Def
HyperthroidismClassification
Hypothroidism
Primary
Secondary
Etiology






Family predisposition
Female sex
Stress
Infection
Toxic multinodular goiter
Secondary-TSH producing
adenoma




AutoimmuneReduced intake of iodine
Infections
Total or partial resection
of gland
 Drugs- amiodarone,
interferon alpha
 Idiopathic
Predisposition
Female sex, family predis, endemic
region with lack pf iodide
Symptoms
 Rapid weight loss
 Sweating
 Increased HR with
premature beads or
arrythmia
 Systolic arterial hypertension
 Weakness
 Fatigue
 Easy tiredness
 Sexual impotence in menloss of hair
 Menstrual disturbances
 In some cases secondary
diabetes mellitus
 Fatigue
 Exhausation
 Weight gain
 Bradycardia
 Amenorrhea
 Decreased libido
 Coarse voice
 Bradycardia
Physical exam
 Reduced weight
 Muscle waste and
decreased muscle
strength
 Possible subfebrile
temp
 + signs of Grefe
 Bilateral
exophthalmos with
hyperthyroid stare
 Thyroid gland is
enlarged with
tenderness during
palpitation








Hyperadrenocortismincreased synthesis of
cortisol due to hyperplasia
or tumours
Primary
 Hyperplasia or tumours
of the cortex of
suprarenal gland
Secondary
 Adenoma of the frontal
part of pituitary gland





Fatigue
Proximal muscle weakness
Weight gain often with
edema
Elevated systolic and
diastolic BP
Hyperacidity




Obesity
Loss of scalp hair,
axillary hair, pubic
hair
Macroglossia
Low HR and systolic
BP
Periorbital puffiness
Bradypsychia
Bradylalia- slowness
in speech
Edema
Obesity affecting
the body while the
limbs are thin
Moon shaped face
Buffalo hump
Purple striae over
abdomen, buttocks
Lab/instrumental
 Decreased cholesterol
and increased
triglycerides
 Slightly increased
glucose
 Increased FT3
 Decreased TSH and
TTH
 Ultrasound of thyroid
gland
 Low levels of calcium
in secondary, high in
primary
 ECG
 Increased cholesterol
and low blood glucose
 Increased TSH and
TTH
 Decreased FT3 and
FT4
 Ultrasound Fine needle aspiration
biopsy
 Secondary- MRI of
pituitary gland
 ECG bradycardia with
low QRS complexes
 increased blood sugar
and WBC
 decreased potassium
 possible elevated liver
enzymes
 Increased levels of
cortisol rhythm
Complication
Thyrotoxic crisis
Thyrotoxic
cardiomyopathy
Toxic hepatitis
Pericarditis
Ischemic Heart disease
Myxedema coma

Prolonged treatment with
corticosteroids (bronchial
asthma, connective tissue
and other types of
autoimmune)
Ectopic ACTH- due to
bronchial or other tumour
secreting similar ACTH
substances




Pain in bones due to
osteoporosis
Secondary diabetes mellitus
Menstrual irregularities
Decreased libido in men and
women
Primary
 Due to atrophy of the
cortex and the suprarenal
gland caused by
infections, autoimmune
disease, amyloidosis
Secondary
 Due to tumours or
postpartum ischemic
infarction of pituitary
gland









Excessive weakness
Easy tiredness
Vertigo
Drowsiness
Low bP
Orthostatism
Nausea
Abdominal pain
Loss of appetite and weight

Hypoadrenocortismdecreased synthesis of
secretion of corticosteroids




GOUT
Form of inflammatory
arthritis characterised by
recurrent attacks of a red,
tender, hot, swollen joint




Crystallisation of uric acidoccur because of genetic,
diet or decreased
excretion of urate
Diet- consumption of
alcohol, fructose
sweetened drink, meat
and seafood
PRPS- mutation
Medical condition= Gout
frequently occurs in
combo with other medial
problem, metabolic
syndrome, kidney








A red, hot, tender, swollen
joint
MTP joint at base of toe is
most often affected
Can affect ankle, knees ,
wrist and elbow
Fever
Fatigue
Malaise
Hyperuricemia
Limited range of motion



lower back, upper
thighs
acanthosis
nigricans-axilla

Hyperpigmentation
– face, breasts,
elbows, lines of the
palms and
gum(increased
secretion of
melanocyte
stimulation
hormone)
Reduced fat and
muscle tissue
Menstrual
disturbances
Obsese
Skin looks red and
shiny
Tophi may appear
around joints, pinna
of ear

















