Block 9 Disease Processes week 1 Flashcards
What are Acidic dyes ?
- React with CATIONIC (positively charged components of cells)
- Example EOSIN - stains pink/ red.
Cytoplasm is most commonly stained pink
What are basic dyes ?
- React with ANIONIC (negatively charged components of cells)
- Example HEMATOXYLIN - stains purplish/blue
DNA in nucleolus stains blue.
What is Autophagy ?
Autophagy allows your body to break down and reuse old cell parts so your cells can operate more efficiently.
Autophagy is your body’s cellular recycling system. It allows a cell to disassemble its junk parts and repurpose the salvageable bits and pieces into new, usable cell parts. A cell can discard the parts it doesn’t need.
It is “turned on” when the cell is in starvation
Different types of necrosis ?
- Coagulative necrosis: less blood flow, tissue dies ( ischemia). All body exception is brain
- Colliquative / liquefactive necrosis: when cells die you the tissue completely or partially turns into a liquid. Associated more with brain.
- Caseous necrosis: tissue becomes cheese like in appearance.
Most common cause is TB where granulomas form in the lungs.
What is Dysplasia ?
- An increase in abnormal cell growth or development.
- Precancerous state
What is Metaplasia?
- Metaplasia is the conversion of one adult tissue type into another
- Gastric intestinal metaplasia is a precancerous change of the mucosa of the stomach with intestinal epithelium
Hypersensitivity reactions
Type 1: Immediate hypersensitivity
Type 2: Cytotoxic hypersensitivity
Type 3: immune complex hypersensitivity
Type 4: delayed type hypersensitivity reaction
Outline the structure of skin & the morphological differences between thin & thick skin ?
Skin also known as the Integumentary System.
3 layers:
-Epidermis
- Dermis
- Hypodermis
Epidermis:
- multiple layers of KERATINOCYTES.
- keratinocytes secrete glycolipids - prevent water seeping out of teh body
- keratinocytes contain cholesterol precursors which when activated by UVB are converted to Vitamin D.
- contains MELANOCYTES - give colour.
Dermis:
- Two layers: papillary layer and reticular layer
- Collagen, elastin, blood vessels, hair follicles, nerves, macrophages found in this area.
- Regulates temp with blood vessels
Hypodermis (subcutaneous layer) :
- contains adipocytes aswell as nerves, lymphatics and more blood vessels.
Difference between thick and thin skin ?
Can divide skin into thin and thick skin.
-
What are the five layers of the epidermis ?
Five layers of epidermis:
- Corneum - outermost layer of dead keratinocytes
- Lucidum
- Granulosum - contain keratin held together by desmosomes
- Spinosum - synthesize keratin. cells in this area area called keratinocytes
- Basalis - high mitotic activity ( divide to produce all the cells that migrate to the surface of the skin)
Meissner’s corpuscles ?
- Found in the dermis layer of the skin, in the dermis papillae
- they have mechanoreceptors which sense physical pressure or movement - specialized to detect light touch and low frequency vibrations
Pacinian corpuscles ?
- Sense course touch, pressure and high frequency vibrations
Skin appendages
- Skin appendages include hair and nails they are found in dermis ( middle layer)
-Hair is made up of keratinocytes and melanocytes
Sweat
Contains:
-water
-electrolytes
- dermcidin ( helps destroy bacteria)
Function: cool down body
ECCRINE gland is a sweat gland
APOCRINE glands are also sweat glands.
Secretions contain more lipids and proteins.
Located in armpits and genitals
Key terms
Hypertrophy: increase in size of cells
Hyperplasia: increase in the number of cells
Weight training: physiologic hypertrophy
Increased urinary frequency: pathologic hyperplasia
Endometrial proliferation: pathologic hyperplasia
Amyotrophic lateral sclerosis ( Lou Gehrig disease) - neurodegeneration of upper and lower motor neurons resulting in respiratory failure:
physiologic hyperplasia.
In response to states of anemia, interstitial cells of the kidneys and liver release the substance erythropoietin (EPO). This compound stimulates erythropoiesis in bone marrow, causing CD34+ hematopoietic stem cells to undergo physiologic hyperplasia to produce more red blood cells.
Neoplasia
This is classified as disordered cell growth, quite similar to dysplasia. However, the distinction is that neoplasia is malignant and irreversible. This is the basis of cancer.
Dysplasia
- Disordered change in type and growth of cells
Calcification ?
