys, do not produce adequate amounts of steroid hormones, primarily cortisol, but may
also include impaired aldosterone production which regulates sodium, potassium and water
retention. Craving for salt or salty foods due to the urinary losses of sodium is common.
Addison's disease and congenital adrenal hyperplasia can manifest as adrenal
insufficiency. If not treated, adrenal insufficiency may result in severe abdominal pains,
diarrhea, vomiting, profound muscle weakness and fatigue, depression, hypotension,
weight loss, kidney failure, changes in mood and personality, and shock. An adrenal crisis
often occurs if the body is subjected to stress, such as an accident, injury, surgery, or
severe infection; death may quickly follow.
Adrenal insufficiency can also occur when the hypothalamus or the pituitary gland, both
located at the base of the skull, does not make adequate amounts of the hormones that
assist in regulating adrenal function. This is called secondary adrenal insufficiency and is
caused by lack of production of ACTH in the pituitary or lack of CRH in the
hypothalamus.
36

Causes of acute adrenal insufficiency are mainly Waterhouse-Friderichsen syndrome,

sudden withdrawal of long-term corticosteroid therapy and stress in patients with
underlying chronic adrenal insufficiency. The latter is termed critical illnessrelated
corticosteroid insufficiency.
For chronic adrenal insufficiency, the major contributors are autoimmune adrenalitis,
tuberculosis, AIDS and metastatic disease. Minor causes of chronic adrenal insufficiency
are systemic amyloidosis, fungal infections, hemochromatosis and sarcoidosis.
Addisons disease is a rare, chronic endocrine disorder in which the adrenal glands do not
produce sufficient steroid hormones (glucocorticoids and often mineralocorticoids). It is
characterised by symptoms, such as abdominal pain and weakness, but under certain
circumstances these may progress to Addisonian crisis, a severe illness in which there
may be very low blood pressure and coma.
The condition arises from problems with the adrenal gland itself, a state referred to as
"primary adrenal insufficiency" and can be caused by damage by the body's own immune
system, certain infections or various rarer causes.
134. Adrenal neoplasms.
Adrenocortical adenoma
Adrenocortical adenomas are benign tumors of the adrenal cortex which are extremely
common. They should not be confused with adrenocortical "nodules", which are not true
neoplasms. The clinical significance of these neoplasms is twofold. A minority of
adrenocortical adenomas are "functional", meaning that they produce glucocorticoids,
mineralcorticoids, and/or sex steroids, resulting in endocrine disorders such as Cushing's
syndrome, Conn's syndrome (hyperaldosteronism), virilization of females, or feminization
of males. Functional adrenocortical adenomas are surgically curable.
Most of the adrenocortical adenomas are less than 2 cm in greatest dimension and less than
50 gram in weight. However, size and weight of the adrenal cortical tumors are no longer
considered to be a reliable sign of benignity or malignancy. Grossly, adrenocortical
adenomas are encapsulated, well-circumscribed, solitary tumors with solid, homogeneous
yellow-cut surface. Necrosis and hemorrhage are rare findings.
Adrenocortical carcinoma
Adrenocortical carcinoma is a rare, highly aggressive cancer of adrenal cortical cells,
which may occur in children or adults. ACC's may be "functional", producing steroid
hormones and consequent endocrine dysfunction similar to that seen in many
adrenocortical adenomas, but many are not. Due to their location deep in the
retroperitoneum, most adrenocortical carcinomas are not diagnosed until they have grown
quite large. They frequently invade large vessels, such as the renal vein and inferior vena
cava, as well as metastasizing via the lymphatics and through the blood to the lungs and
other organs. The most effective treatment is surgery, although this is not feasible for many
patients, and the overall prognosis of the disease is poor. Chemotherapy, radiation therapy,
and hormonal therapy may also be employed in the treatment of this disease.
Tumors of the Adrenal Medulla

37

The adrenal medulla is located anatomically at the center of each adrenal gland, and is
composed of neuroendocrine (chromaffin) cells which produce and release epinephrine
(adrenaline) into the bloodstream in response to activation of the sympathetic nervous
system. Neuroblastoma and pheochromocytoma are the two most important tumors which
arise from the adrenal medulla. Both tumors may also arise from extra-adrenal sites,
specifically, in the paraganglia of the sympathetic chain.
Neuroblastoma
Neuroblastoma is an aggressive cancer of immature neuroblastic cells (precursors of
neurons), and is one of the most common pediatric cancers, with a median age at diagnosis
of two years. Adrenal neuroblastoma typically presents with a rapidly enlarging abdominal
mass. Although the tumor has often spread to distant parts of the body at the time of
diagnosis, this cancer is unusual in that many cases are highly curable when the spread is
limited to the liver, skin, and/or bone marrow. Neuroblastic tumors often produce elevated
levels of catecholamine hormone precursors and homovanillic acid, and may produce
severe watery diarrhea through production of vasoactive intestinal peptide. Treatment of
neuroblastoma includes surgery and radiation therapy for localized disease, and
chemotherapy for metastatic disease.
Pheochromocytoma
Pheochromocytoma is a neoplasm composed of cells similar to the chromaffin cells of the
mature adrenal medulla. Pheochromocytomas occur in patients of all ages, and may be
sporadic, or associated with a hereditary cancer syndrome (neurofibromatosis type I). Only
10% of adrenal pheochromocytomas are malignant, while the rest are benign tumors. The
most clinically important feature of pheochromocytomas is their tendency to produce large
amounts of the catecholamine hormones epinephrine (adrenaline) and norepinephrine. This
may lead to potentially life-threatening high blood pressure, or cardiac arrythmias, and
numerous symptoms such as headache, palpitations, anxiety attacks, sweating, weight loss,
and tremor. Most pheochromocytomas are initially treated with anti-adrenergic drugs to
protect against catecholamine overload, with surgery employed to remove the tumor once
the patient is medically stable.
Incidentalomas
An adrenal incidentaloma is an adrenal tumor found by coincidence without clinical
symptoms or suspicion. It is one of the more common unexpected findings revealed by
computed tomography (CT), magnetic resonance imaging (MRI), or ultrasonography.[1]
In these cases, a dexamethasone suppression test is often used to detect cortisol excess, and
metanephrines or catecholamines for excess of these hormones.
135. Diffuse endocrine system. APUD-comas- morphology and clinical course.
The Diffuse Neuro-Endocrine System (DNES) consists of cells from the central nervous
system (CNS), Peripheral nervous system (PNS) and nearly all organs with the common
phenotype: The ability to produce biological active Amines or Peptides which act like
Neurotransmitters (NT), Hormones or Paracrine regulators.
It regroups the old APUD system which stated that all these cells originated from the
neural tube.

38

The Neural Type:

Adrenal medulla
Paraganglia

The Epithelial type:

These include: separate endocrine gland, or parts thereof

Adenohypophysiss
Islets of Langerhans
parathyroid gland
Pineal gland

unicellular glands incorporated in other epithelial cells

GI Tract
Liver
Merkel cells of the Skin
Parafollicular cell of the Thyroid gland
Mammary glands
urogenital system (male and female)
Respiratory system

APUD cells constitute a group of apparently unrelated endocrine cells. These cells share
the common function of secreting a low molecular weight polypeptide hormone. There are
several different types which secrete the hormones secretin, cholecystokinin and several
others. The name is derived from an acronym, referring to the following:

Amine - for high amine content.

Precursor Uptake - for high uptake of (amine) precursors.
Decarboxylase - for high content of the enzyme amino acid decarboxylase (for
conversion of precursors to amines).

Apudoma
In pathology, an apudoma is an endocrine tumour that arises from an APUD cell[2][3] from
structures such as the ampulla of Vater, pancreas, and prostate.
They are derived from neural crest cells.
136. Multiple endocrine neoplasia syndromes.
The term multiple endocrine neoplasia (MEN) encompasses several distinct syndromes
featuring tumors of endocrine glands, each with its own characteristic pattern. In some
cases, the tumors are malignant, in others, benign. Benign or malignant tumors of
nonendocrine tissues occur as components of some of these tumor syndromes.
MEN syndromes are inherited as autosomal dominant disorders.
The MEN syndromes are a group of genetically inherited diseases resulting in proliferative
lesions (hyperplasia, adenomas, and carcinomas) of multiple endocrine organs. Like other

39

inherited cancer disorders, endocrine tumors arising in the context of MEN syndromes
have certain distinct features that contrast with their sporadic counterparts.
MULTIPLE ENDOCRINE NEOPLASIA, TYPE 1
Characterized by abnormalities involving the parathyroid (include both hyperplasia and
adenomas), pancreas (often present with metastatic disease) and pituitary glands
(prolactinoma)
MEN-1 syndrome is caused by germline mutations in the MEN1 tumor suppressor gene,
which encodes a 610amino acid product known as menin.
The dominant clinical manifestations of MEN-1 usually result from the peptide hormones
that are overproduced and include such abnormalities as recurrent hypoglycemia due to
insulinomas, intractable peptic ulcers in persons with Zollinger-Ellison syndrome,
nephrolithiasis caused by PTH-induced hypercalcemia, or symptoms of prolactin excess
from a pituitary tumor.

MULTIPLE ENDOCRINE NEOPLASIA, TYPE 2

MEN-2 is subclassified into three distinct syndromes: MEN-2A, MEN-2B, and familial
medullary thyroid cancer.

MEN-2A, or Sipple syndrome, is characterized by pheochromocytoma, medullary

carcinoma, and parathyroid hyperplasia. Medullary carcinomas are usually
multifocal and are virtually always associated with foci of C-cell hyperplasia in the
adjacent thyroid.

MEN-2B has significant clinical overlap with MEN-2A. Patients develop medullary
thyroid carcinomas, which are usually multifocal and more aggressive than in MEN2A, and pheochromocytomas. However, unlike in MEN-2A, primary
hyperparathyroidism is not present. In addition, MEN-2B is accompanied by
neuromas or ganglioneuromas involving the skin, oral mucosa, eyes, respiratory tract,
and gastrointestinal tract, and a marfanoid habitus, with long axial skeletal features
and hyperextensible joints.

137. Cerebrovascular diseases.

Stroke is the clinical term for a disease with acute onset of a neurologic
deficit as the result of vascular lesions, either hemorrhage or loss of blood
supply.Cerebral infarction follows loss of blood supply and can be
widespread, focal, or affect regions with the least robust vascular
supply.Focal cerebral infarcts are most commonly embolic; if there is
subsequent fragmentation of an embolism, a nonhemorrhagic infarct can
become hemorrhagic.Primary intraparenchymal hemorrhages are typically
due to either hypertension (most commonly in white matter, deep gray matter,
or posterior fossa contents) or cerebral amyloid angiopathy.Spontaneous
subarachnoid hemorrhage is usually caused by a structural vascular
abnormality, such as an aneurysm or arteriovenous malformation.

