MTE - Mod 1-5 Flashcards
What are the four core areas or components of pathophysiology and how do these components assist in understanding disease processes?
- The Aetiology – cause (genetic or acquired)
- Pathogenesis – molecular response
- Morphological response – micro/macro structural alterations caused by pathogenesis
- Clinical manifestation – symptoms/ signs caused by morphological response
Q1. What are the 5 specific leading world-wide causes of death, identify which ones are preventable and how we might prevent them?
- Ischaemic Heart Disease
- COPD
- HIV/AIDS
- Cerebrovascular disease
- Lower Respiratory Infections
Name one important (of many) condition that we need to pour resources into now, to minimize their contribution to mortality in 20 years’ time? How is this condition caused and how do we currently identify it? (see Lecture 1)
Cardiovascular disease
1 in 4 deaths in Australia
Caused by diet, inactivity, tobacco, alcohol, genetic predisposition
Symptoms are angina, chest pain, SOB, numbness in neck, abs
Tests include ECG, stress, MRI
What is the average life expectancy of non-indigenous Australians and Aboriginal and Torres Straight Islander Peoples ? ii) What conditions do Aboriginal and Torres Straight Islander Peoples seem to be suffering from most greatly
First people’s: 50 years
Non-indigenous: 70 years
Leading indigenous diseases: coronary artery disease, stroke, RHD, diabetes, cancer
Describe the some physiological and pathological forms of hypertrophy and atrophy.
Physiological hypertrophy:
Activation of smooth muscle of the uterus (endometrium) during pregnancy (increase in estrogen receptor = increase protein synthesis)
Pathological Hypertrophy:
Thickening of heart muscle, decrease in size of chambers, reduced capacity of the heart to pump blood = heart increase size due to aortic stenosis
Hypertrophy: stretch induces growth factors and protein synthesis
Physiological atrophy: muscle atrophy due to less utilisation of the muscle
Pathological atrophy: cellular injury (starvation, aging, disease) e.g. vascular disease = gyri become smaller and sulci larger = loss of neuronal matter
Main mechanism of physiological hypertrophy & atrophy:
Stretch induces growth factors and protein synthesis
What is the main mechanism that controls physiological hypertrophy and atrophy? (use a diagram to explain)
- Mechanical stretch
- Agonists
- Growth factors
- leads to signal transduction pathways
- transcription factors (Myc, Fos, Jun)
To - Induction of embryonic gene = increased mechanical performance decreased work load
- Synthesis of contractile proteins = increased mechanical performance
- Increased production of growth factors
Using a labelled diagram, identify the differences in cell morphology that occur during apoptosis and necrosis. Hint: firstly, list the morphological features for necrosis/apoptosis and try to include them into your diagram that has three steps beginning with a healthy cell.
Necrosis:
Lack of o2 = ATP depletion = intracellular Na+ accumulation = osmotic swelling = membrane rupture
Swelling of ER and mitochondria = reversible but if injury progresses = cell membrane breaks down causing blebbing = leakage of cell contents triggers inflammatory response
Apoptosis:
Programmed cell death = Condensation of chromatin = membrane blebbing/ apoptotic bodies
. List the four main clinical presentations of necrosis and conditions which may cause each (including target organ). Focus on one form of necrosis and indicate the main mechanism (the how), regarding how necrosis is caused.
Caseous – lungs – tuberculosis – white, cheesy, soft
Liquefactive – brain – hypoxia
Gangrenous – peripheral limbs – diabetes – black skin with putrefaction
Coagulative – heart – MI – firm tissue
Liquefactive necrosis is caused by infections (release of digestive enzymes) and ischemic injury of the brain (MI), it presents as yellow pus
two main pathways of apoptosis. Why do you think apoptosis does not result in an inflammatory response?
