Viruses Modes of Transmission transfer from host ot host 1. Direct I. Contact II.

. Droplet: droplet containing pathogen over a short distance. Sneezing, coughing, talking 2. Indirect I. Vehicle: via inanimate object/substances. Food and drink, cigarettes, clothing, blankets, soil water II. Vector- aliving organism a) Mechanical Vector straight forward transfer. No development or reproduction of the pathogen in the vector. eg. Flies on feces--> food eg. Traechoma by flies from person to person -->blidness b) Biological Vector Pathogen reproduces or develops in the alternate host. Eg, Malaria caused by protozoan parasite; Pasmodium- transmitted by anopheles III. Airborn: droplet nuclie containing pathogen and Proteins- When droplet dries out on surface then swept up and suspended in air for long periods. Factors that determine whether an infection occurs 1. Host factors : ability to resist levels of specific immunity to that pathogen previous exposure vaccine Level of non specific immunity. Eg intact barriers State of health nutritional status behaviour 2. Pathogen Factors Colonization Factors: determine how effective the pathogen is at establishing. Eg. Suitable portal of entry and exit. Eg. Ability to adhere to surfaces. Eg. Reproductive rate 3. Virulent Factors : Ability to cause harm. i. Enzymes needed to break down barriers, damage tissues ii. Ability to resist phagocytosis eg. Bacteria with capsules iii. Ability to evade the immune system eg. Viruses that become latent iv. Ability to change surface protein v. Ability to produce toxins a) Endotoxins: built into bacteria cell walls- in gram neg. Bacteria. Released when bacterium dies. Usually damage blood cells or blood vessel walls. Often also have systemic effects such as high fever b) Exotoxins: continuously produces and released by bacteria by many different species. Wide range of possible effects. Each kind of toxin is highly specific to the aspect of metabolism they attack/interfere. eg. Neurotoxins-c.botulinum, c.tetani Enterotoxin-e.coli strains

Cancer Description: a disease associated with a decrease in ability to regulate cell cycle. Specially associated with againg. Can expect higher incidence as the population ages. Cell cycle Mitosis: produce new cells G1 : Growoth phase. Accumlate resources. Increase in size. Synthzise proteins and RNA. G0: Becomes fully differentiated. Can carryout normal functions and maintenance. S : Synthesis. Duplicate DNA in preperation for Mitosis G2: More protein and RNA synthesis in preparation for Mitosis Cell cycle is regulate by genes. Many of them are two types 1. Protooncogenes: acts as on switches. Initiate changes in the cell cycle to promote proliferation. If they develop a error/mutation they become oncogenes. Which leads to unregulated proliferation (cancer). HER2 cell surface gene. It is implicated and breast and ovarian cancer. 2. Tumour Suppressor Genes: act as off switches. They reduce cell cycle process and lead to a decrease in proliferation. P53, RAS, BrCA1 Whether you develop cancer or not depends on the presence of oncogenes or mutated tumour suppressor genes or both. But for cancer to develop you need the presence of initiators and promoters. Intiators: Factors that cause the changes in genes i.e mutations. And these are onco or tumour suppresor genes. Many possibilites can include Radiation: electromagnetic or Particle i. UV-sun ii. X-ray Chemical exposure: chemotherapy, pharmaceutical, pesticides Viral infections: HPV, HBV, HCV Cigarettes Promotors: Dont cause mutations but they enable growth i. ii. iii. iv. High hormone levels: with reproduction cancer presence of sex hormones--> increase grwth high fat diet excess alcohol cigarettes

Normally you need recurring exposure to intiators and promotos to develop cancer Characterisics Benign Somewhat differentiated similar to orginal tissue Tumors have clear bounderies Grow moderlty High adhere levels Malignant -undifferentated Unclear boundersies Irregualr shape Grow rapidly Low adhereince level

How to do cancers spread 3 Wyas 1. Invasiveeness expan to and infilrate adajacet tissue 2. Metastisis cells break loose and spread in blood/lymp to distant sites 3. seeding tumour in open vacity spread through cavity. Colorectal cancer can spread to liver thru pelvic abdominal cavity How cancer causes problems infilration and destruction of tisseus loss of function distrpt endocrine produce approriate hormones distrupt blood flow compress adjacent tissuesGI obstruction, airway obstruction. Increased intercranial pressure Interfere with metabolism eg. Catchexia, tissue wasting.

How to treat surgery chemo radiation therapy-targets rapidly diving cells. Homone therapy: tamoxofen binds to estrogen receptos --> decrease tumour growth Nutritional Therapy Gene Therapy Stress: Response to a variety of challenges. Include physical stressors. Trauma ie. Surgery. 1. Psychological school, work 2. Emotional relationships Stress response: Marshelles your resources and helps you to deal with stressors 2 responses 1. short term responses controlled by hypothalamus via ANSSNS, all or none response. All SNS nerves respond at once. All thoaric lumber SNA nerves are interconnected by the chain ganglia

SNS response: Useful but high metablic cost 1. 2. 3. 4. 5. 6. 7. pupil dilation-improves peripheral and low light vision increase HR peripheral Constriction Increased BP Increased blood flow to critical tissue; heart and brain, skeletal mm. Increased Sweat; remove excess heat Stimulate adrenal medulla to secrete horomones: norepinephrine- stimulates effects of SNS for a longer period. Epinephrine: increase blood glu, increase metabolic rate, increased performance, increase o2 use and glucose use, and increase co2, heat production, bronchodialtion, increase ventilation, increase gas exchange, vasodilate blood vessels to sk.mm and heart.

Long term stress response: hypothalamus via endocrine - increase glucocorticoids from adrenal cortex