40

Hypoxia, Ischemia, and Infarction

The brain requires a constant delivery of glucose and oxygen from the blood.
Cerebral blood flow remains constant over a wide range of blood pressure and
intracranial pressure because of autoregulation of vascular resistance.
Global Cerebral Ischemia
This pattern of widespread ischemic/hypoxic injury occurs when there is a
generalized reduction of cerebral perfusion, usually below systolic pressures
of less than 50mmHg, such as in cardiac arrest, shock, and severe
hypotension.
Morphology
In the setting of global ischemia, the brain is swollen, with
wide gyri and narrowed sulci. The cut surface shows poor
demarcation between gray and white matter. The
histopathologic changes that attend irreversible ischemic
injury (infarction) are grouped into three categories. acute
neuronal cell change characterized initially by
microvacuolization, followed by cytoplasmic eosinophilia.
Later occur necrosis of tissue, influx of macrophages, vascular
proliferation, and reactive gliosis. Repair, seen after 2 weeks,
is characterized by removal of all necrotic tissue, loss of
organized CNS structure, and gliosis.
Border zone infarcts are wedge-shaped areas of infarction that occur in those
regions of the brain and spinal cord that lie at the most distal fields of arterial
perfusion. In the cerebral hemispheres, the border zone between the anterior
and the middle cerebral artery distributions is at greatest risk. Damage to this
region produces a band of necrosis over the cerebral convexity a few
centimeters lateral to the interhemispheric fissure. Border zone infarcts are
usually seen after hypotensive episodes.
Focal Cerebral Ischemia
Cerebral arterial occlusion leads to focal ischemia and-if sustained-to
infarction of CNS tissue in the distribution of the compromised vessel. The
major source of collateral flow is the circle of Willis.
Morphology
The macroscopic appearance of a nonhemorrhagic infarct
changes in time. the tissue becomes pale, soft, and swollen,
and the corticomedullary junction becomes indistinct. the
brain becomes gelatinous and friable, and the previously illdefined boundary between normal and abnormal tissue
becomes more distinct as edema resolves in the adjacent tissue
that has survived.
Acute hemorrhages are characterized by extravasation of blood with
compression of the adjacent parenchyma. Old hemorrhages show an area of
41

cavitary destruction of brain with a rim of brownish discoloration. On

microscopic examination, the early lesion consists of a central core of clotted
blood surrounded by a rim of brain tissue showing anoxic neuronal and glial
changes as well as edema.
An unruptured saccular aneurysm is a thin-walled outpouching of an artery.
At the neck of the aneurysm, the muscular wall and intimal elastic lamina
stop short and are absent from the aneurysm sac itself; the sac is made up of
thickened hyalinized intima. The adventitia covering the sac is continuous
with that of the parent artery . Rupture usually occurs at the apex of the sac
with extravasation of blood into the subarachnoid space, the substance of the
brain, or both.
138. Tumors of central nervous system.
Tumors of the nervous system have unique characteristics that set them apart from
neoplastic processes elsewhere in the body.
Histologic distinction between benign and malignant lesions may be more subtle in
the CNS than in other organs.The pattern of growth of low-grade lesions (low
mitotic rate, cellular uniformity, and slow growth) may still include infiltration of
large regions of the brain, thereby leading to serious clinical deficits and poor
prognosis.The anatomic site of the neoplasm can have lethal consequences
irrespective of histologic classification; for example, a benign meningioma, by
compressing the medulla, can cause cardiorespiratory arrest. Moreover, the ability
to resect a lesion may be limited because of its location.The pattern of spread of
primary CNS neoplasms differs from that of other tumors. Although even the most
highly malignant gliomas rarely metastasize outside the CNS, the subarachnoid
space does provide a pathway for spread so that seeding along the brain and spinal
cord can occur.
GLIOMAS
Gliomas, the most common group of primary brain tumors, include astrocytomas,
oligodendrogliomas, and ependymomas.
Astrocytoma
The two major categories of astrocytic tumors are infiltrating astrocytomas and noninfiltrating neoplasms, of which the most common are the pilocytic astrocytomas. These
tumor types have characteristic histologic features, distribution within the brain, age
groups typically affected, and clinical course.
Morphology. The gross appearance of diffuse astrocytoma is that of a poorly defined,
gray, infiltrative tumor that expands and distorts the invaded brain. These tumors range
in size from a few centimeters to enormous lesions that replace an entire hemisphere.
The cut surface of the tumor is either firm or soft and gelatinous; cystic degeneration
may be seen. The tumor may appear well demarcated from the surrounding brain tissue,
but infiltration beyond the outer margins is always present.
Oligodendroglioma

42

Patients may have had several years of neurologic complaints, often including seizures.
The lesions are found mostly in the cerebral hemispheres, with a predilection for white
matter.
Morphology. On gross examination, oligodendrogliomas are well-circumscribed,
gelatinous, gray masses, often with cysts, focal hemorrhage, and calcification. On
microscopic examination, the tumors are composed of sheets of regular cells with
spherical nuclei containing finely granular chromatin (similar to normal
oligodendrocytes) surrounded by a clear halo of cytoplasm .
NEURONAL TUMORS
The most common CNS tumor containing mature-appearing neurons (ganglion cells) is
ganglioglioma, since there is usually an admixed glial neoplasm. Most of these tumors are
slow growing, but the glial component occasionally becomes frankly anaplastic, and the
disease then progresses rapidly. Lesions that contain mixtures of neuronal and glial
elements often present as a seizure disorder; surgical resection of the tumor is usually
effective in controlling the seizures.
Morphology. Gangliogliomas are most commonly found in the temporal lobe and often
have a cystic component. The neoplastic ganglion cells are irregularly clustered and have
apparently random orientation of neurites. Binucleate forms are frequent. The glial
component of these lesions usually resembles a low-grade astrocytoma, lacking mitotic
activity and necrosis.
Dysembryoplastic neuroepithelial tumor is a rare, lowgrade tumor of childhood that often
presents as a seizure disorder, and has a relatively good prognosis after surgical resection.
These lesions are typically located in the superficial temporal lobe, although other cortical
sites are seen. There is often attenuation of the overlying skull, suggesting that the lesion
has been present for a long time.
Morphology. These lesions typically form multiple discrete intracortical nodules of
small, round cells, arranged in columns around central cores of processes, and are
associated with a myxoid background, known as the specific glioneuronal element.
There are well-differentiated floating neurons that sit in the pools of
mucopolysaccharide-rich fluid of the myxoid background. The larger neurons and the
small, round cells of the specific element express neuronal markers. Surrounding the
nodules, there may be focal cortical dysplasia and sometimes low-grade astrocytoma.
Lesions that show both the specific element and a glial component are termed complex.
Germ Cell Tumors
Primary brain germ cell tumors occur along the midline, most commonly in the pineal and
the suprasellar regions. They account for 0.2% to 1% of brain tumors in people of
European descent but up to 10% in Japanese people. They are tumors of the young, with
90% occurring during the first two decades. Germ cell tumors, particularly teratomas, are
among the more common congenital tumors. Germ cell tumors in the pineal region show a
strong male predominance, which is not seen in suprasellar lesions.
MENINGIOMAS

43

Meningiomas are predominantly benign tumors of adults, usually attached to the dura, that
arise from the meningothelial cell of the arachnoid. Meningiomas may be found along any
of the external surfaces of the brain as well as within the ventricular system, where they
arise from the stromal arachnoid cells of the choroid plexus. Prior radiation therapy,
typically decades earlier, is a risk factor for development of meningiomas. Other tumors
such as metastases, solitary fibrous tumors, and a range of poorly differentiated sarcomas
may also grow as dural-based masses.
Morphology. Meningiomas are usually rounded masses with well-defined dural bases
that compress underlying brain but are easily separated from it. Extension into the
overlying bone may be present. The surface of the mass is usually encapsulated with
thin, fibrous tissue and may have a bosselated or polypoid appearance. They may also
grow en plaque, in which the tumor spreads in a sheetlike fashion along the surface of
the dura. This form is commonly associated with hyperostotic reactive changes in the
overlying bone. The lesions range from firm and fibrous to finely gritty, or they may
contain numerous calcified psammoma bodies. Gross evidence of necrosis or extensive
hemorrhage is not present.
Anaplastic (malignant) meningioma is a highly aggressive tumor with the appearance
of a high-grade sarcoma, but retaining some histologic evidence of meningothelial
origin. Mitotic rates are often extremely high. Papillary meningioma (with pleomorphic
cells arranged around fibrovascular cores) and rhabdoid meningioma (with sheets of
tumor cells with hyaline eosinophilic cytoplasm containing intermediate filaments) both
have such a high propensity to recur.
139. Infections in central nervous system - meningitis, encephalitis. Myelitis.
Meningitis It is usually caused by an infection, but may also occur in response to a
nonbacterial irritant introduced into the subarachnoid space (chemical meningitis).
Infectious meningitis is broadly classified into acute pyogenic (usually bacterial
meningitis), aseptic (usually acute viral meningitis), and chronic (usually tuberculous,
spirochetal, or cryptococcal).
Morphology. The normally clear CSF is cloudy and sometimes frankly purulent. In acute
meningitis, an exudate is evident within the leptomeninges over the surface of the brain.
The meningeal vessels are engorged and stand out prominently. The location of the
exudate varies. From the areas of greatest accumulation, tracts of pus can be followed
along blood vessels on the surface of the brain. When the meningitis is fulminant, the
inflammation may extend to the ventricles, producing ventriculitis.
On microscopic examination, neutrophils fill the subarachnoid space in severely affected
areas and are found predominantly around the leptomeningeal blood vessels in less severe
cases. In untreated meningitis, Gram stain reveals varying numbers of the causative
organism. Phlebitis may also lead to venous thrombosis and hemorrhagic infarction of the
underlying brain.
Symptoms: headache and neck stiffness associated with fever, confusion or altered
consciousness, vomiting, and an inability to tolerate light or loud noises.
Causes: Bacterial, Aseptic, Viral, Parasitic, Non-infectious.
Encephalitis: is an acute inflammation of the brain. Encephalitis with meningitis is known
as meningoencephalitis.

44

Symptoms: headache, fever, confusion, drowsiness, and fatigue. More advanced and
serious symptoms include seizures or convulsions, tremors, hallucinations, and memory
problems.

Myelitis: is a disease involving inflammation of the spinal cord, which disrupts central
nervous system functions linking the brain and limbs.
Causes

Infectious mononucleosis
Poliovirus is the cause of poliomyelitis
Cases of Measles myelitis
Herpes simplex, epstein barr virus, cytomegalovirus, and mycoplasma have been
suspected as the eitologic agents of acute disseminated encephalomyelitis.
Retroviruses and Chronic fatigue syndrome-associated virus as well as
enteroviruses have been suspected of being causes of Myalgic encephalomyelits
aka Chronic fatigue syndrome.