Dystrophic calcification: The deposition of calcium salt in degenerated tissues in the absence of a systemic mineral imbalance
Metastatic calcification:
Normal tissue but serum calcium is high
Oedema ?
increased fluid in interstitial tissue space
Outline the pathophysiology of haemorrhage ?
- Hemorrhage is an acute loss of blood from a damaged blood vessel.
Types of skin hemorrhage ?
Petechiae
Purpura
Ecchymosis
Bleeding into the skin can occur from broken blood vessels that form tiny red dots (called petechiae). Blood also can collect under the tissue in larger flat areas (called purpura), or in a very large bruised area (called an ecchymosis).
Embolism ?
- Solid, liquid or gaseous mass carried in the blood to a site distant
form the point of origin
Most common = pulmonary embolism
3 basic layers of skin
Haemodynamics
Haemodynamics is the movement of blood.
Fluid homeostasis requires:
- vessel wall
- osmolarity ( electrolytes /proteins)
- Maintenance of intravascular pressure
Embolism
An embolism is a blocked artery caused by a foreign body, such as a blood clot or an air bubble
Artherosclerosis
Atherosclerosis is thickening or hardening of the arteries caused by a buildup of plaque in the inner lining of an artery
Infarction
Infarction is tissue death or necrosis due to inadequate blood supply to the affected area
Thrombosis
Thrombosis is a blood clot within blood vessels that limits the flow of blood.
Describe fluid balance at capillaries ?
- Fluid balance is maintained by HYDROSTATIC PRESSRURE (HP) and COLLOID OSMOTIC PRESSURE (COP).
- Hydrostatic pressure - drives fluid into tissues
- Colloid Osmotic pressure ( aka oncotic pressure) - is determined mainly by protein concentration ( albumin).
Increased protein concentrations pull water back into microvessels
Edema
Definition: abnormally increased fluid in interstitial tissue space
Lower limb edema can be unliteral and bilateral.
Unilateral lower limb edema is usually caused by a pathological process in the limb itself, such as DVT or compartment syndrome.
Bilateral lower limb edema is usually due to systemic causes like heart, liver, and kidney failure
A more severe type of edema is anasarca, where the whole body develops generalized edema, and can be caused by things like malnutrition, as well as cirrhosis, nephrotic syndrome, or even burns.
Causes of extravasation of water from the vasculature
- Increase in vascular volume/pressure
- Decrease in plasma protein content
- Changes in endothelial cell function (vessel wall)
Edema
Inflammation can also cause edema
Congestive heart failure causes one or both of the heart’s lower chambers stop pumping blood well. As a result, blood can back up in the legs, ankles and feet, causing edema
Hyperemia and Congestion
Hyperemia is more blood than normal going to your body’s tissues or organs. Its an active adaptive process.
Congestion: reduced blood flow out. Passive process caused by impaired venous return from the affected area
Types of congestion
Examples
What are the 3 stages of the homeostatic process ?
Haemorrhage – the process of bleeding
Thrombosis – the process of clotting
Fibrinolysis – the process of clot dissolution
Bleeding on the skin ?
Pathalogical thrombus
Mural thrombus vs occlusive thrombus
stable atherosclerotic plaque ( plaque does not move) causes mural thrombus
Unstable atherosclerotic plaque ( fibrous cap ruptures and plaque not attached to the the vessel wall) can cause occlusive thrombus
Thrombus are caused by which 3 main factors :
Endothelial injury
Abnormal blood flow
Hypercoagulability (blood composition
Venoous thromboembolism
Artherosclerosis
Artherosclerosis can lead to …..
Pulmonary embolism
- Blockage of pulmonary artery due to thromboembolism
- There is less lung perfusion ( less blood going tot he lungs)
- Most thromboembolisms arise from lower extremity deep vein thrombosis ( e.g. iliofemoral deep vein thrombosis).
- Upper extremity deep veins are rare
Virchow’s triad
Three risk factors which increase the likelihood of a thromboembolism:
- Endothelial injury
- Stasis of blood flow
- blood hypercoagulability
Ischaemia
Inadequate blood supply to an organ or tissue. Insufficient supply of oxygen and nutrients and accumulation of metabolic waste
Hypoxia
Inadequate oxygen supply to tissue
Infarction
Infarction is tissue death or necrosis due to inadequate blood supply to the affected area
Aneurysm
Blood vessel enlargement caused by vessel wall weakness
Arterial more common than venous
Aneurysm classification
True aneurysm - real enlarged walls
Fusiform: bulge both sides
Saccular: bulge on one side
False aneurysm: blood leaks out of hole in blood vessel wall and blood clots. So enlarged walls but not because of bulge
Aneurysm facts
60 % of true aortic aneurysms occur in the abdominal aorta, 40 % in thoracic aorta. Most between renal artery branch and aortic bifurcation due to less collagen in this area of aorta.
