Revision PE 1

1. Diabetes Mellitus

Section 1
A. Criteria for 1. Fasting blood sugar ≥7.0 mmol/L
diagnosis of 2. Random blood sugar ≥ 11.1 mmol/L with classic hyperglyseamia symptoms
diabetes 3. 2hour oral glucose tolerance test ≥ 11.1 mmol/L
mellitus 4. HbA1c ≥ 6.3%
B. Pre-diabetes 1. Impaired oral glucose tolerance test which is 2hour glucose is 7.8-11
definition mmol/L
2. Impaired fasting glucose – 6.1-6.9 mmol/L

C. Impaired Defined as blood glucose is raised beyond normal levels, but not high enough
glucose to warrant a diabetes diagnosis. Prediabetes is the same as impaired glucose
tolerance intolerance (IGT) or impaired fasting glucose (IFG).
definition
Section 2
D. Classification of TYPE 1 TYPE 2 GESTATIONAL OTHER TYPES OF
diabetes DIABETES DIABETES MELLITUS
mellitus
E. Pathogenesis β-cell Insulin Diabetes 1.Diseases of
destruction resistance associated with exocrine pancreas.
1.Autoimmune pregnancy 2.Endocrine
-pancreatic disorders –
beta cells acromegaly,
destruction Cushing syndrome,
2.Idiopathic glucagonoma,
pheochromocytom
a ,Hyperthyroidism
3.Drug induced-
Corticosteroids
4.Genetic defect in
the β cells function
5.Infections
F. Age of incidence Age <20-years- Adult-onset 5-7% of all Genetic defect in
old. pregnancies. beta cell function:
Juvenile-onset Usually in second MODY (maturity
and third onset diabetes of
trimesters(less the young).
common in first Different forms of
trimester) autosomal
dominant inherited
diabetes mellitus
that manifest
before age of 25
years and are not
associated with
obesity or
autoantibodies
 Older adults
G. Risk factors Association 1. obesity 1. Recurrent 1.Infection
with 2.High waist- pregnancy loss (congenital rubella
autoimmune to-hip ratio 2.At least one infection)
condition like; (visceral fat birth of child 2.Genetic defects in
i. Hashimoto accumulation) diagnosed with insulin function
thyroiditis 3.Physical fetal macrosomia 3. Glucocorticoid
ii.Type A inactivity 3.Gestational therapy as in
gastritis 4.Hypertension diabetes in prior steroid diabetes
iii.Celiac 5.Dyslipidemia pregnancy 4.Rare
disease 6.History immunological
iv.Primary gestational diseases like stiff
adrenal diabetes person syndrome
insufficiency
Section 3
H. i) Classify the Effects of 1.Mothers are polyuria, polydipsia,
clinical Effects of hyperglycemia asymptomatic and polyphagia, weight
presentation of hyperglycemia may present with loss. Hyperglycemia
DM 1.Polyuria edema,warning include blurred
1.Polyuria signs include vision, lower
2.Polydipsia polyhydramnios,o extremity
2.Polydipsia r large-for- paresthesias, or
3.Polyphagia gestational age yeast infections,
3.Polyphagia infants (>90 th particularly
Benign percentile) balanitis in men
Weight loss, acanthosis
thin nigricans.
appearance is Hyperosmolar
typical for type Non-ketotic
1 diabetic Coma. Non-
patient. ketotic because
Diabetic type 2 DM
ketoacidosis there is still
residual insulin
which can still
suppress
lipolysis and
ketogenesis
ii) List and Kidney disease 1. Maternal; Diabetes
describe the (nephropathy) i.gestational dramatically
complications Heart disease. hypertension increases the risk of
under each class Stroke. Heart and ii.preeclampsia, various
in H i) High blood eclampsia, HELLP cardiovascular
blood vessel
pressure. syndrome,UTI. problems, including
disease.Nerve
Nerve disease 2. Fetal; coronary artery
damage
(neuropathy) i.diabetic disease with chest
Foot problems, (neuropathy) in fetopathy pain (angina), heart
including limbs.Other attack, stroke and
ulcers. nerve narrowing of
Eye disease damage.Kidney arteries
(retinopathy) disease.Eye (atherosclerosis).
 Skin infections. damage.Skin Nerve damage
conditions.Slo (neuropathy): One
w of the most
healing.Hearin common diabetes
g impairment. complications,
nerve damage can
cause numbness
and pain. Nerve
damage most often
affects the feet and
legs but can also
affect your
digestion, blood
vessels, and heart.

