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Brian Assinment
Brian Assinment
Reg No Hsm221-0348/2019
a. Classification
Is divided into;
Genetic defect of beta cell function due to mutations in various enzymes e.g. Hepatocyte
nuclear transcription factor –HNF, glucokinase.
Gestational diabetes mellitus- about 4% pregnant women develop diabetes mellitus due to
metabolic changes during pregnancy.
b. Laboratory diagnosis
I. Urine testing – Urine is tested for presence of glucose and ketones.
Glucosuria:
Benedict’s quantitative tests detects any reducing substance in the urine and is not specific for
glucose.
Dipstick method based on enzyme coated paper strip which turns purple when dipped in urine
containing glucose.
II. Single blood sugar estimation – Method include O-toluidine, somogyl-Nelson and
glucose oxidase. Whole blood or plasma may be used but whole blood values are 15%
lower than plasma values. A grossly elevated single determination of plasma glucose
may be sufficient to make the diagnosis of diabetes.
Performed principally for patients with borderline fasting plasm glucose value (i.e. Between
100-140mm/dl)individuals with fasting value of plasma glucose higher than 126mm/dl and
2hr value after 75gm oral glucose higher than 200mg/dl are labelled as diabetes
N0.2
a) Aetiology
Congenital hypothyroidism:
Myxoedema:
b) Clinical features
Cretinism: These are features observed within a few weeks to months of birth. The baby;
Is slow to thrive
Feeds poorly
Experiences constipation
Has a scaly skin
Has a hoarse cry
Experiences bradycardia
c) Laboratory Findings
TSH test- detects even tiny amounts of TSH in the blood and is the most accurate
measure of thyroid activity available.
T4 test measures the actual amount of circulating thyroid hormone in the blood.
Thyroid autoantibody test- Tests for the presence of thyroid autoantibodies. Most people
with Hashimoto’s disease have those antibodies but people whose hypothyroidism is
caused by other conditions do not.
NO3
A. Clinical Presentation
i. Fever- Slight increase in temperature around the joint.
ii. Joint stiffness
iii. Painful if swelling, which can eventually result in fatigue
iv. Swollen joints
v. Joint deformities and contractures
B. Pathological features
i. Joint stiffness and deformities- Joints become fixed in place by thick hardened pannus
which also may course its displacement and deformities.
ii. Muscle dystrophy- Muscles adjacent to the joint atrophy from disuse and destruction.
iii. Development of pain nodules- Pain nodules over bony prominences may persist or
regress.
C. Complications
i. Osteoporosis
Rheumatoid arthritis itself, along with some medications used for treating rheumatoid
arthritis can increase your risk osteoporosis – a condition that weakens your bones and makes
them more prone to fracture.
These firm bumps of tissue most commonly form around pressure points, such as the elbows.
However these nodules can form anywhere in the body including the lungs.
People who have rheumatoid arthritis are much most likely to experience Sjogren’s
syndrome, a disorder that decreases the amount of moisture in your eyes and mouth.