- Abdominal aorta aneurysm (AAA)
- Thoracic aortic aneurysm
- Cerebral aneurysm
Shock
Shock = clinical state characterised by systemic hypoperfusion (lack of blood flow) leading to reduced delivery of oxygen and nutrients
Types of shock
Hypovolemic shock :
- can be due to hemorrhage - internal bleeding
- can be nonhemorrhagic fluid loss - due to dehydartion so you have less blood volume
Cardiogenic shock:
- injury or obstruction prevents heart from pumping blood efficiently
Distributive Shock:
- Allergic reaction or damage to the nervous system causes blood vessels to vasodilate or become leaky.
Types of distributive shock
Septic shock: caused by infection
Anaphylactic shock: allergic reaction which causes low blood pressure
Neurogenic shock: pain at site of spinal fracture, evidence of spinal injury ( loss of sensation, paralysis, loss of reflexes)
Septic shock
Septic shock
Bacteria
The microbiome is an important contributor to our health
Gram negative and gram positive bacteria
Gram positive: thick layer of peptidoglycan above plasma membrane - can retain dye - purple
Gram negative: thin layer of peptidoglycan between layers of plasma membrane - does not retain dye - pink
- Gram negative have LPS
- Gram positive have Teichoic acid
How does diversity arise ?
- Mutations - mutagens/mistakes during replication
- Genetic exchange - between bacteria by transformation, transduction, conjugation, transposons
Outline the three main ways bacteria use to exchange genetic material ?
Bacteria exchange genetic information using horizontal gene transfer. Which is gene transfer between two already existing organisms.
Donor transfers genetic material to a recipient who is not the donors offspring.
There are 3 ways to do this:
TRANSDUCTION - foreign genetic material introduced via Viruses
CONJUGATION - transfer between two bacteria using cell-cell contact
TRANSFORMATION - uptake of genetic material from the environment
How do bacteria multiply ?
Binary fission
Acid fast bacteria
- are bacteria with a waxy cell wall, high lipid content and lipids in cell wall are made of a complex hydrocarbon called Mycolic acid
- structure is similar to gram positive bacteria.
- will stain red with carbol fushsin and will not decolorise with strong acid alcohol solution
- Myobacterium Turberculosis - Tuberculosis
- Myobacterium leprae - Leprosy
- Nocardia spp. - Norcardiosis
are all examples of acid fast bacteria.
Bacteria without a conventional cell wall
Chlamydia sp.
Mycoplasma sp.
Nomenclature of bacteria
FAMILY, GENERA, SPECIES, STRAIN/ SEROTYPE
Gram negative and gram positive cell wall
Gram positive bacteria can form spores. Spores are bad because they are heat (over 100 degree) resistant, dessication and chemical resistant
Once you have infection with a spore it is very hard to get rid off.
Fastidious
- Some pathogens require some elements from us like vitamins. Some pathogens only grow in our body.
Selective and Differential Media is used to determine which pathogen something is so you can determine what illness someone has
Selective - only lets a spefic type of bacteria grow. If the bacteria your testing for doesn’t grow then its not that bacteria. E.g. you have some mediums where only gram positive bacteria will grow
Differential - the property that is different. Like in this case the dish is either yellow (indicates salmonella) or pink (indicates E.Coli)
Serotyping
The last few letters
What is pathogenic and commensal bacteria ?
Commensal bacteria are microbes that reside on the surface or mucosa of the body without causing harm.
Pathogenic bacteria - microbes that cause disease
Koch’s Postulates
Proving that a specific microorganism causes a specific disease (1890).
Purpose: to establish a causal relationship between a pathogen and disease.
There are 4 criteria:
1. Find candidate bacterium in every cause of the disease.
- Isolate bacterium from the host, grow in pure culture
- Show that cultured bacteria causes the same disease in a healthy subject.
- Isolate bacterium from experimental subject.
Problems with this method:
- Some pathogens such as bacteria which cause syphillis and leprosy are very difficult to grow in an artificial medium.
- Also viruses cannot be grown in pure culture they replicate in cells.