2. Arthritis

Section 1
A. Classification Autoimmune Infective/septic Degenerativ Gout
of arthritis e
B. State the Rheumatoid Septic arthritis Osteoarthri 1.Uric acid
most arthritis tis (gouty
common arthritis)
cause/type
2.Calcium
pyrophosph
ate
deposition
C. Describe the Hematogenous 1.Aging - An
pathogenesis 1.Autoimmune spread (most 2.Mechanic inflammator
pathogenesis reaction triggered common) al stresses y crystal
by -From a distant on the joint arthropathy
unknown antigen > site (e.g., 3.Genetic – that is
> activation of T abscesses, link to caused by
lymphocytes wound chromosom the
 infection, es 2 and 11 precipitation
2. Genetic septicemia) 4.Bone and
susceptibility gene -Disseminated density deposition
in class II infection (e.g., 5.Deficient of uric acid
HLA locus > gonorrhea) estrogen crystals in
activation of T cells Direct synovial
contamination Changes in fluid and
3. Cytokines -Iatrogenic (e.g., composition tissues.
released by T joint injection, and It is typically
lymphocytes(IL1 arthrocentesis , mechanical associated
and TNF) arthroscopy ) properties with
stimulates synovial -Trauma (e.g., of the hyperuricem
cells open wounds cartilage ia, but can
proliferation and around the joint, also occur if
activate penetrating 1.Increased uric acid
inflammatory trauma) in water levels are
mediators Contiguous content normal.
a. further spread (e.g.,
inflammation > septic bursitis, 2.Decreased
cartilage osteomyelitis) in
destruction proteoglyca
b. RANKL which n
will activate
osteoclasts to 3.Decreased
further destroy the of type II
bone > erosion of collagen
the subchondral >weakening
bone of the
c.Inflammatory collagen
cells infiltration
and cytokines > 4.Increased
synovial collagen
hyperplasia> breakdown
pannus formation
5.Increased
apoptosis>
reduced
number of
chondrocyte
s.

1.Weakenin
g of the
cartilage.
2.Attempt
to repair
3.Stimulatio
n of the
chrondrocyt
es at the
deeperblaye
 r to
proliferate
4.To
produce
proteoglyca
ns and new
collagen
5.Failure of
repair

6. Then,
Fibrillation ,
cracking and
softening of
the cartilage
> Sloughing
of full
thickness of
cartilage
>Exposure
of the
subchondral
bone >
Sclerosis of
the
underlying
bone +
Tendency of
small bone
fractures +
Cysts
formation +
Osteophytes
formation

(Mild
chronic
inflammatio
n)
D. Age of > 65 years.♀ > ♂ -Septic arthritis Increases Sex: ♀ < ♂
incidence is increasingly with age Peak
common among incidence:
persons older 30–60 years
than 65 years
especially
immunosuppres
sed individuals.
E. Risk factors / Risk factors -Prosthetic Modifiable 1.Family
for septic include: implant risk factors history of
arthritis the 1.Genetic -Interventions -Obesity gout
common disposition: (e.g., intra- -Excessive 2.Heavy
 organisms associated with articular joint loading drinking
and the HLA-DR4 and HLA- injections) or overuse
source of DR1 -Underlying joint (mechanical
infection 2.Environmental disease, stress)
factors (e.g., especially Nonmodifia
smoking) rheumatoid ble risk
3.Hormonal factors arthritis factors
(premenopausal - -Age (> 55
women are at the Immunosuppres years)
highest risk, sed state -Family
suggesting a -Diabetes history
predisposing role mellitus -History of
of female sex -Age > 80 years joint injury
hormones) -Chronic skin or trauma
4.Infection infections -Anatomic
5.Obesity -IV drug us factors
6.Family history of causing
RA -Staphylococcus asymmetric
aureus al joint
-Idiopathic Most common stress
inflammatory in adults and -Hemophilic
autoimmune children > 2 hemarthros
disorder of years es and
unknown etiology Frequently deposition
found in diseases
patients with that stiffen
arthritis cartilage
following -Sex
invasive joint
procedures

-K. kingae: most

common in
infants and
children ≤ 2
years
-Streptococci
-N. gonorrheae
-Gram-negative
rods esp. E. coli
and P.
aeruginosa

