• Need to know the etiology
• Method of transmission

Etiological Agent: Treponema pallidum

Transmission: Sexual contact, or passed through the placenta after 4th month (miscarriage) or child born with syphillis

1st Stage of Syphillis

(Primary Stage)

Formation of a chancre; a small ulcer of the mucus membranes

Lasts 4-6 weeks, highly infectious

2nd Stage of Syphillis

(Secondary Stage)

Occurs several months after the chancre has healed; produces a systemic infection with fever, lymphadenopathy, skin rash, and shallow mucus membrane ulcerations

Persists for several weeks and may reoccur

3rd Stage of Syphillis

(Tertiary Stage)

Neissera gonnorhoeae

Transmission:  Sexual contact, can spread to neonate (gonococcal ophthalmia neonatorum)

Primarily infects mucosa of the cervix and urethra

Signs include profuse vaginal discharge; pain and burning on urination

May spread to the oviducts -> acute salpingitis, scar tissue, and infertility

Urethritis:

Signs are purulent urethral discharge, pain and burning on urination

Also can spread to the intenal reproductive organs -> scarring and infertility

Can infect the rectal mucosa -> purulent bloody mucoid discharge

Pharyngeal/tonsillar infection -> sore throat

Gets into blood system -> Goes systemic

Causes fever, joint pain, multiple small abscesses on the skin, can effedct tendons, heart valves, and meninges

Herpes simplex virus; 6 types: HSV-1, HSV-2, Cytomegalovirus, varicella-zoster virus, Epstein-Barr virus, HSV-6

Transmission:  Contact with broken herpes blister, passed to neonate when they pass through the vaginal canal, close person-to person contact, airborne droplets

Causes singles primarily in adults

Initial Symptom: pain and paresthesia of an affected dermatone, an area innervated by a single spinal nerve

Vesicular eruptions the occur along the region of the dermatone

Causes chicken pox primarily in children

Pruritic vessels appear on the face, trunk, and scalp then spread to the limbs

Spread by close person-to-person contact and airborne droplets

Primary lesions; formation of vesicles that rupture to ulcers

Virus will persist in the tissue and flare up periodically causing recurrent infections

Chlamydia trachomatis;

Now the most common sexually transmitted disease

Transmission:  Sexual Contact

Genital Chlamydial Infections

Treatment

Human Papillomavirus (HPV)

Results in Condylomata acuminate (genital warts)

1. HIV invades the helper T cells and the viral RNA is converted into DNA by viral reverse trascriptase and inserted in the host cell's genome
2. Virus proliferates in infected cells and sheds into the blood and body fluids
3. Progressive destruction of the T cells
4. Immune system collapse

Common Infections In AIDS

Viruses

Common infections in AIDS

Fungi

Common infection in AIDS

Protozoa

Common infections in AIDS

Bacteria

Relatively slow growth

Typicall remains localized

Possesses a fibrous capsule

Slow growth, expands, remains localized, well differentiated

Relatively rapid, disorganized growth

Aggressive localized invasion

Demonstrates metastasis

Rapid growth, infiltrates, metastasis by bloodstream and lymphatics, poorly differentiated

Ectodermal

Benign: Epithelioma

Malignant: Carcinoma

Ectodermal

Benign: Adenoma

Malignant: Adenocarcinoma

Ectodermal

Malignant melanoma

Ectodermal

Both types -> Glioma

May be named after specific cell type e.g. Astrocytoma

mesodermal and endodermal origin

Sarcoma

Benign: Lipoma

Malignant: Liposarcoma

mesodermal and endodermal origin

Sarcoma

Benign: Chondroma

Malignant: Chondosarcoma

mesodermal and endodermal origin

Sarcoma

Benign: Osteoma

Malignant: Osteosarcoma

mesodermal and endodermal

Sarcoma

Benign: Fibroma

Malignant: Fibrosarcoma

mesodermal and endodermal origin

Sarcoma

Benign: leiomyoma (commonly occurs in the uterus)