Types

Acute disseminated encephalomyelitis

Myalgic encephalomyelitis aka Chronic fatigue syndrome
Poliomyelitis
Transverse myelitis

140. Demyelinating diseases of the nervous system.

Demyelinating diseases of the CNS are acquired conditions characterized by preferential
damage to myelin, with relative preservation of axons. The clinical deficits are due to the
effect of myelin loss on the transmission of electrical impulses along axons. The natural
history of demyelinating diseases is determined, in part, by the limited capacity of the CNS
to regenerate normal myelin and by the degree of secondary damage to axons that occurs
as the disease runs its course.
MULTIPLE SCLEROSIS
Multiple sclerosis (MS) is an autoimmune demyelinating disorder characterized by distinct
episodes of neurologic deficits, separated in time, attributable to white matter lesions that
are separated in space.
Morphology. MS is a white matter disease that is best appreciated in sections of the brain
and spinal cord. Lesions appear as multiple, well-circumscribed, somewhat depressed,
glassy, graytan, irregularly shaped plaques In the fresh state these are firmer than the
surrounding white matter (sclerosis). Plaques can be found throughout the white matter
and also extend into gray matter, since these have myelinated fibers running through them.
The size of lesions varies considerably, from small foci that are only recognizable
microscopically to confluent plaques that involve large portions of the centrum semiovale.
The lesions often have sharply defined borders. Plaques commonly occur adjacent to the
lateral ventricles. They are also frequent in the optic nerves and chiasm, brainstem,
ascending and descending fiber tracts, cerebellum, and spinal cord.
NEUROMYELITIS OPTICA

45

The development of synchronous (or near synchronous) bilateral optic neuritis and spinal
cord demyelination is referred to as neuromyelitis optica or Devic disease. White cells are
common in the CSF, often including neutrophils. Within the damaged areas of white
matter, there is typically necrosis, an inflammatory infiltrate including neutrophils, and
vascular deposition of immunoglobulin and complement. These lesions have been
suggested to be mediated by humoral immune mechanisms. Many affected individuals
show antibodies to aquaporins, which are in part responsible for maintenance of astrocytic
foot process and thus the integrity of the blood-brain barrier.
ACUTE DISSEMINATED ENCEPHALOMYELITIS AND ACUTE NECROTIZING
HEMORRHAGIC ENCEPHALOMYELITIS
Acute disseminated encephalomyelitis (ADEM, perivenous encephalomyelitis) is a diffuse,
monophasic demyelinating disease that follows either a viral infection or, rarely, a viral
immunization. Symptoms include headache, lethargy, and coma.
Acute necrotizing hemorrhagic encephalomyelitis is a fulminant syndrome of CNS
demyelination, typically affecting young adults and children. The illness is almost
invariably preceded by a recent episode of upper respiratory infection, most often of
unknown cause.
Morphology. In ADEM, macroscopic examination of the brain shows only grayish
discoloration around white-matter vessels. On microscopic examination, myelin loss
with relative preservation of axons can be found throughout the white matter. In the early
stages, polymorphonuclear leukocytes can be found within the lesions; later,
mononuclear infiltrates predominate.
Central pontine myelinolysis is characterized by loss of myelin (with relative preservation
of axons and neuronal cell bodies) in a roughly symmetric pattern involving the basis
pontis and portions of the pontine tegmentum but sparing the periventricular and subpial
regions. Lesions may be found more rostrally; it is extremely rare for the process to extend
below the pontomedullary junction. Morphologically there is myelin loss without evidence
of inflammation; neurons and axons are well preserved. Again, because of the monophasic
nature of the disease all lesions appear to be at the same stage of myelin loss and reaction.

141. Toxic encephalopathies.

Chronic solvent encephalopathy is a degenerative neurologic disorder caused by exposure
to toxic substances like organic solvents.
Causes: Toxic encephalopathy can be caused by various chemicals, some of which are
commonly used in everyday life. These harmful chemicals can be inhaled (in the case of
air fresheners) or applied (in the case of perfumes). The substances diffuse into the brain
rapidly, as they are lipophilic and readily transported across the bloodbrain barrier. This is
a result of increased membrane solubility and local blood flow, with central nervous
system (CNS) solvent uptake being further increased with high levels of physical activity
Signs and symptoms: Toxic encephalopathy has a wide variety of symptoms, which can
include memory loss, small personality changes/increased irritability, insidious onset of
concentration difficulties, involuntary movements, fatigue, seizures, arm strength
problems, and depression.

46

Treatment: Diet changes and nutritional supplements may help some patients. To reduce or
halt seizures, anticonvulsants may be prescribed. Dialysis or organ replacement surgery
may be needed in some severe cases.
142. Infectious diseases - classification according to the mode of transmission of the
infectious agents. Sepsis. Septicemia. Septicopyemia.

Sepsis is a potentially deadly medical condition that is characterized by a

whole-body inflammatory state (called a systemic inflammatory response
syndrome) and the presence of a known or suspectedinfection. The body
may develop this inflammatory response by the immune
system tomicrobes in the blood, urine, lungs, skin, or other tissues. A lay
term for sepsis is blood poisoning, also used to describe septicaemia.
Severe sepsis is the systemic inflammatory response, plus infection, plus
the presence of organ dysfunction.
Septicemia is a related medical term referring to the presence of
pathogenic organisms in the bloodstream, leading to sepsis. Severe sepsis
is usually treated in the intensive care unit with intravenous
fluids and antibiotics.
Signs and symptoms: sepsis is characterized by presence of
acute inflammation present throughout the entire body, and is, therefore,
frequently associated with fever and elevated white blood cell count
(leukocytosis) or low white blood cell count and lower-than-average
temperature, and vomiting. The modern concept of sepsis is that the host's
immune response to the infection causes most of the symptoms of sepsis,
resulting in hemodynamic consequences and damage to organs. This host
response has been termed systemic inflammatory response
syndrome (SIRS) and is characterized by an elevated heart rate, high
respiratory rate, abnormal white blood cell count and elevated or lowered
body temperature.

Sepsis is differentiated from SIRS by the presence of a known or

suspected pathogen.
This immunological response causes widespread activation of acute-phase
proteins, affecting the complement system and the coagulation pathways,
which then cause damage to the vasculature as well as to the organs. Various
neuroendocrine counter-regulatory systems are then activated as well, often
compounding the problem. Even with immediate and aggressive treatment, this
may progress to multiple organ dysfunction syndrome and eventually death.
Septicopyemia: a form of sepsis, in which the leading suppurative processes are at the
gates of a bacterial infection and embolism ("metastasis pus") with the formation of
abscesses in many organs and tissues, in contrast to the signs of septicemia giperergii
appear very moderate, so the disease does not have the rough. Main role in the
development septicopyemia belongs aureus and Pseudomonas aeruginosa.
143. Viral diseases. Viral respiratory disorders. Grippe.
Parainfluenza-3 virus is an RNA virus classified in the Paramyxovirus
family. Infections caused by PI-3 are common in cattle. Although PI-3 is
capable of causing disease, it is usually associated with mild to subclinical

47

infections. The most important role of PI-3 is to serve as an initiator that

can lead to the development of secondary bacterial pneumonia. Clinical
signs include pyrexia, cough, serous nasal and lacrimal discharge, increased
respiratory rate, and increased breath sounds.
Bovine respiratory syncytial virus is an RNA virus classified as a
pneumovirus in the Paramyxovirus family. This virus was named for its
characteristic cytopathic effectthe formation of syncytial cells. In
additional to cattle, sheep and goats can also be infected by respiratory
syncytial viruses. Gross lesions include a diffuse interstitial pneumonia
with subpleural and interstitial emphysema along with interstitial edema.
These lesions are similar to and must be differentiated from other causes of
interstitial pneumonia.
Grippe: is an infectious disease of birds and mammals caused by RNA
viruses of the family Orthomyxoviridae, the influenza viruses. The most
common symptoms are chills, fever, runny nose, sore throat, muscle pains,
headache (often severe), coughing, weakness/fatigue and general
discomfort. One of the mechanisms is believed to be the inhibition of
adrenocorticotropic hormone (ACTH) resulting in lowered cortisol levels.
Knowing which genes are carried by a particular strain can help predict
how well it will infect humans and how severe this infection will be
Flu can occasionally lead to pneumonia, either direct viral pneumonia or
secondary bacterial pneumonia, even for persons who are usually very
healthy.
Typically, influenza is transmitted through the air by coughs or sneezes,
creating aerosols containing the virus. Influenza can also be transmitted by
direct contact with bird droppings or nasal secretions, or through contact
with contaminated surfaces.
Treatment: People with the flu are advised to get plenty of rest, drink plenty
of liquids, avoid using alcohol and tobacco and, if necessary, take
medications such as acetaminophen (paracetamol) to relieve the fever and
muscle aches associated with the flu.
144. Viral disorders of digestive tract: Mumps, viral enteritis and diarrhea.
Mumps is a viral disease of the human species, caused by the mumps virus.
Painful swelling of the salivary glands (classically the parotid gland) is the most
typical presentation. Painful testicular swelling (orchitis) and rash may also occur.
The symptoms are generally not severe in children. In teenage males and men,
complications such as infertility orsubfertility are more common, although still rare
in absolute terms. The disease is generally self-limiting, running its course before
receding, with no specific treatment apart from controlling the symptoms with pain
medication.
Signs and symptoms: Parotid inflammation, Fever, Headache, Pancreatitis,
Orchitis, dry mouth, sore face and/or ears and occasionally in more serious cases,

48

loss of voice. Fever and headache are prodromal symptoms of mumps, together
with malaise and anorexia.
Viral enteritis:
Viral enteritis is an inflammation of the intestinal tract caused by a virus. Viruses that
cause enteritis include: Parvovirus, Coronavirus, Herpesvirus, Astrovirus, Enterovirus,
Reovirus.
Viral enteritis is easily transmitted to susceptible dogs.
These viruses attack the lining of the intestinal tract, destroying certain portions of the
absorptive villi and thereby causing the characteristic signs of their disease
entities:Depression, Fever, Loss of appetite, Vomiting, Diarrhea, Blood in the stools, Heart
muscle damage may occur with some of these viral infections.
Diarrhea:
Abnormally swift passage of waste material through the large intestine, with consequent
discharge of loose feces from the anus. Diarrhea may be accompanied by cramping. The
disorder has a wide range of causes. It may, for example, result from bacterial or viral
infection; from dysentery, either amoebic or bacillary; from impaired absorption of
nutrients; from eating coarse or highly seasoned foods or drinking large quantities of
alcoholic beverages; from poisons such as arsenic or mercury bichloride; or from drugs
administered to reduce high blood pressure. Excessive amounts of thyroid hormones,
parathyroid hormone deficiencies, irritable bowel syndrome, and uremia (an excess of
nitrogenous wastes in the blood) all may cause diarrhea. Most cases of diarrhea are not
serious and do not require treatment; dehydration can be prevented by drinking plenty of
clear liquids. Diarrhea caused by an infection can often be treated with antibiotics
145. Viral disorders with exanthemas or skin rashes: Measles (rubeola),
Rubella (German measles), Smallpox.
Measles, is an infection of the respiratory system caused by a virus, specifically
a paramyxovirus of the genus Morbillivirus. Morbilliviruses, like other
paramyxoviruses, are enveloped, single-stranded, negative-sense RNA viruses.
Symptoms include fever, cough, runny nose, red eyes and a
generalized, maculopapular, erythematous rash.Koplik's spots seen inside the
mouth are pathognomonic (diagnostic) for measles, but are not often seen, even
in real cases of measles, because they are transient and may disappear within a
day of arising
Complications with measles are relatively common, ranging from relatively mild
and less serious diarrhea, to pneumonia, Otitis media and acute encephalitis (and
rarely subacute sclerosing panencephalitis); corneal ulceration leading to corneal
scarring. Complications are usually more severe in adults who catch the virus.
There is no specific treatment for measles. Most patients with uncomplicated
measles will recover with rest and supportive treatment.
Rubella is a disease caused by the rubella virus. Rubella is a common childhood
infection usually with minimal systemic upset although transient arthropathy may
occur in adults. Serious complications are very rare.

