Early
Intermediate
Late
Terminal

Early wound healing events

Hemostasis
Platelet aggregation
Intrinsic and extrinsic coagulation cascade
Thrombin, fibrin
Vasoconstriction

Inflammation
Vasodilatation
Increase in vascular permeability
Chemotaxis
Cellular response

Intermediate wound healing events

Mesenchymal cell chemotaxis and proliferation
Angiogenesis
Epithelisation
2-4 days after injury
Mediated by cytokines

Fibroblasts- migration and proliferation
Smooth muscle

Angiogenesis- reconstruction of vasculature
Stimulate: High lactate, acidic Ph, low O2 tension
Endothelial cell migration and proliferation

Epithelisation
Partial thickness- Cells derived from wound edges and epithelial appendages.
Incisional wound: cellular migration over less then 1 mm. Wound sealed in 24-48h.

Cellular detachment
Migration
Proliferartion
differentiation

Late wound healing events

Collagen synthesis
3 helical polypeptide chains
Lysine and proline hydroxylation
Required for cross-linking

Wound contraction

Centripetal movement of the wound edges toward the center. ( 0.6-0.7 mm/day)
Begins at 4-5 days
Maximal contraction 12-15 days
Trivial component in closed incisional wounds, significant for closure of open wounds
Rate- depends on tissue
Circular wounds- slower closure but avoid stenosis

Mechanism- cell mediated processes, not requiring collagen synthesis
Myofibroblasts- fibroblasts with myofilaments in cytoplasm
Appear in wound day 3-21
Located in periphery- pull wound edges together.
Contractures- contraction across joint surface

Terminal wound healing events

Remodeling- turnover of collagen. Type 3 replaced by type 1
Day 21- net accumulation of wound collagen becomes stable
Wound bursting strength- 15% of normal.
Week 3-6- greatest rate of increase
6 weeks- 80-90% of eventual strength.
6 months maximum strength ( 90% ). Process continues for 12 months

Cytokines and growth factors

Primary mediators in wound healing.
Endo, para, auto, intracrine function
EGF
FGF
PDGF
TGF

Which of the following is primarily responsible for tensile strength in a healing wound 4 days after injury?

Collagen
Elastin
Fibrin
Fibronectin
Hyaluronic acid

Which of the following is primarily responsible for tensile strength in a healing wound 6 weeks after injury?

Myofibroblasts
Fibrin
Fibronectin
Collagen
Collagen cross linking

Infection
foreign body/ necrotic tissue, hematomas
local/ systemic factors
type of surgery

Hypoxia and smoking
O2 delivery necessary for cellular respiration and hydroxylation of proline and lysine
Smoking- vasoconstriction, atherosclerosis, carboxyhemoglobin.

Radiation
Collagen synthesized to abnormal degree- fibrosis
Fibrosis of vessels- (media)-occlusion
Thinned epidermis, pigmentation
Limited access of inflammatory cells and cytokines- impaired healing
Damage to fibrocytes and keratinocytes.

Systemic factors

Malnutrition
Limited AA supply for collagen synthesis
Consumption of proteins d/t CHD and fat deficiency.
Vit C deficiency- diminished hydroxylation of lysine and proline,
Vit D- impaired bone healing
Zinc- inhibition in cellular proliferation and defficient granulation tissur formation

Normal healing is accelerated by which of the following?
VitC
VitA
Zinc
Increased local oxygen tension
Scarlet red

Cancer
Cachexia, anorexia
Altered host metabolism.
Protein catabolism
Abnormal inflammatory cell response

Old Age

Diabetes
Impaired healing ( decreased chemotaxis and phagocyte function )
Risk of infection

Hypertrophic scars and kelloids

Excessive healing processes- increase in net collagen synthesis raised thickened scar
Keloid- Extension beyond wound margin, familial, may develop up to 1 year, rarely subside
Hypertrophic scar- Confined to wound margin, light skinned, early after injury, may subside, cause contractures
Tx- excision, steroid injection, pressure garments, radiation tx

Types of wound closure
Primary closure
Approximation of acutely disrupted tissue with sutures, staples or tape
Secondary wound closure
Open wound margins approximate by biologic contraction

If a patient requires reoperation 1 month after a midline abdominal incision which of the following promotes the most rapid gain in strength of the new incision
Separate transverse incision
Midline scar is excised with a 1 cm margin
Midline incision reopended without scar excision
Rate of strength ganed is not effected by incision technique