Malignant: Leiomyosarcoma

mesodermal and endodermal origin

Sarcoma

Benign: Rhabdomyoma

Malignant: Rhabdomyosarcoma

Will usually be malignant, rarely benign

Teratoma

All 3 origin tissues

ALWAYS BENIGN

Leukemia

Lymphoma (Hodgkin's disease, Non-Hodgkin's disease, Burkitt Lymphoma)

Hodgkin's Disease

Lymphoma

Non-Hodgkin's Disease

Lymphoma

Structural characteristics of tumor and tumor cells

6 different points

• Pleomorphism-  All look different
• Disorganization
• Biochemical changes- increased glycolysis regardless of oxygen availability; loss of specialized function
• Anaplasia- different growth, w/o growth, not normal growth
• Autonomy- Cells are social by chemical messengers, self-ruling
• Increased mitotic figures

Number of new cells

(minus)

Number of cells lost

Oncogenesis

(heredity)

Heredity appears to be a factor, not a direct cause.

There is an increased propensity for development of a particular cancer

Any chemical or physical environment agent that increases the frequency of mutation.

Not all are carcinogenic

Any substance that promotes the development of cancer.

All are mutagens.

Environmental Fators in Oncogenesis

Physical Factors

Environmnetal Factors in Oncogenesis

Polycyclic Hydrocarbons

Environmental Factors in Oncogenesis

Benzopyrene

Environmental Factors in Oncogenesis

Nitrosamines

Formed when nitrite ions react with amino acids in the body

Ascorbic acid inhibits nitrosamine formation

(lunch meats, salami, etc)

Environmental Facors in Oncogenesis

Inorganic Carcinogens

Environmental Factors in Oncogenesis

Alcohol

Clinical Manifestations of Cancer

8 different points

Clinical Manifestations of Cancer:

Tissue Destructions

Disruption of normal tissue and compression of blood vessels

Obstruction o duct or lumen of tubular organs

Clinical Manifestations of Cancer:

Infection

Clinical Manifestations of Cancer:

Pain

Clinical Manifestations of Cancer:

Fatigue

Clinical Manifestations of Cancer:

Cachexia

Clinical Manifestations of Cancer:

Hormonal Effects

Clinical Manifestations of Cancer:

Paraneoplastic syndromes

Treatment of Cancer

6 different points

Adult: 5 year survival rates

Pediatric:  Look at period of risk time determined by the age of the child at diagnosis +9 months of intrauterine time; up to approximately 16 years of age.

(ex. 5 yrs old '5+5+9mths=10 years and 9 months')

4 Major categories of how blood coagulation is disrupted:

Abnormalities of small blood vessels

4 major categories of how blood coagulation is disrupted:

Abnormalities of platelet function

4 major categories of how blood coagulation is disrupted:

Defieciency of one or more of the plasma coagulation factors

These deficiencies usually result in Hematomas.  Only 3 hereditary bleeding disorders occur with any frequency:

Hemophilia A

Hemophilia B

von Willebrand disease

4 major categories of blood coagulation disruption:

Liberation of thromboplastic material into circulation

Laboratory test to evaluate hemostasis (5):

Platelet Counts

Laboratory test to evaluate hemostasis (5):

Bleeding Time

Laboratory test to evaluate hemostasis (5):

Partial thromboplastin time

Laboratory test to evaluate hemostasis (5):

Prothrombin Time

Laboratory test to evaluate hemostasis (5):

Thrombin Time

• Slowing or stasis of blood flow
• Damage to the blood vessel wall
• An increase in the coagulability of the blood

Areas where thrombosis can occur:

Venous

Areas where thrombosis can occur:

Arterial

Areas where thrombosis can occur:

Intracardiac

• Elevated blood coagulation proteins
• Estrogen in hormonal birth control
• Heredity
• Cancer

Part of a thrombus that has broken free and is now ciculating within the cardiovascular system

Most emboli are thromboemboli, but other material can occasionally cause embolism

Types of Embolus (4):

Fat Embolism

Types of Embolus (4):