Acth is decreased
primary hypercortism
CT scan
PET scan and MRI
MRI
ECG with hypertrophy
of LV with ST-T
changes
Increased K+
Low sodium
Low BP glucose
Reduced level of
cortisol and
aldosterone with
increased ACTH
CT
MRI
Synovial fluid analysisBlood testhyperuricemia, blood
plasma level
>420micromols, 360 in
females
RF
ANA
Ultrasound- to detect
urate crystal in a joint
X-ray- joint X-ray can
be used in ruling out
other causes of joints
CT/MRI
Rheumatoid arthritis
failure,hemolytic
anaemia
 Medication- diuretics
 Obesity and diabetes= risk
factor
Cause is unknown, it is an
autoimmune disease-some genetic
and environmental factors


Etiology




Genetic predispositionfamily history of RA- HLADR1 and HLADR4
Environmental- Smoking,
silica exposure, infections
Obesity
F sex







Swollen, tender and warm
joints-MCPA, PIP, MTP
Joint stiffness-usually worse
in morning and after
inactivity
Rheumatoid nodule in skin
Fatigue
Fever
Local osteoporosis around
inflamed joints
Periodontitis and tooth loss
Pericarditis
Carpal tunnel syndrome





Persistent
symmetric
polyarthritis that
affects hands and
feet
Pain upon walking
Ulnar deviation
Buttonhole
deformity
Swan neck
deformity






RF is increased about
80% of people with RA
APCA
Antinuclear BBlood- sedimentation
rate, CRP, kidney
function
X-ray- decreased bone
density, bone erosion,
narrowing of joint
space
Ultrasound MRI
• Eyes = episcleritis or
scleritis. More
common is the indirect
effect of
keratoconjunctivitis
sicca, which is a
dryness of eyes and
mouth caused by
lymphocyte infiltration
of lacrimal and salivary
glands.
• Heart = endocarditis,
pericarditis, L ventricle
failure,
• Renal amyloidosis as
a consequence of
untreated chronic
inflammation
• Joint damage, joint
deformity]
DMARD
ANTIFLARES
Ankylosing spondylitis- type
of arthritis where there is
long term inflammation of
the joints of the spine.


Idiopathic
Combination of genetic
and environmental factors
>90 of those affecting
have HLA-B27









Chronic dull pain in the
lower back or gluteal region
Pain often severe at rest may
improve during physical
activity
Worse at nigh w morning
stiffness
Loss of spinal mobility
Loss of chest expansion w/a
limitation of ant. Flexion,
lat.flexion and extension of
lumbar spine
Fatigue
Fever
Malaise
Enthesitis- achilles
tendonitis, plantar fasciitis




Autoimmune connective
disorders
Systemic lupus
erythematosus
Environmental
tiggergenetic factor
immune system cant clear
effectively nuclear
antigen immune
response desposition in
tissues
SLE is presumably caused by
genetic susceptibility coupled w/an
environmental trigger which
results in defects in immune
system
One of the factors associated with
SLE is vit D def
Risk factors- smoking, direct
sunlight, F sex, black Asian and
ethnicity, medication











Systemic- low grade fever,
photosensitivity
Mouth and nose- ulcers
Face- butterfly rash
Fatigue
Loss of appetite
Joint pain- arthritis
Discord rash-scar
Pleuritis, pericarditis
Kidney disorder
Blood disorder-anemia
Neurological disorder




Schober testmeasure degree of
lumbar forward
flexion as the
patients bends over
as though touching
toes
Gaenslen testpatient supine, hip
joint is maximally
flexed on one side
and the opposite
hip is extended
Chin brown
measurement- AS
often have necks
that angle forward
sharply as the spine
stiffens
Chest expansioncompromised
Cyanosis(secondary
to resp compl)
Butterfly rash
Rash over body







CRP
Sedimentation rate
HLAB27 Ag test
Increase ESR
X-ray
MRI
Ultrasound


ANA test +
Blood workhematological
disorder- leukopenia,
lymphopenia
Urine serologyprotein in urine
MRI scan


Vertebral fractures