49

Acquired rubella is transmitted via airborne droplet emission from the upper
respiratory tract of active cases (can be passed along by the breath of people sick
from Rubella. The virus may also be present in the urine, feces and on the skin.
There is no carrier state: the reservoir exists entirely in active human cases.
DAGNOSS: Rubella virus specific IgM antibodies are present in people recently
infected by Rubella virus but these antibodies can persist for over a year and a
positive test result needs to be interpreted with caution. The presence of these
antibodies along with, or a short time after, the characteristic rash confirms the
diagnosis.
Smallpox was an infectious disease unique to humans, caused by either of
two virus variants, Variola major and Variola minor.
Once inhaled, variola major virus invades the oropharyngeal (mouth and throat) or
the respiratory mucosa, migrates to regional lymph nodes, and begins to multiply.
In the initial growth phase the virus seems to move from cell to cell, but around the
12th day, lysis of many infected cells occurs and the virus is found in
the bloodstream in large numbers (this is called viremia), and a second wave of
multiplication occurs in the spleen, bone marrow, and lymph nodes. The initial or
prodromal symptoms are similar to other viral diseases such as influenza and
the common cold: fever , muscle pain, malaise, headache and prostration. As
the digestive tract is commonly involved, nausea and vomiting and backache often
occur.
The prodrome, or preeruptive stage, usually lasts 24 days. By days 1215 the
first visible lesionssmall reddish spots calledenanthemappear on mucous
membranes of the mouth, tongue, palate, and throat, and temperature falls to near
normal. These lesions rapidly enlarge and rupture, releasing large amounts of
virus into the saliva .Smallpox virus preferentially attacks skin cells, causing the
characteristic pimples (called macules) associated with the disease. A rash
develops on the skin 24 to 48 hours after lesions on the mucous membranes
appear.
146. Herpes virus disease: Herpes simplex (HSV I) and Herpes genitalis (HSV II)
infections. Chicken pox (Varicella) and Herpes Zoster.
Herpes simplex virus 1 and 2, are two members of the
herpes virus family, Herpesviridae, that infect humans. Both HSV-1 (which
produces most cold sores) and HSV-2 (which produces most genital herpes)
are ubiquitous and contagious.
They can be spread when an infected person is producing and shedding the virus.
Symptoms of herpes simplex virus infection include watery blisters in
the skin or mucous membranes of the mouth, lips or genitals. Lesions heal with
a scab characteristic of herpetic disease. Sometimes, the viruses cause very mild
or atypical symptoms during outbreaks. However, as neurotropic and
neuroinvasive viruses, HSV-1 and -2 persist in the body by becoming latent and
hiding from the immune system in the cell bodies of neurons. After the initial
or primary infection, some infected people experience sporadic episodes of
viral reactivation or outbreaks. In an outbreak, the virus in a nerve cell becomes
active and is transported via the neuron's axon to the skin, where virus replication
and shedding occur and cause new sores .HSV-1 and -2 are transmitted from
contact with an infectious area of the skin during reactivations of the virus.
Treatment usually involves general-purpose antiviral drugs that interfere with viral

50

replication, reducing the physical severity of outbreak-associated lesions and

lowering the chance of transmission to others. Studies of vulnerable patient
populations have indicated that daily use of antivirals such
as acyclovir and valacyclovir can reduce reactivation rates.

Herpes genitalis refers to a genital infection by Herpes simplex virus. The typical
manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of genital
sores consisting of inflamed papules and vesicles on the outer surface of the
genitals, resembling cold sores, that usually appear 47 days after sexual
exposure to HSV for the first time.
In males, the lesions occur on the glans penis, shaft of the penis or other parts of
the genital region, on the inner thigh, buttocks, or anus. In females, lesions appear
on or near the pubis, labia, clitoris, vulva, buttocks or anus. Other common
symptoms include pain, itching, and burning. After 23 weeks, existing lesions
progress into ulcers and then crust and heal, although lesions on mucosal
surfaces may never form crusts.
Acyclovir is an antiviral drug used against herpes viruses, varicella-zoster,
and Epstein-Barr Viruses. This drug reduces the pain and the number of lesions in
the initial case of genital herpes. Furthermore, it decreases the frequency and
severity of recurrent infections.
Chickenpox is a highly contagious illness caused by
primary infection with varicella zoster virus (VZV).
It usually starts with vesicular skin rash mainly on the body and head rather than at
the periphery and becomes itchy, raw pockmarks, which mostly heal without
scarring. On examination, the observer typically finds lesions at various stages of
healing. Chickenpox is an airborne disease spread easily through coughing or
sneezing of ill individuals or through direct contact with secretions from the rash. A
person with chickenpox is infectious one to two days before the rash appears.
The onset of illness with chickenpox is often characterized by symptoms
including myalgia, itching, nausea, fever, headache, sore throat, etc. In children,
the first symptom is usually the development of a papular rash, which begins on
the trunk and then spreads to the face and limbs
Varicella treatment mainly consists of easing the symptoms as there is no
actual cure of the condition. Some treatments are however available for relieving
the symptoms while theimmune system clears the virus from the body.
Herpes zoster, is a viral disease characterized by a painful skin rash
with blisters in a limited area on one side of the body, often in a stripe.
Varicella zoster virus can become latent in the nerve cell bodies and less
frequently in non-neuronal satellite cells of dorsal root, cranial
nerveor autonomic ganglion, without causing any symptoms.
The earliest symptoms of herpes zoster, which include headache, fever,
and malaise, are nonspecific and are commonly followed by sensations of burning
pain, itching, hyperesthesia (oversensitivity), or paresthesia. The pain may be mild
to extreme in the affected dermatome, with sensations that are often described as
aching, numbing, and can be interspersed with quick stabs of agonizing painIf the
rash has appeared, identifying this disease requires only a visual examination,
since very few diseases produce a rash in a dermatomal pattern. However, herpes
simplex virus (HSV) can occasionally produce a rash in such a pattern.

51

147. Cytomegalic inclusion disease.

Cytomegalic inclusion body disease (CIBD) is caused by infection from the
cytomegalic virus (CMV), a type of herpes virus that can lie dormant after
initial infection and then reactivate periodically throughout life. The virus
causes enlargement of cells of some organs and the development of
inclusion bodies- discrete masses of cellular material-in the cytoplasm or
nucleus of these cells. : An infection due to cytomegalovirus and marked by
nuclear inclusion bodies in enlarged infected cells.
Causes of Cytomegalic Inclusion Disease

infection,
genetic defect,
environmental stress
It is most commonly transmitted when an uninfected person
comes in contact with infected body fluids and then touches his or
her mouth or nose, at which point the virus is absorbed into the
mucous membranes.
In a fetus, newborn, or a person with a compromised immune
system, CIBD can be much more severe.

What are the symptoms of Cytomegalic Inclusion Disease?

shed the virus in their body fluids, such as saliva, urine, blood,
tears, semen, or breast milk.
Bone pain.
Fatigue
CIBD can be apparent as a lung infection, excessive bleeding,
anemia, liver damage, etc.
Swollen lymph glands.

Cytomegalic Inclusion Disease Treatment

The main treatment includes the use of the antiviral drugs, such
as ganciclovir and acyclovir to prevent infection in the people who
are suffering from weak immune system and to reduce their viral
load.
High titer immunoglobulin (IVIG, CytoGam) may also be
prescribed for infected people with some impaired immune
system.

148. Infectious mononucleosis.

Infectious mononucleosis is an infectious, widespread viral disease caused by the
EpsteinBarr virus (EBV), one type of herpes virus.
The signs and symptoms of infectious mononucleosis vary with age.
The classic symptoms of mononucleosis are a sore
throat, fever, fatigue, malaise, pharyngeal inflammation, vomiting, petechiae and
loss of appetite. Common signs include lymphadenopathy (enlarged lymph

52

nodes), splenomegaly (enlarged spleen), hepatitis (refers to inflammation of

hepatocytescells in the liver) and hemolysis (the bursting of red blood cells).
Morphology: Reactive (or atypical) lymphocytosis is seen in this high-oil magnification
view of the peripheral blood. These reactive lymphocytes have pleomorphic reticular
nucleii, peripheral basophilia of cytoplasm, and scalloped cell borders some of which
appears to stream into red cells. Slight rouleaux is also present.
Treatment: Infectious mononucleosis is generally self-limiting, so only symptomatic
and/or supportive treatments are used.[23] Rest is recommended during the acute
phase of the infection, but activity should[citation needed] be resumed once acute
symptoms have resolved. Nevertheless, heavy physical activity and contact sports
should be avoided to mitigate the risk of splenic rupture, for at least one month
following initial infection or splenomegaly has resolved, as determined by a
treating physician.
149. Viral diseases of the Central Nervous system: Poliomyelitis.
Poliomyelitis is an acute, viral, infectious disease spread from person to person,
primarily via the fecal-oral route .
Although approximately 90% of polio infections cause no symptoms at all, affected
individuals can exhibit a range of symptoms if the virus enters the blood stream. In
about 1% of cases, the virus enters the central nervous system, preferentially
infecting and destroying motor neurons, leading to muscle weakness and
acute flaccid paralysis. Different types of paralysis may occur, depending on the
nerves involved. Spinal polio is the most common form, characterized by
asymmetric paralysis that most often involves the legs. Bulbar polio leads to
weakness of muscles innervated by cranial nerves. Bulbospinal polio is a
combination of bulbar and spinal paralysis.
Two basic patterns of polio infection are described: a minor illness which does not
involve the central nervous system (CNS), sometimes called abortive poliomyelitis,
and a major illness involving the CNS, which may be paralytic or nonparalytic
Rarely, the infection produces minor symptoms; these may include
upper respiratory tract infection (sore throat and
fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain,
constipation or, rarely, diarrhea), and influenza-like illness. Most patients with CNS
involvement develop nonparalytic aseptic meningitis, with symptoms of headache,
neck, back, abdominal and extremity pain, fever, vomiting, lethargy and irritability.
CAUSE
Poliomyelitis is caused by infection with a member of the genus Enterovirus known
as poliovirus (PV). This group of RNA viruses colonize thegastrointestinal
tract[1] specifically the oropharynx and the intestine. Three serotypes of
poliovirus have been identifiedpoliovirus type 1 (PV1), type 2 (PV2), and type 3
(PV3)each with a slightly different capsid protein.[14] All three are
extremely virulent and produce the same disease symptoms.
TRANSMSSON
Poliomyelitis is highly contagious via the oral-oral (oropharyngeal source) and
fecal-oral (intestinal source) routes.

53

DAGNOSS
A laboratory diagnosis is usually made based on recovery of poliovirus from a
stool sample or a swab of the pharynx. Analysis of the patient's cerebrospinal
fluid (CSF), which is collected by a lumbar puncture ("spinal tap"), reveals an
increased number of white blood cells (primarily lymphocytes) and a mildly
elevated protein level.
TREATMENT
There is no cure for polio. The focus of modern treatment has been on providing
relief of symptoms, speeding recovery and preventing complications. Supportive
measures include antibiotics to prevent infections in weakened
muscles, analgesics for pain, moderate exercise and a nutritious diet.[55] Treatment
of polio often requires long-term rehabilitation, including physical therapy, braces,
corrective shoes and, in some cases, orthopedic surgery
150. Viral diseases of the Central Nervous system: Rabies.
Rabies is a viral disease that causes acute encephalitis (inflammation of the brain)
inendotherms. It is zoonotic , most commonly by a bite from an infected subject.
For a human, rabies is almost invariably fatal if postexposure prophylaxis is not
administered prior to the onset of severe symptoms. The rabies virus infects the
central nervous system, ultimately causing disease in the brain and death.
The rabies virus travels to the brain by following the peripheral nerves. Once the
rabies virus reaches the central nervous system and symptoms begin to show, the
infection is effectively untreatable and usually fatal within days.
SING AND SYM.
The period between infection and the first flu-like symptoms is normally two to
twelve weeks, but can be as long as two years. Soon after, the symptoms expand
to slight or partial paralysis, cerebral
dysfunction, anxiety, insomnia, confusion, agitation, abnormal behavior, paranoia,
terror, hallucinations, progressing to delirium. The production of large quantities of
saliva and tears coupled with an inability to speak or swallow are typical during the
later stages of the disease; this can result in hydrophobia, in which the patient has
difficulty swallowing because the throat and jaw become slowly paralyzed, shows
panic when presented with liquids to drink, and cannot quench its thirst
Treatment after exposure (receiving the vaccines), known as post-exposure
prophylaxis (PEP), is highly successful in preventing the disease if administered
promptly, in general within ten days of infection. Begun with little or no delay, PEP
is 100% effective against rabies.[9] In the case in which there has been a
significant delay in administering PEP, the treatment should be administered
regardless of that delay, as it may still be effective
151. AIDS.
Acquired immune deficiency syndrome is a disease of the human immune
system caused by the human immunodeficiency virus (HIV). The illness interferes
with the immune system making people with AIDS much more likely to
get infections, including opportunistic infections and tumors that do not affect
people with working immune systems. This susceptibility gets worse as the
disease continues.
54

