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Disorder of Carbohydrate Metabolism-1
Disorder of Carbohydrate Metabolism-1
CARBOHYDRATE
METABOLISM
hyperglicemia hypoglicemia
Increased thirst
Increased urination
Weight loss in spite of increased appetite
Fatigue
Nausea and vomiting
Frequent infections including those of the
bladder, vagina, and skin
Blurred vision
Note: Usually there are no symptoms.
People (usually with type 1 diabetes) may
also present with diabetic ketoacidosis, a
state of metabolic dysregulation
characterized by the smell of acetone; a
rapid, deep breathing known as
Kussmaul breathing; nausea; vomiting and
abdominal pain; and an altered states of
consciousness.
A rarer but equally severe possibility is
hyperosmolar nonketotic state, which is more
common in type 2 diabetes and is mainly the result
of dehydration. Often, the patient has been drinking
extreme amounts of sugar-containing drinks, leading
to a vicious circle in regard to the water loss.
A number of skin rashes can occur in diabetes that
are collectively known as diabetic dermadromes.
Causes
Type 1 diabetes is also partly inherited and then
triggered by certain infections, with some
evidence pointing at Coxsackie B4 virus. There is
a genetic element in individual susceptibility to
some of these triggers which has been traced to
particular HLA genotypes (i.e., the genetic "self"
identifiers relied upon by the immune system).
However, even in those who have inherited the
susceptibility, type 1 diabetes mellitus seems to
require an environmental trigger.
Causes
The cause of diabetes depends on the
type. Type 2 diabetes is due primarily to
lifestyle factors and genetics.
Diagnosis
Diabetes mellitus is characterized by recurrent or persistent
hyperglycemia, and is diagnosed by demonstrating any one
of the following
Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL).
Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after
a 75 g oral glucose load as in a glucose tolerance test.
Symptoms of hyperglycemia and casual plasma glucose
≥ 11.1 mmol/L (200 mg/dL).
Glycated hemoglobin (Hb A1C) ≥ 6.5%
Glycosylated hemoglobin and Glucose tolerance test
Complications
Diabetes doubles the risk of vascular problems, including
cardiovascular disease.
Glycated hemoglobin is better than fasting glucose for
determining risks of cardiovascular disease and death
from any cause
The complications of diabetes mellitus are far less
common and less severe in people who have well-
controlled blood sugar levels.
Wider health problems accelerate the deleterious effects
of diabetes. These include smoking, elevated cholesterol
levels, obesity, high blood pressure, and lack of regular
exercise.
Complications of diabetes
mellitus
Acute
Complications of diabetes
mellitus
Diabetic ketoacidosis
Hyperglycemia hyperosmolar state
Hypoglycemia
Diabetic coma
Respiratory infections
Chronic
Complications of diabetes
mellitus
Angiopathy Chronic
elevation of blood
glucose level leads
to damage of blood
vessels
The endothelial
cells lining the
blood vessels take
in more glucose Fundus photo showing scatter laser
than normal, since surgery for diabetic retinopathy
they do not depend
on insulin.
Galactosemia
This is hereditary illness. In it’s base lies an
blockade of galactose metabolism. In organism
intermediate metabolits accumulate. There are two
the main forms of galactosemia on base of
transferase insufficiency and on base of
galactokinase insufficiency.
transferase insufficiency
galactokinase insufficiency
Glycogenoses
Simple carbohydrates deposit in
organism as polysaccharides. In muscles
and liver accumulates glycogen. It consist
of 4 % of liver weight and 2 % of muscles
weight. Muscles glycogen is used as of
ready fuel source for immediate
guaranteeing by energy. Liver without
interruption provides cerebrum and
erythrocytes with glucose .
Synthesis and splitting of glycogen are
exactly adjusted and coordinated
processes. Attached to immediate need in
glucose –cells of pancreas secret
glucagone. It activates adenylatcyclase of
hepatic cells. Adenilatcyclase stimulates
derivation of cAMP. Under action of cAMP
takes place activation of proteinkinase and
this enzyme raises activity
glycogenphosphorilase and oppresses
activity of glucogensynthase.
Glycogenosis type I – Girke’s
disease. Girke’s disease cause
deficit of glucose-6-phosphatase.
This enzyme provides 90 % of
glucose which disengages in liver
from glycogen.
It play central role in normal glucose
homeostasis. Glucose which
disengages attached to disintegration
of glycogen or is derivated in process
of gluconeogenesis obligatory goes
over stage of glucose-6-phosphate.
Enzyme glucose-6-phosphatase
tears away a phosphate group from
glucose. There free glucose is
formed it goes out in blood.
Attached to Girke’s disease stage of
Girke’s disease
tearing phosphate group is blocked.
There are no free glucose
hypoglycemia occur.
Hypoglycemia arises. Attached to
Girke’s disease glycogen is deponed
in liver and kidneys.
Type ІІ glycogenosis – Pompe’s disease.
Illness is related to deficit of lysosomal
enzyme – sour maltase, or -1,4-
glucosidase. This enzyme slits glycogene to
glucose in digestive vacuoles. Attached to
it’s deficit glycogen accumulates at first in
lysosomes and then in cytosole of
hepatocytes and myocytes.
Type ІІІ glycogenosis – Cori’s disease,
Forbs’ disease. This illness is named
limitdecstrinosis. In it’s base lies a deficit of
amylo-1,6-glucosidase. Degradation of
glycogen pauses in sites of branching.
Glycogen accumulates in liver and muscles.
Cure is diet with big proteins maintenance.
Type ІV glycogenosis – Anderson’s
disease. It is called by deficit of amilo-
1,4,1,6-transglucosidase (branching
enzyme). As result of this There is derivated
anomalous glycogen with very long
branches and rare points of branching. It is
not exposed to degradation and
accumulates in liver, heart, kidneys, spleen,
lymphatic nods, skeletal muscles. Glycogen storage disease II (Micro)
The myofibers are engorged with glycogen. On cross sections the myofibrils are pushed to the periphery.
Despite the thick walls, this is not hypertrophy. These patients present with congestive failure.
Type V glycogenosis – McArdel’s
disease. It’s cause is deficit of
phosphorilase of myocytes. Typical
pain displays in muscles after
physical loading. Glycogene does
not slit only in muscles. Here it
accumulates. In liver mobilization of
glycogen comes normal.
Type VІ glycogenosis – Hers’
disease. Illness arises as result of
insufficiency of hepatic
phosphorilase complex. Glycogen
accumulates in liver. Typical sign is
hepatomegalia.
Type VІІ glycogenosis. Illness
essence is in oppression of muscle
phosphofrutkinase. Symptoms are
similar to McArdles disease.