Intrinsic:
Cell injury bcl-2 family sensor bcl-2 family effector bax, bak mitochondria leaks cytochrome c and pro-apoptotic protein initiator caspase executioner caspases cell death
Extrinsic:
Receptor ligand interaction receptor adaptor protein inhibitor caspases executioner caspases endonuclease activation, cytoskeleton breakdown cell death
Why do you think apoptosis does not result in an inflammatory response?
Apoptosis causes cellular shrinking + fragmentation – organelles are packed into apoptotic bodies and engulfed by phagocyte without releasing any intracellular substance outside also membrane remains intact = no stimulation for inflammation
Describe some of the most common intracellular accumulations. How are these accumulations formed and how are they detected? Pick one of these accumulations and describe the effects on the cell? (ie. mechanisms and end result)
Normal accumulations:
- Water
- Lipids
- Proteins
- Electrolytes
Abnormal accumulations:
- Substances – silica, carbon
- Infectious agents – viruses
- Synthesis – triglycerides
Pick one of these accumulations and describe the effects on the cell? (ie. mechanisms and end result)
Fatty Liver – hepatic steatosis
Lipoprotein accumulation is formed when lipid catabolism & accumulation is disturbed. Micro = clear vacuoles surrounding the hepatocytes
Define ->
Transudate
Exudate
Extravasion
Chemotaxis
Transudate:
Escaped fluid from the blood vessel into the interstitial space – water, ions, no inflammation
Exudate:
Escape of fluid, leaks out of blood vessels into other tissues/ IF. Fluid contains high protein, cellular debris, inflammatory cells, occurs late inflammation
Extravasion:
Leakage of plasma fluid and proteins through the widened interendothelial spaces into the tissues = oedema – caused by acute inflammation
Chemotaxis:
Locomotion along a chemical gradient
- Describe how neutrophils and macrophages (and other cells involved in inflammation) might be assessed from biopsy/tissue sections.
Staining in histopathology
- H & E staining – purple nucleus with pink proteins/cytoplasm
What are the main differences in the appearance of neutrophils and macrophages (in terms of the time of infiltration and visual appearance/use drawings/images)
Neutrophils only last 24 hours before macrophages come in. neutrophils are smaller compared to macrophages. Nuclei have 2-5 lobules and stained dark purple. More abundant so easy to spot
Macrophages change from monocytes once they leave the blood, resulting in structural change. They then engulf foreign bodies creating vesicle in the cytoplasm
Beyond the completion of a tissue biopsy, what other techniques can be employed to detect different white blood cell populations in the human body?
Haematology would use Blood film analysis to identify morphological features and full blood count.
• Leishman’s (Romanowski) stain - Eosin and Methylene blue dissolved in methanol.
Broadly describe the processes involved in inflammation. Relate these and name the four cardinal signs that might alert you to acute injury and infection.
Tissue injury vasodilation increased Blood flow erythema, calor
Vasodilation increased vascular permeability plasma proteins & leukocytes leak from blood vessels swelling & oedema
Leukocyte recruitment (loose attachment + rolling) increased blood flow in site of inflammation & vascular permeability influx of leukocytes into tissue leukocyte proliferation
Past 24hrs systemic response fever, sweating, shivering neutrophils replaced by monocytes
4 cardinal signs:
1. Rubor – red
2. Calor – heat
3. Tumor – swelling
4. Dolor – pain
What are the four cardinal signs ?
- Rubor – red
- Calor – heat
- Tumor – swelling
- Dolor – pain
Define the Systemic Inflammatory Response Syndrome (SIRS) and its presentation. How does this differ from the acute cardinal signs of acute inflammation above? Provide some examples of conditions/situations that might be associated with a SIRS response.