HIV is transmitted in many ways, such as: vaginal, oral or anal sex; blood
transfusion; contaminated hypodermic needles; and exchange between mother
and baby during pregnancy, childbirth, and breastfeeding. It can be transmitted by
any contact of a mucous membrane or the bloodstream with a bodily fluid that has
the virus in it.
SINNG AND SYM.
The symptoms of AIDS are primarily the result of conditions that do not normally
develop in individuals with healthy immune systems. Most of these conditions are
infections caused by bacteria, viruses, fungi and parasites that are normally
controlled by the elements of the immune system that HIV damages.Opportunistic
infections are common in people with AIDS.These infections affect nearly
every organ system.. People with AIDS also have an increased risk of developing
various cancers such as Kaposi's sarcoma, cervical cancer and cancers of the
immune system known as lymphomas. Additionally, people with AIDS often have
systemic symptoms of infection like fevers, sweats(particularly at night), swollen
glands, chills, weakness, and weight loss.
CAUSE
AIDS is the ultimate clinical consequence of infection with HIV. HIV is
a retrovirus that primarily infects vital organs of the human immune system such
as CD4+ T cells (a subset of T cells), macrophages and dendritic cells. It directly
and indirectly destroys CD4+ T cells..
TREATMENT
There is currently no publicly available HIV vaccine or cure for HIV or AIDS. The
only known methods of prevention are based on avoiding exposure to the virus or,
failing that, an antiretroviral treatment directly after a highly significant exposure,
called post-exposure prophylaxis (PEP).[113] PEP has a very demanding four week
schedule of dosage. It also has very unpleasant side effects
including diarrhea, malaise, nausea and fatigue
152. Rickettsial Diseases: Typhus fever (epidemic typhus).
Typhus is any of several similar diseases caused by Rickettsia prowazekii bacteria.
Rickettsiae morphology: The rickettsial organisms in common with the elementary bodies
of vaccinia virus and all bacteria would appear to have a limiting membrane which
surrounds a substance that seems to be protoplasmic in nature; numbers of dense granules
are embedded in the inner protoplasm.
Symptoms include severe headache, a sustained high fever, cough, rash,
severe muscle pain, chills, falling blood pressure, stupor,sensitivity to light,
and delirium. A rash begins on the chest about five days after the fever appears,
and spreads to the trunk and extremities. A symptom common to all forms of
typhus is a fever which may reach 39 C
TREATMENT
The infection is treated with antibiotics. Intravenous fluids and oxygen may be
needed to stabilize the patient. The mortality rate is 10% to 60%, but is vastly
lower (close to zero) if intracellular antibiotics such as tetracycline are used before
8 days. Infection can also be prevented by vaccination.
55

153. Staphilococcal infections.

Streptococcus is a genus of spherical Gram-positive bacteria belonging to
the phylum Firmicutes and the lactic acid bacteria group. Cellular
division occurs along a single axis in these bacteria, and thus they grow in
chains or pairs.
Alpha-hemolytic
Pneumococci

S. pneumoniae (sometimes called Pneumococcus), is a leading cause of

bacterial pneumonia and occasional etiology of otitis
media, sinusitis, meningitis and peritonitis.

Inflammation is thought to be the major cause of how pneumococcus causes

disease, hence the inflammatory nature of the diagnoses assocaited with it.
The Viridans group: alpha-hemolytic

S. mutans, a contributor to dental caries

S. mitis, mostly found around cheek region
S. sanguinis, no preference of locations
S. salivarius, mostly found on the dorsal side of the tongue
S. salivarius ssp. thermophilus, used in the manufacture of some cheeses and
yogurts
S. constellatus, occasional human pathogen, notable as colonies grown on
blood agarsmell strongly of caramel

Beta-hemolytic
Alpha-hemolytic S. viridans (right) and beta-hemolytic S. pyogenes (left)
streptococci growing on blood agar
Group A
S. pyogenes, also known as Group A Streptococcus (GAS), is the causative
agent in Group A streptococcal infections, including streptococcal
pharyngitis ("strep throat" AmE), acuterheumatic fever, scarlet fever,
acute glomerulonephritis and necrotizing fasciitis. Strep. pyogenes is the
other major cause of streptococcal infection in humans, after
pneumococcus. Group A Streptococcus infection is generally diagnosed
with a Rapid Strep Test (AmE) or by culture. Rheumatic fever, a disease that
affects the joints, kidneys and heart valves, is a consequence of untreated
strep A infection caused not by the bacterium itself. Rheumatic fever is
caused by the antibodies created by the immune system to fight off the
infection cross-reacting with other proteins in the body. This cross-reaction
causes the body to essentially attack itself and leads to the damage above.
Group B
S. agalactiae, or GBS, causes pneumonia and meningitis in neonates and
the elderly, with occasional systemic bacteremia. They can also colonize the
intestines and the female reproductive tract, increasing the risk for premature
rupture of membranes and transmission to the infant
56

Group C
This group includes S. equi, which causes strangles in horses,[10] and S.
zooepidemicus - S. equi is a clonal descendent or biovar of the ancestral S.
zooepidemicus - which causes infections in several species of mammals, including
cattle and horses. Streptococcus dysgalactiae is also a member of Group C, haemolytic streptococci that can cause pharyngitis and other pyogenic infections
similar to Group A streptococc
Group D (enterococci)
Many former Group D streptococci have been reclassified and placed in the
genus Enterococcus
For example, Streptococcus faecalis is now Enterococcus faecalis. The remaining
nonenterococcal Group D strains include Streptococcus bovis and Streptococcus
equinus.
Nonhemolytic streptococci rarely cause illness. However, weakly hemolytic group
D beta-hemolytic streptococci and Listeria monocytogenes (which is actually a
Gram-positive bacillus) should not be confused with nonhemolytic streptococci.
Group F streptococci
Group F streptococci were first described in 1934 by Long and Bliss amongst the
"minute haemolytic streptococci
Group G streptococci
These streptococci are usually, but not exclusively, beta-hemolytic. Streptococcus
canis is an example of a GGS which is typically found on animals, but can cause
infection in humans.
154. Streptococcal infections. Scarlet fever.
Scarlet fever is a disease caused by erythrogenic toxin (a bacterial exotoxin)
released by Streptococcus pyogenes.
Morphology: the shape of the bacteria that causes scarlet fever, Streptococcus pyogenes,
also known as Group A strep, are spherical and form chains.
Symptoms include sore throat, fever and a characteristic red rash. Scarlet fever is usually
spread by inhalation.
Treatment: Other than the occurrence of the diarrhea, the treatment and course of
scarlet fever are no different from those of any strep throat. In case of penicillin
allergy, clindamycin or erythromycincan be used with success.
155. Streptococcal infections. Erysipelas.
Erysipelas is an acute streptococcus bacterial infection[2] of the deep epidermis
with lymphatic spread.
SIGNS
Patients typically develop symptoms including
high fevers, shaking, chills, fatigue, headaches, vomiting, and general illness

57

within 48 hours of the initial infection. The erythematous skin lesion enlarges
rapidly and has a sharply demarcated raised edge. It appears as a red, swollen,
warm, hardened and painful rash, similar in consistency to an orange peel. More
severe infections can result in vesicles, bullae, and petechiae, with possible
skin necrosis. Lymph nodes may be swollen, and lymphedema may occur. Fat
tissue is most susceptible to infection, and facial areas typically around the eyes,
ears, and cheeks. Repeated infection of the extremities can lead to chronic
swelling.
ETIOLOGY
Most cases of erysipelas are due to Streptococcus pyogenes (also known as betahemolytic group A streptococci), although non-group A streptococci can also be
the causative agent. Historically, the face was most affected; today the legs are
affected most often.[3] The rash is due to an exotoxin, not the Strep. bacteria itself
and is found in areas where no bacteria are present - e.g. the infection may be in
the nasopharynx, but the rash is found usually on the face and arms. Erysipelas
infections can enter the skin through minor trauma, eczema, surgical incisions and
ulcers, and often originate from strep bacteria in the subject's own nasal
passages. Infection sets in after a small scratch or abrasion spreads resulting in
toxaemia. Erysipelas does not affect subcutaneous tissue. It does not release pus,
only serum or serous fluid. Subcutaneous edema may lead the physician to
misdiagnose it as cellulitis, but the style of the rash is much more well
circumscribed and sharply marginated than the rash of cellulitis.
TREATMENT
Depending on the severity, treatment involves either oral or intravenous
antibiotics, using penicillins, clindamycin or erythromycin. While illness symptoms
resolve in a day or two, the skin may take weeks to return to normal.
156. Meningococcal infections: Neisseria meningitidis.

Meningococcal disease describes infections caused by the bacterium Neisseria

meningitidis (also termed meningococcus). It carries a high mortality rate if
untreated. While best known as a cause of meningitis, widespread blood infection
(sepsis) is more damaging and dangerous. Meningitis and Meningococcemia are
major causes of illness, death, and disability in both developed and under
developed countries worldwide.
Neisseria meningitidis, often referred to as meningococcus, is a bacterium that
can cause meningitis[1] and other forms of meningococcal diseasesuch
as meningococcemia, a life threatening sepsis. N. meningitidis is a major cause of
morbidity and mortality during childhood in industrialized countries. it appears as
a Gram-negative diplococcus and cultures of the bacteria test positive for the
enzyme oxidase.
Meningococcus is spread through the exchange of saliva and other respiratory
secretions during activities like coughing, kissing, and chewing on toys. Though it
initially produces general symptoms like fatigue, it can rapidly progress from fever,
headache and neck stiffness to coma and death. The symptoms are easily
confused with those of meningitis caused by other organisms such as Hemophilus
influenzae and Streptococcus pneumoniae.[4] Death occurs in approximately 10%

58

of cases. Those with impaired immunity may be at particular risk of

meningococcus.