-S. epidermidis
-H. influenzae
-M. tuberculosis
and atypical
mycobacteria
-B. burgdorferi
(Lyme disease
F. List the 1. Morning
 American stiffness of more
rheumatolog than 1 hour most
y diagnostic mornings for at
criterias forleast 6 weeks.
rheumatoid 2. Arthritis and
arthritis soft-tissue swelling
of more than 3 of
14 joints or joint
groups,present for
at least 6 weeks.
3.Arthritis of hand
joints,present for
at least 6 weeks.
4.Symmetric
arthritis,present
for at least 6
weeks.
5.Subcutaneous
nodules
6.Rheumatoid
factor at a level
above 95th
percentile
7.Radiological
changes suggestive
of joint erosion
Section 2
G. What is A pannus is a
pannus and membrane of
describe the granulation tissue
process of composed of
development mesenchyme- and
of pannus bone marrow-
derived cells.
Formation of the
pannus stimulates
the release of IL-1,
platelet-derived
growth factor,
prostaglandins,
and substance P by
macrophages,
which ultimately
cause cartilage
destruction and
bone erosion.
Pannus formation
occurs in these
steps;
1. In a healthy
joint, the smooth
synovium is just a
few cells thick. The
synovium
produces synovial
fluid, which
lubricates and
nourishes a joint.
2. Rheumatoid
arthritis causes
white blood cells
to attack healthy
synovium. This
attack is the start
of inflammation.
3. The white blood
cells release
chemicals
(cytokines) that
prompt the
synovium’s blood
vessels to multiply
(hypervascularizati
on). As blood
vessels multiply,
blood flow
increases.
4. The increased
blood flow
encourages
synovium’s cells to
multiply. As more
cells are produced,
the synovium
thickens.
5. Microscopic,
finger-like
projections grow
on the normally
smooth surface of
the synovium.
These projections,
called villi, make
pannus tissue
rough and uneven.
6. The thickening
synovium requires
space and invades
the space in
between a joint’s
bones. It spreads
over the surface of
 the bones and
their protective
layer of articular
cartilage. It also
pushes out at the
edges of the joint,
making it look
swollen. The
development of
pannus can cause
joint damage and
symptoms such as
inflammation,
pain, and swelling.
H. What is -Rheumatoid
rheumatoid nodules are firm
nodule lumps that appear
under the skin in
up to 20% of
patients with RA.
They usually occur
overexposed joints
that are subject to
trauma, such as
the finger joints
and elbows.
- Rheumatoid
nodules: central
fibrinoid necrosis
with palisading
histiocytes
(epithelioid cells)

3. Prostate disease

Prostatic Carcinoma of prostate

hyperplasia
Benign/Malignant Benign Malignant
Pathogenesis Is benign glandular Prostate cancer is marked by an uncontrolled
and stromal (malignant) growth of cells in the prostate gland.
hyperplasia of the Prostate cancer develops when the rates of cell
transitional zone of division exceed those of cell death, leading to
the prostate. uncontrolled tumor growth.
Clinical features Irritative -Fatigue
symptoms -Loss of appetite
-Urinary frequency -Weight loss
-Urinary urgency -Urinary retention
and urge -Hematuria
incontinence -Incontinence
-Nocturia -Hydronephrosis (associated with flank pain and renal
-Occasionally failure
dysuria -Bone pain (due to bone metastasis, especially in the
Obstructive lumbosacral spine)
symptoms -Neurological deficits (due to spinal cord
-Hesitancy compression)
-Straining to -Lymphedema (caused by obstructing metastases in
urinate the lymph nodes) leading to:
-Poor and/or Swelling
intermittent Pain
stream (not Rednes
continuous)
-Prolonged
terminal dribbling
-Sensation of
incomplete voiding
-Acute urinary
retention
Additional
symptoms: gross
hematuria
Digital rectal
examination (DRE)
findings:
symmetrically
enlarged, smooth
(no nodules), firm,
nontender prostate
with rubbery or
elastic texture

Morphology -Most common localization: peripheral zone

(microscopic) -Differentiated (posterior lobe) of prostate.
 prostatic cells -Most common type: adenocarcinoma expressing PSA
- Possible corpora
amylacea

Method of metastasis -prostate cancer metastasis occurs most often in the

lymph nodes and the bones.
Prostate cancer metastasis occurs when cells break
away from the tumor in the prostate. The cancer cells
can travel through the lymphatic system or the
bloodstream to other areas of the body.

Tumour markers -Prostate-specific antigen (PSA)

Grading system
(Describe)