• The setting: requirements
• Privacy
• Comfortable surroundings
• An appropriate setting arrangement

Factors which influence doctor-patient communication

• Patient-related factors (patient’s feel at that time)
• Physical symptoms
• Psychological factors related to illness and/or medical care (e.g. anxiety., depression, anger, denial)
• Previous experience of medical care
• Current experience of medical care

Factors which influence doctor-patient communication

• Doctor-related factors
• Training in communication skills
• Self-confidence in ability to communicate’personality
• Physical factors (e.g. Tirdeness)
• Psychological factors (e.g. Anxiety)

Factors which influence doctor-patient communication

• Others
• The patient’s beliefs about health and illness
• The problem they wish to discuss
• Their expectation of the doctor will do (often based on previous experience)
• How they perceive the doctor

The setting of the inteview

• In each case every effort should be made to provide a setting that facilitates communication
• Privacy is essencial
• Try to avoid interruptions and make sure that the lighting and temperature are as comfortable as possible
• The arrangements of the seat
• There are 3 possible setting (see pictures)
• Try to drag a chair when we’re having consultation with the patient is on the bed. This would create the same “level”, so the patient wont feel threatened

Guideline for conducting an interview

• Beginning the interview
• Greet the patient by name and shake hands, if it seems appropriate
• Ask the patient to sit down
• Introduce yourself
• Explain the purpose of the interview
• Say how much time is available
• Explain the need to take the notes and ask if this is acceptable

The main part of the interview

• Maintain a positive atmosphere, warm manner, good eye contact
• Use open question at the beginning
• Listen carefully
• Be alert and responsive to verbal and non ferbal cues
• Facilitate the patient, both verbally and non-verbally
• Use spesific questions when appropriate
• Calrify what the patient has told you
• Encourage the patient to be relevant

Ending the interview

• Summaries what the patient has told you and ask if your summary is accurate
• Ask if the would like to add anything
• Thank the patient

What is it?
A disease in which bones become fragile and more likely to break.
Breaks usually occur in the hip, spine and wrist

What causes osteoporosis?
Scientist have not yet learned all the reasons this occurs.
When you are young your body makes new bone faster than it breaks down old bones.
As you get older, this process slows down and you start losing bone density.
The risk for osteoporosis depends on how much bone mass you attained between ages 25 and 35 and how fast you lose it.

Risk Factors
Anorexia nervosa or bulimia
Diet low in calcium
Use of certain medications
Low testosterone levels in men
An inactive lifestyle
Cigarette smoking
Excessive use of alcohol
Being Asian or Caucasian

Bone Health
Bones are living tissue, they provide structural support, protect vital organs and store calcium.
Until age 30, we store and build bone effectively.
As part of the aging process, bones begin to break down faster than they are formed.
Accelerates after menopause. Estrogen is the hormone that protects against bone loss.

Bone Mass Density
The National Osteoporosis Foundation
Recommends you have a BDT if:
You use medications that cause osteoporosis
You have type I diabetes, liver disease, kidney disease or a family history
You experience early menopause
You’re postmenopausal over 50 and have at least one risk factor.
You’re postmenopausal over 65 and never had a test.

Calcium
Is needed for heart muscles, and nerves to function properly.
Inadequate amounts contribute to osteoporosis.
Appropriate calcium intake falls between 1000 and 1300 mg a day

How to get enough Calcium every day!
Follow the Food Guide Pyramid
for Dietary Calcium Sources
Dairy- low fat yogurt, skim milk, cheese, chocolate pudding, ice milk, ice cream or frozen yogurt.
Protein- tofu, sardines, salmon
Vegetables- turnip greens, Bok Choy, Broccoli, collard greens
Other foods: vegetable lasagna, cheese enchilada, cheese pizza, calcium fortified orange juice.

Exercise
Exercising regularly in childhood and adolescence can ensure that you will reach peak bone density.
Need to participate in weight bearing exercise. For example, walking, dancing, jogging, stair climbing, racquet sports and hiking.

Medications
There is no cure, but several medications have been approved.
Each stops or slows bone loss, increases bone density, and reduces fracture risk.
Estrogen Replacement,
Alendronate,raloxitene and risedronate are prescribed to prevent and treat the disease.

Bone-Building Checklist
Maintain a calcium rich diet.
Get plenty of vitamin D
Engage in weight-bearing exercise
Don’t smoke and limit alcohol intake
Consider Hormone Replacement or other medications if you are at risk.