Amnionic Fluid Embolism

Types of Embolus (4):

Air Embolism

Types of Embolus (4):

Foreign Material Embolism

• Pump must be properly constructed so that it is free of mechanical defects
• Pump must have a system of unidirectional valves that function properly
• Pump must have adequate fuel supply
• Pump must be used within its rated capacity so that it will function properly or not wear out faster
• Pump motor must function smoothly and efficiently

• Ventricular septal defects (VSD)
• Atrial septal defects (ASD)
• Patent ductus arteriosus
• Coarctation of the aorta
• Tetralogy of Fallot

5 major congenital structural defects of the heart:

Atrial Septal Defects (ASD)

5 major congenital structural defects of the heart:

Patent ductus arteriosus (PDA)

5 major congenital structural defects of the heart:

Coarctation of the aorta

5 major congenital structural defects of the heart:

Tetralogy of Fallot

Valvular Stenosis:

Mitral Stenosis

Valvular Stenosis:

Aortic Stenosis

Valvular Stenosis:

Tricuspid and Pulmonary Stenosis

Valvular insufficiency/incompetence:

Mitral insufficiency

Valvular insuffieciency/incompetence:

Aortic Insufficiency

Valvular insufficiency/incompetence:

Tricuspid and pulmonary insufficiency

Coronary Heart Disease:

Risk Factors (5)

• Genetics
• Elevated blood lipids
• Hypertension
• Smoking
• Diabetes

• Sudden occlusion o a coronary artery usually by a thrombosis formation
• Hemorrhage into an atheromatous plaque
• Arterial Spasm
• Sudden greatly increase myocardial O2 requirements

Complications with MI:

Arrhythmias

Complications with MI:

Cardiogenic Shock

Complications with MI:

Intracardial Thrombosis

Complications with MI:

Cardiac Rupture

Complications with MI:

Myocardial Scarring

Complications with MI:

Pericardial Disease- Acute Pericarditis

Non-specific inflammatory response to a variety of injuries:

• Result in pericardial effusion, causes fibrin deposition in the serous membranes which may hear a friction rub as the roughened membranes slide past each other during the cardiac cycle
• May have to perform pericardiocentesis to remove the excess pericardial fluid to decrease pressure of the heart

Complications with MI:

Pericardial Disease- Chronic pericarditis

Complications with MI:

Papillary muscle dysfunction

Complications with MI:

Complete Heart Failure

• Size of infarct
• Patient's age
• Development of complications
• Presence of other disease processes

• Congestion: backup of blood into the upstram vasculature due to decreased forward flow
• Activation of circulatory compensations to try and maintain cardiac output
• Cardiac output decline: occurs when the compensatory mechanisms fail
• Death:  Ultimate end of CHF

(literally without blood) is a decreased erythrocyte number or a decrease in the quantity of hemoglobin with the RBCs

Decrease in the quantity of hemoglobin within the RBCs- iron deficiency- actually can see an increase in RBC's, but still anemia

Increased erythrocyte number.

Can be due to:

Decreased plasma volume

Abnormal proliferation of RBCs in the bone marrow

Excessive erythropoietin (released from kidneys)

Genetic disease where the body becomes overloaded with iron

There is an accumulation of iron that leads to organ damage, followed by scarring, and permanent derangement of organ function.  Manifestations of the disease take years to develop; tan to brown skin, diabetes, cirrhosis, heart failure.

Treatment:  repeated phlebotomies (withdrawal of blood) until iron stores are depleted and the periodic for life

Thrombocytopenia:

Primary thrombocytopenia

Decreased plate numbers

Associated with antiplatelet autoantibodies

The bone marrow produces platelets ut are rapidly destroyed; often encountered in children and subsides spontaneously after a short time; tends to be chronic in adults

Thrombocytopenia:

Secondary Thrombocytopenia Purpura

Decreased platelet numbers.

Drugs, chemicals damage the bone marrow.

Bone marrow infiltrated by leukemic cells or metastatic carcinoma.