TREATMENT
Persons with confirmed N. meningitidis infection should be hospitalized
immediately for treatment with antibiotics ( Third-generation cephalosporin
antibiotics (i.e. cefotaxime, ceftriaxone) ).
157. Gonococcal infections: Neisseria gonorrhoeae - Gonorrhea.
Gonorrhea Gonorrhea is a common sexually transmitted infection caused by the
bacterium Neisseria gonorrhoeae. Gonorrhea is most frequently spread during
sexual contact. However, it can also be transmitted from the mother's genital tract
to the newborn during birth, causing ophthalmia neonatorum and systemic
neonatal infection. In women, the cervix is the most common site of gonorrhea,
resulting in endocervicitis and urethritis, which can be complicated by pelvic
inflammatory disease (PID). In men, gonorrhea causes anterior urethritis.
Neisseria gonorrhoeae is a species of Gram-negative coffee bean shaped
diplococci bacteria responsible for the sexually transmitted infection gonorrhea .
Symptoms of infection with N. gonorrhoeae differ depending on the site of
infection. Note also that 10% of infected males and 80% of infected females are
asymptomatic. The usual symptoms in men are burning with urination and penile
discharge. Women, on the other hand, are asymptomatic half the time or
have vaginal discharge and pelvic pain.
Infection of the genitals can result in a purulent (or pus-like) discharge from the
genitals which may be foul smelling. Symptoms may include inflammation,
redness, swelling, and dysuria.
N. gonorrhoeae can also
cause conjunctivitis, pharyngitis, proctitis or urethritis, prostatitis and orchitis.
If N. gonorrhoeae is resistant to the penicillin family of antibiotics,
then ceftriaxone (a third-generation cephalosporin) is often used. Sexual partners
should also be notified and treated.
In both men and women if gonorrhea is left untreated, it may spread locally
causingepididymitis or pelvic inflammatory disease or throughout the body,
affecting joints and heart valves. Half of women with gonorrhea
are asymptomatic while others have vaginal discharge, lower abdominal pain
or pain with intercourse. Most men who are infected have symptoms such
as urethritis associated with burning with urination and discharge from the penis.
One of the complication of gonorrhea is systemic dissemination resulting in
skin pustules or petechia, septic arthritis, meningitis orendocarditis.
158. Infections of childhood: Whooping cough (Bordetella pertussis)

59

Pertussis, also known as whooping cough s a highly contagious bacterial

disease caused by Bordetella pertussis.
SIGN AND SYM.
The classic signs of pertussis are a paroxysmal cough, inspiratory whoop,
and vomiting after coughing. The cough from pertussis has been documented to
cause subconjunctival hemorrhages, rib fractures, urinary incontinence, hernias,
post-cough fainting, and vertebral artery dissection. If there is vomiting after a
coughing spell or an inspiratory whooping sound on coughing, the likelihood that
the illness is pertussis is nearly doubled.
DIAGNOSIS
Methods used in laboratory diagnosis include culturing of nasopharyngeal swabs
on Bordet-Gengou medium, polymerase chain reaction(PCR), direct
immunofluorescence (DFA), and serological methods.
PREVENTATON
The primary method of prevention for pertussis is vaccination
Common complications of the disease include pneumonia, encephalopathy,
earache, or seizures.
159. Infections of childhood: Diphtheria.
Diphtheria is an upper respiratory tract illness caused by Corynebacterium
diphtheriae, a facultative anaerobic, Gram-positive bacterium.
It is characterized by sore throat, low fever, and an adherent membrane
(apseudomembrane) on the tonsils, pharynx, and/or nasal cavity. A milder form of
diphtheria can be restricted to the skin.
Less common consequences include myocarditis (about 20% of
cases) and peripheral neuropathy (about 10% of cases). t is a contagious disease
spread by direct physical contact or breathing the aerosolized secretions of
infected individuals.
SIGN AND SYM.
The symptoms of diphtheria usually begin two to seven days after infection.
Symptoms of diphtheria include fever of 38C or above, chills, fatigue, bluish skin
coloration, sore throat, hoarseness, cough, headache, difficulty swallowing, painful
swallowing, difficulty breathing, rapid breathing, foul-smelling bloodstained nasal
discharge and lymphadenopathy. Symptoms can also include cardiac arrhythmias,
myocarditis, and cranial and peripheral nerve palsies.
Clinical criteria

Upper respiratory tract illness with sore throat

Low-grade fever (>102F is rare)
An adherent pseudomembrane of the tonsil(s), pharynx, and/or nose.

TREATMENT
The disease may remain manageable, but in more severe cases, lymph nodes in
the neck may swell, and breathing and swallowing will be more difficult. Abnormal

60

cardiac rhythms can occur early in the course of the illness or weeks later, and can
lead to heart failure. Diphtheria can also cause paralysis in the eye, neck, throat,
or respiratory muscles.
160. Enteropathogenic Bacteria: E. coli enteric infections
E. coli is a gram-negative bacterium that can produce a bloody diarrhea due to
toxins it secretes when it infects human intestinal tracts.
The symptoms of E. coli infection may include a low fever, nausea,
vomiting, stomach cramps, and bloody diarrhea.
E. coli is notorious because it can cause additional complications in children and
the elderly; renal failure, anemia, and dehydration especially for children (termed
HUS or Hemolytic-uremic syndrome) and spontaneous bleeding, organ failures,
and mental changes in the elderly . Some of these patients develop disabilities or
die.
Diagnosis is definitively made when E. coli is isolated, usually from the patient's
stool, and identified as serotype 0157 by immunologic tests.
Most E. coli infections resolve spontaneously and require no treatment; however
supportive treatment is usually quickly required if the patient becomes dehydrated,
anemic, or develops HUS or TTP. The majority of E. coli infections have excellent
outcomes.
If complications develop such as severe dehydration, anemia, HUS or TTP, the
outcomes can decline from good to poor quickly. Prevention consists of eating well
cooked foods, especially hamburger, and drinking treated or pasteurized fluids.
Avoiding touching or eating any food that may be contaminated with any animal or
human waste will help prevent the infection. There is no E. coli vaccine available
for humans.
161. Enteropathogenic Bacteria: Salmonella infections - Salmonelosis.
Salmonella infection is a common bacterial disease that affects the intestinal tract.
Salmonella bacteria typically live in animal and human intestines and are shed
through feces. Humans become infected most frequently through contaminated
water or food sources.
Salmonellosis is an infection with Salmonella bacteria. Most people infected
with Salmonella develop diarrhea, fever, vomiting, andabdominal cramps 12 to 72
hours after infection.
There are different kinds of Salmonella, including S. bongori and S. enterica.
Symptoms are usuallygastrointestinal, including nausea, vomiting, abdominal
cramps and bloody diarrhea with mucus. Headache, fatigue and rose spots are
also possible.
treatment: intravenous fluids to treat the dehydration, and may be
given medications to providesymptomatic relief, such as fever reduction. In severe

61

cases, the Salmonella infection may spread from the intestines to

the blood stream, and then to other body sites, and can cause death unless the
person is treated promptly with antibiotics.
The bacterium induces responses in the animal it is infecting, and this is what
typically causes the symptoms, rather than any direct toxin produced. Symptoms
are usually gastrointestinal, including nausea, vomiting, abdominal cramps and
bloody diarrhea with mucus. Headache, fatigue and rose spots are also possible.
These symptoms can be severe, especially in young children and the elderly.
Symptoms last generally up to a week, and can appear 12 to 72 hours after
ingesting the bacterium.
162. Enteropathogenic Bacteria: Salmonella infections - Typhoid Fever.
Salmonella infection is a common bacterial disease that affects the intestinal tract.
Salmonella bacteria typically live in animal and human intestines and are shed
through feces. Humans become infected most frequently through contaminated
water or food sources.
Typhoid fever, also known as Typhoid,[1] is a common worldwide bacterial
disease, transmitted by the ingestion of food or water contaminated with
the feces of an infected person, which contain the bacterium Salmonella enterica,
serovar Typhi.[2][3] The bacteria then perforate through the intestinal wall and
are phagocytosed by macrophages.
After the ingestion of contaminated food or water, the Salmonella bacteria invade the small
intestine and enter the bloodstream temporarily. The bacteria are carried by white blood
cells in the liver, spleen, and bone marrow. The bacteria then multiply in the cells of these
organs and reenter the bloodstream. Patients develop symptoms, including fever, when the
organism reenters the bloodstream. Bacteria invade the gallbladder, biliary system, and the
lymphatic tissue of the bowel. Here, they multiply in high numbers. The bacteria pass into
the intestinal tract and can be identified for diagnosis in cultures from the stool tested in
the laboratory. Stool cultures are sensitive in the early and late stages of the disease but
often must be supplemented with blood cultures to make the definite diagnosis.

Symptoms: poor appetite;

abdominal pain;
headaches;
generalized aches and pains;
fever, often up to 104 F;
lethargy (usually only if untreated);
intestinal bleeding or perforation (after two to three weeks of the disease);
diarrhea or constipation.

163. Enteropathogenic Bacteria: Salmonella infections - Bacillary Dysentery.

Salmonella infection is a common bacterial disease that affects the intestinal tract.
Salmonella bacteria typically live in animal and human intestines and are shed
through feces. Humans become infected most frequently through contaminated
water or food sources.
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Bacillary dysentery is a type of dysentery, and is a severe form of shigellosis.

Bacillary dysentery is associated with species of bacteria from
the Enterobacteriaceae family. Shigellosis is caused by one of several types
of Shigella bacteria.
One characteristic of bacillary dysentery is blood in stool,[7] which is the result of
invasion of themucosa by the pathogen.
TREATMENT
Dysentery is initially managed by maintaining fluid intake using oral rehydration
therapy. If this treatment cannot be adequately maintained due to vomiting or the
profuseness of diarrhea, hospital admission may be required for intravenous fluid
replacement.
164. Cholera (Vibrio cholerae).
Cholera is an infection of the small intestine caused by the bacterium Vibrio
cholerae.
Transmission occurs primarily by drinking water or eating food that has been
contaminated by the feces of an infected person (even an asymptomatic one). The
severity of the diarrhea and vomiting can lead to
rapid dehydration and electrolyte imbalance, and death in some cases. The
primary treatment is with oral rehydration solution (ORS) to
replace water and electrolytes; if this is not tolerated or does not provide quick
enough treatment, intravenous fluids can also be used. Antibiotics are beneficial in
those with severe disease to shorten its duration and severity.
SIGN AND SYM
The primary symptoms of cholera are profuse, painless diarrhea and vomiting of
clear fluid. These symptoms usually start suddenly, one to five days after ingestion
of the bacteria. The diarrhea is frequently described as "rice water" in nature and
may have a fishy odor.
TREATMENT
cholera can be successfully treated with oral rehydration therapy (ORT), which is
highly effective, safe, and simple to administer. Antibiotic treatments for one to
three days shorten the course of the disease and reduce the severity of the
symptoms.
165. Clostridia: Tetanus.
Tetanus is a medical condition characterized by a prolonged contraction of skeletal muscle
fibers.
The primary symptoms are caused by tetanospasmin, a neurotoxin produced by the Grampositive, rod-shaped, obligate anaerobic bacterium Clostridium tetani.
Tetanus affects skeletal muscle.
C. tetani usually enters a host through a wound to the skin, then it replicates. Once
an infection is established, C. tetani produces two

63

exotoxins, tetanolysin and tetanospasmin. Eleven strains of C. tetani have been

identified, which differ primarily in flagellar antigens and in their ability to produce
tetanospasmin.
Tetanospasmin is a neurotoxin that causes the clinical manifestations of tetanus.
Tetanus toxin is generated in living bacteria, and is released when the
bacteria lyse, such as during spore germination or vegetative growth. A minimal
amount of spore germination and vegetative cell growth are required for toxin
production
166. Zoonotic Bacteria: Anthrax.
A zoonosis is any infectious disease that can be transmitted
fromanimals to humans or from humans to animals. The emergence of a pathogen
into a new host species is called disease invasion.
Anthrax is an acute disease caused by the bacterium Bacillus anthracis. Most
forms of the disease are lethal, and it affects both humans and other animals.
There are effective vaccines against anthrax, and some forms of the disease
respond well to antibiotic treatment.
SINGS AND SYM.
Respiratory infection in humans initially presents with cold or flu-like symptoms for
several days, followed by severe (and often fatal) respiratory collapse.
Gastrointestinal infection in humans is most often caused by eating anthraxinfected meat and is characterized by serious gastrointestinal difficulty, vomiting of
blood, severe diarrhea, acute inflammation of the intestinal tract, and loss of
appetite.
Cutaneous anthrax infection in humans shows up as a boil-like skin lesion that
eventually forms an ulcer with a black center . The black eschar often shows up as
a large, painless necrotic ulcer at the site of infection.
TREATMENT
Anthrax cannot be spread directly from person to person, but a person's clothing
and body may be contaminated with anthrax spores. Effective decontamination of
people can be accomplished by a thorough wash-down with antimicrobial effective
soap and water. Waste water should be treated with bleach or other anti-microbial
agent.
167. Zoonotic Bacteria: Plague.
A zoonosis is any infectious disease that can be transmitted
fromanimals to humans or from humans to animals. The emergence of a pathogen
into a new host species is called disease invasion.
Bubonic plague is a zoonotic disease, circulating mainly among small rodents
and their fleas,[1] and is one of three types of infections caused by Yersinia
pestis (formerly known as Pasteurella pestis), which belongs to the
family Enterobacteriaceae. Without treatment, the bubonic plague kills about two
out of three infected humans within 4 days.
SIGN AND SYM.
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The most infamous symptom of bubonic plague is an infection of the lymph glands
(lymphadenitis), which become swollen and painful and are known as buboes.
Acral gangrene: Gangrene of the extremities such as toes, fingers, lips and tip of
the nose.[5]