Whether a infection occurs and disease develops after being exposed to a pathogen depends on:
- Where bacterium is in/enters in the host
- Bacterial species or strains
- The host
Normally sterile sites (microbe free) or with very low bacterial counts include:
FLUIDS:
- Blood, Cerebrospinal fluid, Urine
TISSUES/ORGANS:
- Muscles, glands, brain
Disease related terminology
Strict pathogen - always causes disease
e.g. mycobacterium tuberculosis ( causes TB)
plasmodium species ( causes malaria)
rabies virus ( causes rabies)
Opportunistic pathogen - part of the normal microbial flora
Faculative pathogen - can grow and survive in environment aswell as host
Bacteria virulence factors
Streptococcus pneumoniae
- will use sugar residues as an energy source
- pneumolysins - toxin which causes damage. Example of exotoxin.
Beta - haemolysin
Botulinum toxin
This is why young children shouldn’t have honey, because can produce toxin.
Cholera toxin
Salmonella
Listeria monocytogens
- Pregnant women are told not to eat soft cheese because of the risk of this pathogen causing meninigitis in the foetus
Methods pathogens use to evade immune system
- Hide: enter cell and stay intracellular
- Phase variation/Antigenic variation
- Molecular mimicry
- Modify or block host immune response
Burns to the skin
- Burns to the skin damage skin and proteins
- This impairs the skin barrier which causes:
- impaired thermoregulation - loss of body heat
- impaired fluid retention - large water, protein loses from skin and affected tissue
- Loss of microbial barrier function - high risk of infection
Types of burns
1st degree burn ( superficial burn)
2nd degree burn ( superficial patrial thickness burn)
2nd degree burn ( deep partial thickness burn)
3rd degree burn ( full thickness burn)
4th degree burn ( full thickness burn)
Causes of burns
Thermal burns anything above 44 degrees Celsius
Chemical burns - exposure to corrosive substances
Electrical burns
Radiation burns
Response to burns
First degree burns: maintain moist skin barrier with antimicrobial burn dressing
Second degree: daily burn dressing with topical antimicrobial
Deep second degree: antibiotics to prevent sepsis
Atherosclerosis
Atherosclerosis is thickening or hardening of the arteries caused by a buildup of plaque in the inner lining of an artery.
Atherosclerosis, which develops from fatty plaque buildup, is a common type of arteriosclerosis.
Arteriosclerosis
Arteriosclerosis is a type of vascular disease where the blood vessels carrying oxygen away from the heart (arteries) become damaged from factors such as high cholesterol, high blood pressure, diabetes and certain genetic influences.
Atherosclerosis is the hardening of any artery (even though it’s usually medium- to large-sized arteries) which is caused by the buildup of plaque.
These plaques are called atheromatous plaques and happen in the innermost wall called the tunica intima.
Tunica intima protects blood vessel wall from blood and secretes proteins to prevent blood from clotting.
Your tunica intima (endothelium) can et damaged by LDL, chemicals from smoking and high blood pressure.
The weak walls allow LDL to enter the endothelial wall.
WBC called monocytes follow the LDL and break them down. However if there is too much LDL macrophages can die. So macrophages filled with LCL are stuck in the damaged endothelial wall - they are called foam cells.
As foam cells build up we get a fatty streak which blood can clot on. Platelets begin to gather at the damaged endothelium and release platelet-derived growth factor, which in turn encourages the growth of smooth muscle cell.
The growing smooth muscle cell secretes collagen, proteoglycans and elastin fibrous cells that form a wall around the fatty streak preventing blood clotting. This is called a fibrous cap and with the fatty streak we now have a plaque.
Build up of calcium.
An atheromatous plaque can cause reduced blood flow
- If blood flow is reduced in the coronary arteries ANGINA and MYOCARIDAL INFARCTIONS can occur.
The building up of plaque also weakens the artery walls, which means it can lead to aneurysms
The building up of plaque also weakens the artery walls, which means it can lead to aneurysms which explains why atherosclerosis is a main cause of abdominal aortic aneurysms.
Artherosclerosis and kidneys
But the complications of atherosclerosis don’t stop there! If we move on to the kidneys, plaque build up in the renal arteries reduces blood flow to the kidney, and tricks the kidney into thinking blood pressure is low.
The kidneys then activate the renin-angiotensin-aldosterone system which unnecessarily increase blood volume in the body, causing hypertension.
Process of infarction
- Have artery with plaque if the shell gets exposed platelets are attracted to the plaque and fully occlude the blood vessel.
Risk factors of atheroma
High cholesterol and triglyceride levels.
High blood pressure.
Smoking.
Type 1 diabetes.
Obesity.
Physical inactivity.
High saturated fat diet.
Amlodipine
Side effects of amlodipine is swelling