WHAT IS A BAD NEWS..??
Why is it difficult to give bad news??

may feel responsible and fears being blamed
not knowing how best to do it
possible inhibition
reluctance to change the exiting doctor-patient relationship
Fear of upsetting the patient’s exiting family roles

Not knowing the patient their resources and limitations
Fear of the implications for the patient
Fear of the patient’s emotional reaction
Uncertainty as to what may happen next
Lack of clarity about own role as a health-care provider

Options for managing difficult situations

To whom should bad news be given?
Who should give bad news?
When should bad news be given?
Should you give hope and reassurance along with bad news?

How to give bad news
There are five main consideration:
Personal preparation
The physical setting
Talking to the patient and responding to their concerns
Arranging follow-up or referral
Feedback and handover to professional colleagues

Dengue fever is an acute mosquito-borne infection caused by the dengue viruses. This is found in tropical and sub-tropical regions around the world. For instance, dengue fever is an endemic illness in many countries in South East Asia. The dengue viruses encompass four different stereotypes, each of which can lead to dengue fever and dengue hemorrhagic fever.

Clinical features

Dengue fever is clinically characterized by sudden onset of high fever, severe headache, pain behind the eyes, muscle and joint pains, anorexia, nausea and rash. Young children may exhibit a milder non-specific febrile illness with rash.

Dengue hemorrhagic fever is a severe and potentially fatal complication of dengue fever. Initially, the features include high fever, which lasts two to seven days and can be as high as 40-41 oC, facial flush and other non-specific constitutional symptoms of dengue fever. Later, it may be followed by the manifestation of bleeding tendency such as skin bruises, nose or gum bleeding, and possibly internal bleeding. In severe cases, it may progress to circulatory failure, shock and die.

Immunity is gained against that stereotype after recovery from its infection. However, no effective protection is conferred against subsequent infection by the other three stereotypes.

Mode of transmission

Dengue fever is transmitted to humans through by the bites of female Aedes mosquitoes which are infected with a dengue virus. It cannot be spread directly from human to human. In Hong Kong, the principal vector Aedes aegypti is not found, but the prevailing species Aedes albopictus can also spread the disease.

Incubation period

The incubation period ranges from 3 to 14 days, commonly 4 to 7 days.

Management

There is no specific medication for dengue fever or dengue hemorrhagic fever. Dengue fever is mostly self-limiting. Symptomatic treatment is given to provide relief from fever and pain. Patients with dengue hemorrhagic fever should be treated promptly with supportive management. The mainstay of the treatment is to maintain the circulating fluid volume. With appropriate and timely treatment, mortality rate should be less than 1%.

Prevention

At present, no effective vaccine for dengue fever is available. Therefore, the best preventive measure is to eliminate pockets of stagnant water that serve as sites of mosquito breeding, and to avoid mosquito bites.

The hypertension in each of these dignoses is classified as:
Mild : Systolic > 140 mmHg and/or diastolic > 90 mmHg
Severe : Systolic > 160 mmHg and/or diastolic > 110 mmHg

The only cure for hypertension in pregnancy is delivery

Pathophysiology of Hypertension in Pregnancy
Normal : Arachdonic acid triggers two pathways:
1. Prostacycline: Decreases blood pressure via: decreased vasoconstriction, Increased uteroplacental blood flow
2. Thromboxane: Increases blood pressure via: increased vasoontriction, decreased uteroplacental blood flow

In Pregnancy-Hypertensive States
The balance is thought to be tipped toward the thromboxane pathway.
Hypertension related deaths in pregnancy account for 15% of maternal deaths
Chronic hypertension and pregnancy
If during pregnandy a chronic hypertensive patient’s systolic blood pressure rises by 30 mmHg or diastolic rises by 15 mmHg, it is pregnancy induced hypertension superimposed on chronic hypertension.
Management
Mild : Early and serial ultrasounds, biophysicals
Severe : serial ultrasounds and biophysicals, antihypertensives (methyldopa/nifedipine)

PREGNANCY INDUCED HYPERTENSION
Defined as hypertension during pregnancy in a previously normotensive woman (the patient had normal blood pressure prio to 20 weeks gestation)

Subsets of pregnancy-induced hypertension
1. Pregnancy induced hypertension
2. Preeclampsia : renal involvement leads to proteinuria
3. Eclampsia : central nervous system involvement leads to seizures
4. HELLP Syndrome : the clinical picture is dominated by hematoloic and hepatic manifestations