Chills
General ill feeling (malaise)
High fever
Muscle Cramps[6]
Seizures
Smooth, painful lymph gland swelling called a bubo, commonly found in the
groin, but may occur in the armpits or neck, most often at the site of the initial
infection (bite or scratch)
Pain may occur in the area before the swelling appears
Skin color changes to a pink hue in some extreme cases
Bleeding out of the cochlea will begin after 12 hours of infection

Other symptoms include heavy breathing, continuous blood vomiting, aching

limbs, coughing, and extreme pain.
TREATMENT
Several classes of antibiotics are effective in treating bubonic plague. These
include aminoglycosides such
as streptomycin and gentamicin,tetracyclines (especially doxycycline), and
the fluoroquinolone ciprofloxacin.
168. Hemorrhagic Fever.
The viral hemorrhagic fevers (VHFs) are a diverse group of animal and human
illnesses that are caused by four distinct families of RNA viruses: the
families Arenaviridae, Filoviridae, Bunyaviridae, and Flaviviridae. All types of VHF
are characterized by fever and bleeding disorders and all can progress to high
fever, shock and death in many cases.
ETIOLOGY:
The family Arenaviridae include the viruses responsible for Lassa
fever and Argentine, Bolivian, Brazilian and Venezuelan hemorrhagic fevers.

The family Bunyaviridae include the members of the Hantavirus genus that
cause hemorrhagic fever with renal syndrome (HFRS), theCrimean-Congo
hemorrhagic fever (CCHF) virus from the Nairovirus genus, and the Rift Valley
fever (RVF) virus from the Phlebovirusgenus.
The family Filoviridae include Ebola virus and Marburg virus.
Finally, the family Flaviviridae include dengue, yellow fever, and two viruses in
the tick-borne encephalitis group that cause VHF: Omsk hemorrhagic
fever virus and Kyasanur Forest disease virus

Signs and symptoms :

fever and bleeding diathesis. Manifestations of VHF often also include flushing of
the face and chest, petechiae, frank bleeding,edema, hypotension, and shock.
65

Malaise, myalgias, headache, vomiting, and diarrhea occur frequently. Definitive

diagnosis is usually made at a reference laboratory with
advancedbiocontainment capabilities.
clinical signs:
The findings of laboratory investigation vary somewhat between the viruses but in
general there is a decrease in the total white cell count particularly
the lymphocytes, a decrease in theplatelet count, an increase in
the serum liver enzymes and an increase in both the prothrombin (PT) and
activated partial thromboplastin times (PTT). The hematocrit may be elevated. The
serum urea and creatine may be raised but this is dependent on the hydration
status of the patient. The bleeding time tends to be prolonged.
treatment:
Medical management of VHF patients may require intensive supportive care.
Antiviral therapy with intravenous ribavirin may be useful in Bunyaviridae and
Arenaviridae infections . Prophylactic (preventive) ribavirin may be effective for
some bunyavirus and arenavirus infections.
169. Treponemes: Syphilis - Etiology, stages.
Syphilis is a sexually transmitted infection caused by
the spirochete bacterium Treponema pallidum subspecies pallidum. The primary
route of transmission is through sexual contact; however, it may also be
transmitted from mother to fetus during pregnancy or at birth, resulting
incongenital syphilis.
The signs and symptoms of syphilis vary depending in which of the four stages it
presents (primary, secondary, latent, and tertiary). The primary stage classically
presents with a single chancre (a firm, painless, non-itchy skin ulceration),
secondary syphilis with a diffuse rash which frequently involves the palms of the
hands and soles of the feet, latent syphilis with little to no symptoms, and tertiary
syphilis withgummas, neurological, or cardiac symptoms.
STAGES
Primary syphilis is typically acquired by direct sexual contact with the infectious
lesions of another person. Approximately three to 90 days after the initial exposure
(average 21 days) a skin lesion, called a chancre, appears at the point of contact.
This is classically a single, firm, painless, non-itchy skin ulceration with a clean
base and sharp borders. The lesion, however, may take on almost any form. In the
classic form, it evolves from a macule to a papule and finally to an erosion or ulcer.
Secondary syphilis occurs approximately four to ten weeks after the primary
infection. symptoms most commonly involve the skin, mucous membranes,
and lymph nodes. Other symptoms may include fever, sore throat, malaise, weight
loss, hair loss, and headache.
Latent syphilis is defined as having serologic proof of infection without symptoms
of disease. Early latent syphilis may have a relapse of symptoms. Late latent
syphilis is asymptomatic, and not as contagious as early latent syphilis.
Tertiary syphilis may occur approximately three to 15 years after the initial
66

infection, and may be divided into three different forms: gummatous syphilis,
late neurosyphilis and cardiovascular syphilis. Without treatment, a third of
infected people develop tertiary disease. People with tertiary syphilis are not
infectious.
Gummatous syphilis or late benign syphilis usually occurs one to 46 years after
the initial infection, with an average of 15 years. This stage is characterized by the
formation of chronic gummas, which are soft, tumor-like balls of inflammation
which may vary considerably in size. They typically affect the skin, bone, and liver,
but can occur anywhere.
Neurosyphilis refers to an infection involving the central nervous system. It may
occur early, being either asymptomatic or in the form of syphilitic meningitis, or late
as meningovascular syphilis, general paresis, or tabes dorsalis, which is
associated with poor balance and lightning pains in the lower extremities.
Cardiovascular syphilis usually occurs 1030 years after the initial infection. The
most common complication is syphilitic aortitis, which may result
in aneurysm formation
170. Acquired Primary Syphilis.
Primary syphilis is typically acquired by direct sexual contact with the infectious
lesions of another person. Approximately three to 90 days after the initial exposure
(average 21 days) a skin lesion, called a chancre, appears at the point of contact.
This is classically a single, firm, painless, non-itchy skin ulceration with a clean
base and sharp borders. The lesion, however, may take on almost any form. In the
classic form, it evolves from a macule to a papule and finally to an erosion or ulcer.
171. Secondary Syphilis.
Secondary syphilis occurs approximately four to ten weeks after the primary
infection.[4] While secondary disease is known for the many different ways it can
manifest, symptoms most commonly involve the skin, mucous membranes,
and lymph nodes.[9]
Symptoms
The most common symptom is a skin rash, which varies in appearance, yet
frequently involves the palms and soles. Lesions called mucous patches may be
seen in or on the mouth, vagina, or penis.
Moist, warty patches may develop on the genitalia or skin folds. These are called
condylomata lata.
During secondary syphilis, additional symptoms such as fever, general ill feeling,
loss of appetite, muscle aches, joint pain, enlarged lymph nodes, and hair loss may
occur.
Treatment
Antibiotics are used to treat syphilis. The antibiotic of choice is penicillin, yet
doxycycline may be used as an alternative in individuals with a penicillin allergy.
For treatment of syphilis during pregnancy, penicillin is the drug of choice
67

Possible Complications

The complications of syphilis are related to the development of the syndromes

associated with tertiary syphilis:
Cardiovascular complications (aortitis and aneurysms)
Destructive lesions of the skin and bones (gummas)
Neurosyphilis
In addition, untreated secondary syphilis during pregnancy may spread the disease
to the developing baby. This is called congenital syphilis.
172. Tertiary Syphilis.
In tertiary syphilis, the infection-causing organisms have continued to grow for
years. Pockets of damage, or lesions, affects various tissues such as the bones, skin,
nervous tissue, heart, and arteries. These areas are called gummas, and are very
destructive. Tertiary syphilis is less frequently seen today than in the past because
of early detection and adequate treatment.

Symptoms of tertiary syphilis depend on which organ systems have been affected.
They vary widely and are difficult to diagnose. In individuals with tertiary syphilis,
the primary and secondary stages of syphilis usually have been long forgotten.
Medical findings of aortic aneurysms and neurological problems require astute
diagnostic ability to link them to syphilis. Some of the symptomatic problems are
listed below.
Cardiovascular syphilis which affects the aorta and causes aneurysms or valve
disease
Central nervous system disorders (neurosyphilis)
Infiltrative tumors of skin, bones, or liver (gumma)
Treatment
The treatment of syphilis is determined by the length of time the person has been
infected.
Syphilis can be treated with antibiotics such as penicillin, G benzathine,
doxycycline, or tetracycline (for patients who are allergic to penicillin). Length of
treatment depends on the extent of the infection and factors such as the person's
overall health.
For treating syphilis during pregnancy, only penicillin is recommended.
173. Congenital Syphilis.
Congenital syphilis is syphilis present in utero and at birth, and occurs when a
child is born to a mother with secondary syphilis. Untreated syphilis results in a
high risk of a bad outcome of pregnancy, including mulberry molars in the fetus.
Syphilis can cause miscarriages,premature births, stillbirths, or death of newborn
babies. Some infants with congenital syphilis have symptoms at birth, but most
develop symptoms later. Untreated babies can have deformities, delays in

68

development, or seizures along with many other problems such as rash,

fever, hepatosplenomegaly, anemia, and jaundice. Sores on infected babies are
infectious. Rarely, the symptoms of syphilis go unseen in infants so that they
develop the symptoms of late-stage syphilis, including damage to their bones,
teeth, eyes, ears, and brain.
CLASSFCATON
EARLY
This is a subset of cases of congenital syphilis. Newborns may be asymptomatic
and are only identified on routine prenatal screening. If not identified and treated,
these newborns develop poor feeding and rhinorrhea. By definition, early
congenital syphilis occurs in children between 0 and 2 years old.[2] After, they can
develop late congenital syphilis.
LATE
Late congenital syphilis is a subset of cases of congenital syphilis. By definition, it
occurs in children at or greater than 2 years of age who acquired the infection
trans-placentally.
SIGN AND SYM
abnormal x-rays.

Hutchinson's triad, a set of symptoms consisting of deafness, Hutchinson's

teeth (centrally notched, widely-spaced peg-shaped upper central incisors),
and interstitial keratitis (IK), an inflammation of the cornea which can lead to
corneal scarring and potentially blindness.
mulberry molars (sixth year molars with multiple poorly developed cusps).
frontal bossing.
poorly developed maxillae.
enlarged liver.
enlarged spleen.
other skin rash.
sabre shins.
anemia.
lymph node enlargement.
jaundice.
pseudoparalysis.
snuffles, the name given to rhinitis in this situation. When chronic, this can
lead to saddle nose deformity.
rhagades, linear scars at the angles of the mouth and nose result from
bacterial infection of skin lesions.
Higoumenakis sign, enlargement of the sternal end of clavicle in late
congenital syphilis.

Death from congenital syphilis is usually through pulmonary hemorrhage.

TREATMENT
If a pregnant mother is identified as being infected with syphilis, treatment can
effectively prevent congenital syphilis from developing in the unborn child,
especially if she is treated before the sixteenth week of pregnancy. The child is at

69

greatest risk of contracting syphilis when the mother is in the early stages of
infection, but the disease can be passed at any point during pregnancy, even
during delivery (should the child have not contracted it already). However, a
woman in the secondary stage of syphilis decreases her child's risk of developing
congenital syphilis by 98% if she receives treatment before the last month of
pregnancy.[6] An afflicted child can be treated using antibiotics much like an adult,
however any developmental symptoms are likely to be permanent.
174. Mycobacteria: Tubercullosis- etiology. Pathogenesis, classification.
Tuberculosis (TB) is a chronic, progressive infection with a period of latency
following initial infection. It occurs most commonly in the lungs. Pulmonary
symptoms include productive cough, chest pain, and dyspnea. Diagnosis is most
often by sputum culture and smear. Treatment is with multiple antimicrobial drugs..
Etiology
TB properly refers only to disease caused by Mycobacterium tuberculosis. Similar
disease occasionally results from the closely related mycobacteria, M. bovis, M.
africanum, and M. microti.
TB results almost exclusively from inhalation of airborne particles (droplet nuclei)
containingM. tuberculosis. They disperse primarily through coughing, singing, and
other forced respiratory maneuvers by people who have active pulmonary TB and
whose sputum contains a significant number of organisms (typically enough to
render the smear positive). People with pulmonary cavitary lesions are especially
infectious. Droplet nuclei containing tubercle bacilli may remain suspended in
room air currents for several hours, increasing the chance of spread. However,
once these droplets land on a surface, it is difficult to resuspend the organisms
(eg, by sweeping the floor, shaking out bed linens) as respirable particles.
Transmission is enhanced by frequent or prolonged exposure to a patient who is
dispersing large numbers of tubercle bacilli in overcrowded, enclosed, poorly
ventilated spaces; thus, people living in poverty or in institutions are at particular
risk. Health care practitioners who have close contact with active cases have
increased risk. However, once effective treatment begins, cough rapidly
decreases, organisms are inactivated, and within weeks, TB is no longer
contagious.
Classification based on the pathogenesis of TB
Class 0
No exposure to TB; not infected.
No history of exposure, negative reaction to the tuberculin skin test.
Class 1
Exposure to TB; No evidence of infection.
History of exposure, negative reaction to a tuberculin skin test given at least 10
weeks after exposure.
Class 2
70

TB Infection; No TB disease.
Positive reaction to the tuberculin skin test, negative smears and cultures (if
done), no clinical or x-ray evidence of TB disease.
Class 3
Current TB disease.
Positive culture for M. Tuberculosis (if done), or a positive reaction to the
tuberculin skin test and clinical or x-ray evidence of current TB disease.
Class 4
Previous TB disease (not current).
Medical history of TB disease, or
Abnormal but stable x-ray findings for a person who has a positive reaction to
the tuberculin skin test, negative smears and cultures (if done), and no clinical
or x-ray evidence of current TB disease
Class 5
TB suspected.
Signs and symptoms of TB disease, but evaluation not complete.

175. Primary Tuberculosis.

primary tuberculosis n.
Tuberculosis caused by infection with tubercle bacilli andcharacterized
by the formation of a primary complex in the lungsconsisting of a small
peripheral pulmonary focus and hilar orparatracheal lymph node involve
ment; it may cavitate and healwith scarring or progress.
Except for the rare intestinal (bovine) tuberculosis and the even more
uncommon skin, oropharyngeal, and lymphoidal primary sites, the
lungsare the usual location of primary infections. As detailed earlier ,
the initial focus of primary infection is the Ghon complex, which
consists of
1. a parenchymal subpleural lesion, often just above or just
below the interlobar fissure between the upper and the lower
lobes, and
2. enlarged caseous lymph nodes draining the parenchymal
focus.
Primary TB can also present as a lower lobe pneumonia. The course
and fate of this initial infection is variable, but in most cases patients
are asymptomatic, and the lesions undergo fibrosis and calcification.
Exceptionally, particularly in infants and children or immunodeficient
adults, progressive spread with cavitation, tuberculous pneumonia, or
miliary tuberculosis may follow a primary infection.

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Tuberculosis Symptoms
You may not notice any symptoms of illness until the disease is quite advanced.
Even then the symptoms -- loss of weight, loss of energy, poor appetite, fever, a
productive cough, and night sweats -- might easily be blamed on another disease.

Only about 10% of people infected with M. tuberculosis ever develop

tuberculosis disease. Many of those who suffer TB do so in the first few years
following infection, but the bacillus may lie dormant in the body for decades.
Although most initial infections have no symptoms and people overcome them,
they may develop fever, dry cough, and abnormalities that may be seen on
a chest X-ray.
176. Secondary Tuberculosis.
The infection can become reactivated if the Mycobacteria are able to rupture the
tubercle and spread through the lungs. This reactivation typically happens to those
with a weakened or suppressed immune system.
Most cases of secondary pulmonary tuberculosis
represent reactivation of an old, possibly subclinical infection.
During primary infection, bacilli may disseminate, without producing
symptoms, and establish themselves in sites with high oxygen tension,
particularly the lung apices. Reactivation in such sites occurs in no more
than 5 to 10% of the cases of primary infection. Secondary
tuberculosis, however, tends to produce more damage to the lungs than
does primary tuberculosis
The subsequent course of the secondary lesions is variable. They either
may heal spontaneously, result in a fibrocalcific nodule (with therapy),
or progress along the many pathways, discussed next.
Tuberculosis Symptoms
You may not notice any symptoms of illness until the disease is quite advanced.
Even then the symptoms -- loss of weight, loss of energy, poor appetite, fever, a
productive cough, and night sweats -- might easily be blamed on another disease.

Only about 10% of people infected with M. tuberculosis ever develop

tuberculosis disease. Many of those who suffer TB do so in the first few years
following infection, but the bacillus may lie dormant in the body for decades.
177. Fungal Diseases -- Candidiasis, aspergilosis. Histoplasmosis.
Candidiasis is a fungal infection (mycosis) of any of the Candida species
(all yeasts), of which Candida albicans is the most common.
Candidiasis encompasses infections that range from superficial, such as oral
thrush and vaginitis, to systemic and potentially life-threatening diseases.
Superficial infections of skin and mucosal membranes by Candida causing
local inflammation and discomfort are common in many human populations. While
clearly attributable to the presence of the opportunistic pathogens of the
genus Candida, candidiasis describes a number of different disease syndromes
that often differ in their causes and outcomes

72

SINGS AND SYM.

Most candidial infections are treatable and result in minimal complications such as
redness, itching and discomfort, though complication may be severe or fatal if left
untreated in certain populations. In immunocompetent persons, candidiasis is
usually a very localized infection of the skin or mucosal membranes, including
the oral cavity (thrush), the pharynx or esophagus, the gastrointestinal tract,
the urinary bladder, or the genitalia (vagina, penis).
Candidiasis is a very common cause of vaginal irritation, or vaginitis, and can also
occur on the male genitals. In immunocompromisedpatients, Candida infections
can affect the esophagus with the potential of becoming systemic, causing a much
more serious condition, afungemia called candidemia
DIAGNOSIS
Diagnosis of a yeast infection is done either via microscopic examination or
culturing.
TREATMENT
In clinical settings, candidiasis is commonly treated with antimycotics
the antifungal drugs .
Aspergillosis is an infection or allergic response due to the Aspergillus fungus.
Symptoms of allergic bronchopulmonary aspergillosis may include:

Cough
Coughing up blood or brownish mucus plugs
Fever
General ill feeling (malaise)
Wheezing
Weight loss

Treatment: A fungus ball is usually not treated (with antifungal medicines) unless
there is bleeding into the lung tissue. In that case, surgery is needed. Invasive
aspergillosis is treated with several weeks of an antifungal drug called
voriconazole
If symptoms do occur, they may include: Fever and chills, Cough and chest
pain when breathing in, Joint pain, Mouth sores, Red skin bumps (erythema
nodosum), most often on the lower legs.
Histoplasmosis: is a disease caused by the fungus Histoplasma capsulatum. Symptoms
of this infection vary greatly, but the disease primarily affects the lungs. Occasionally,
other organs are affected; this is called disseminated histoplasmosis, and it can be fatal if
left untreated.
Histoplasmosis is common among AIDS patients because of their suppressed immunity. In
immunocompetent individuals, past infection results in partial protection against ill effects
if reinfected.

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TREATMENT
Most of the time, histoplasmosis clears up without treatment. Resting and taking
medication can control a fever.
178. Protozoa Diseases - Amebiasis.
Amebiasis is an infection of the intestines caused by the parasite Entamoeba
histolytica. Entamoeba histolytica can live in the large intestine (colon) without
causing disease. However, sometimes, it invades the colon wall, causing colitis,
acute dysentery, or long-term (chronic) diarrhea. The infection can also spread
through the blood to the liver and, rarely, to the lungs, brain, or other organs.
Risk factors for severe amebiasis include:

Alcoholism
Cancer
Malnutrition
Older or younger age
Pregnancy

Most people with this infection do not have symptoms. If symptoms occur, they are
seen 7 to 10 days after being exposed to the parasite.
Mild symptoms:

Abdominal cramps
Diarrhea
Fatigue
Excessive gas
Rectal pain while having a bowel movement (tenesmus)
Unintentional weight loss

Severe symptoms:

Abdominal tenderness
Bloody stools
Fever
Vomiting

Treatment depends on the severity of infection. Usually, metronidazole is given by

mouth for 10 days.
If you are vomiting, you may need to receive medications through a vein
(intravenously) until you can tolerate them by mouth. Antidiarrheal medications are
usually not prescribed because they can make the condition worse.
After treatment, the stool should be rechecked to make sure that the infection has
been cleared.
179. Blood and tissue protozoa: Malaria.

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Malaria is a mosquito-borne infectious disease of humans and other animals

caused by eukaryotic protists of the genus Plasmodium. The disease results from
the multiplication of Plasmodium parasites within red blood cells, causing
symptoms that typically include fever and headache, in severe cases progressing
to coma or death.
Symptoms of malaria include fever, shivering, arthralgia (joint
pain), vomiting, anemia (caused by hemolysis), jaundice, hemoglobinuria, retinal
damage,[15] and convulsions. The classic symptom of malaria is cyclical
occurrence of sudden coldness followed by rigor and then fever and sweating
lasting four to six hours.
MEDCATONS
Several drugs, most of which are also used for treatment of malaria, can be taken
preventively. Chloroquine may be used where the parasite is still
sensitive.[59] However due to resistance one of three
medications: mefloquine (Lariam), doxycycline (available generically), and the
combination of atovaquone and proguanil hydrochloride (Malarone) is frequently
needed.[59] Doxycycline and the atovaquone and proguanil combination are the
best tolerated with mefloquine associated with higher rates of neurological and
psychiatric symptoms.
180. Tapeworm: Echinococcosis.
Echinococcosis, which is often referred to as hydatid disease or echinococcal
disease, is a parasitic disease that affects both humans and other mammals, such
as sheep, dogs, rodents and horses.[1]
There are three different forms of echinococcosis found in humans, each of which
is caused by the larval stages of different species of the tapeworm of
genus Echinococcus.
The first of the three and also the most common form found in humans is cystic
echinococcosis (also known as unilocular echinococcosis), which is caused
by Echinococcus granulosus. The second is alveolar echinococcosis (also
known as alveolar colloid of the liver, alveolar hydatid disease, alveolococcosis,
multilocular echinococcosis, small fox tapeworm), which is caused
by Echinococcus multilocularis and the third is polycystic echinococcosis (also
known as human polycystic hydatid disease, neotropical echinococcosis), which is
caused by Echinococcus vogeli.
all disease-causing species of Echinococcus are transmitted to intermediate hosts
via the ingestion of eggs and are transmitted to definitive hosts by means of eating
infected, cyst-containing organs. The incubation period for all species
of Echinococcus can be months to years or even decades.[13] It largely depends
on the location of the cyst in the body and how fast the cyst is growing.
TREATMENT
surgical , sometimes surgical with chemotherapy ,

75