Complication
• Heart failure
• Cerebral hemorrhage
• Placental abruption
• Fetal growth restriction
• Fetal death

Management

Mild : observe, bed rest
Severe : always hospitalize + antihypertensive pharmacotherapy (hydralazine or labetalol short term, nifedipine or methyldopa long term)
In pregnancy induced hypertension we must monitor for intrauterine growth retardation and progression to superimposed preeclampsia

Severe Pregnancy induced hypertension usually occurs in the third trimester

Generally for all pregnancy-hypertensive states:
If > 36 weeks/fetal lung maturity : Induce labor
If < 34 weeks/fetal lung immaturity : steroids plus expectant management
If fetal or maternal deterioration at any gestational age, induce labor

PREECLAMPSIA
Preeclampsia is pregnancy induced hypertension with proteinuria +/- pathological edema. It is classified as mild or severe
Preeclampsia rarely develops before 20 weeks and usually occurs in a first pregnancy
Preeclampsia is usually asymptomatic; itscrucial to pick up during routine prenatal visits

Criteria for mild preeclampsia
• Blood pressure : ? 140 systolic or ? 90 diastolic
• Proteinuria : 300 mg to 5 g/24 hrs ( normal : < 300 mg/24 hrs in pregnancy, < 150 mg/24 hrs in nonpregnant state)

Manifestations of severe disease
• Blood pressure : > 160 systolic or > 110 diastolic
• Proteinuria : 5 g/24 hrs
• Elevated serum creatinine
• Oliguria (< 500 ml/24 hrs)
• Symptoms suggesting end organ involvement (headache, visual disturbances, epigastric pain)
• Pulmonary edema
• Hepatocellular dysfunction
• Thrombocytopenia
• IUGR or oligohydramnions
• Microangiophatic hemolysis
• Grand mal seizures (eclampsia)

Predisopsing Factors
• Nulliparity
• Family history of preeclampsia-eclampsia
• Multiple fetuses
• Diabetes
• Chronic vascular disease
• Renal disease
• Hydatidiform mole
• Fetal hydrops

HELLP SYNDROME

Hellp syndrome is a manifestation of preeclampsia with hemolysis, elevated liver enzyms and low platelets. In contrast to typical presentations of preeclampsia, it is associated with :
• High morbidity
• Multiparous mothers
• Mothers older than 25
• Less than 36 weeks gestation
The prime objectives in severe cases are to forestall convulsions, prevent intracranial hemorrhage and serious damage to other vital organs, and deliver a healthy infant

Diagnosis of Preeclampsia

Once preeclampsia is suspected, the following tests should be done :
• Blood : Electrolytes, blood urea nitrogen (BUN), creatinine, liver function tests (LFTs) (ALT, AST), complete blood count (CBC), uric acid, and platelet count
• Urine : Sediment, 24 hour protein, 24 hour creatinine
• Fetal : ultrasound, nonstress test, biophysical profile

Management

Varies depending on severity of disease and gestational age of fetus:
Mild Preeclampsia
• Hospitalize, observe, bedrest, low-salt diet, monitor labs closely

Severe Preeclampsia

• Hospitalize, bed rest, low salt, low calories
• Antihypertensive pharmacotherapy: hydralazine or labetalol short term nifedipine or methyldopa long term
• Anticonvulsive theraphy : magnesium sulfate

Plus the following :
• If > 36 weeks/fetal lung maturity : induce labor
• If < 34 weeks/fetal llung immaturity : steroids plus expectant management
• If fetal or maternaldeterioration at any gestational age : induce labor
The only cure is delivery

ECLAMPSIA

Criteria : Mild or severe preeclampsia ; generalized seizures
25% of seizures are before labor, 50 % of seizures are during labor, 25% of seizures are post labor (maybe encountered up to 10 days post partum)

Management

1. Control of the convulsions (magnesium sulvate IV and IM). Magnesium toxicity is associated with loss of patellar reflexes. Treat with calcium gluconate 10% solution 1g iv
2. Correction of hypoxia and acidosis
3. Blood Pressure control (hydralazine or labetolol)
4. Delivery after control of convulsions

Antihypertensive agents used in pregnancy
Short term control : hydralazine , labetolol
Long term control : methyldopa, nifedipine, atenolol