• Severe localised acute inflammation
• LPS (lipopolysaccharide) recognition –> cytokines released and circulate systemically
o Fever results in response to infection: cytokines (IL1 + TNF) induces:
Arachidonic acid (prostaglandin synthesis) metabolism
Protein synthesis increases (in liver):
• C reactive protein (CRP)
• Fibrinogen
• Serum amyloid A (SAA)
o Leukocytosis: > 20000 cells in blood cell counts
Caused by accelerated release of leukocytes from marrow
• Bacterial infections: neutrophilia
• Viral infections: lymphocytosis
o Increase in pulse, BP and decreased sweating to maintain pressure & minimise heat loss
o Eg. Sepsis in severe cases: massive increase in LPS and IL-1 –> vascular coagulation + decreased BP –> vascular failure + metabolic disturbances
o Difference – response consists of the same cardinal symptoms but more exaggerated, systemic rather than localised
Explain the processes involved in acute inflammation in response to a severe sunburn of the skin. Briefly describe how inflammatory mediators are involved in this process and some not too gruesome images (from online) to show the macroscopic effects over time.
Mast cells activated by heat degranulation and release of histamine and cytokines such as IL-6, IL-1, and TNF vasodilation and increased blood flow causes erythema, calor and rubor immune system activates oedema occurs due increased plasma fluid and protein deposition (extravasation) leukocytes accumulate at the area of injury and pus forms due to the death of neutrophils blistering
Explain the processes involved in chronic inflammation and how it differs from acute inflammation. What is usually the end result of chronic inflammation, as perhaps seen in Duchene Muscular Dystrophy (check online)?
Acute inflammation triggers a healing process including rubor (redness), calor (heat), dallor (pain), and tumor (swelling) immediate onset
• Causes: short term physiological stress
• Dominant leukocyte: Neutrophils
• The microbial agent/damaged cell is eliminated through macrophage apoptosis and out via the lymphatic system
• Morphology: erythema, swelling, neutrophils
• End result: elimination of stimulus and return of normal function
Chronic inflammation surpasses the healing process with no presentation of the cardinal signs and progressive loss of cell/tissue function, delayed onset
• Causes: long term exposure, mycobacterial (tuberculosis), virus, fungus, parasites, autoimmune diseases or prolonged exposure to toxins
• Morphology: no oedema, tissue destruction, fibrosis and granuloma formation
• Dominant leukocyte: macrophages
• Macrophage accumulation
• Excessive prolonged damage
• End result: fibrosis and loss of function eg. tissue damage in atherosclerosis, rheumatoid arthritis, pulmonary fibrosis, tuberculosis
Duchenne Muscular Dystrophy
• Genetic disorder characterised by progressive muscular degeneration/weakness
• Results in chronic inflammation which presents as muscular weakness and cardiac muscle atrophy and leads to early mortality
What common systemic blood markers of inflammation exist and what do they represent/measure?
• Erythrocyte sedimentation rate (ESR),
o The distance red blood cells fall in a test tube in one hour – further decent greater inflammatory response of immune system
• C-reactive protein (CRP) and
o Level of CRP in blood, CRP is made by the liver, sent into bloodstream for inflammation to protect tissues from infection
o It is used to detect the severity of inflammation/ whether you’re responding to treatment
• plasma viscosity (PV)
o Viscosity of patients’ blood
• Troponin- myocardial infarct
• Creatine Kinase- skeletal & cardiac muscle damage
• ALT (Alanine transaminase) & AST (Aspartate transaminase)-liver damage
• leukocyte count- nonspecific infection
Provide 2 conditions that each of the above markers are diagnostic for. What is the approximate ‘reference range’ (normal range) for each in Australia?
ESR – test is nonspecific – only confirms the presence or absence of inflammatory activity in the body
• Conditions
o Autoimmune (RA, Lupus)
o Kidney / thyroid
o Infections
o Anaemia
Define
Tissue Growth
Tissue Repair
Transcription factor
Collagen
Tissue regeneration –
The renewal and growth to repair or replace tissue that is damage/suffered from a disease
Tissue repair –
Compensatory regeneration of tissue followed by surgical, mechanical or chemical induced injury resulting in restoration of structure and function of the tissue
Transcription factor –
Protein that controls rate of transcription of genetic information from DNA to mRNA
Collagen –
Structural protein found in skin and other connective tissue
the possible causes and effects of tissue regeneration and repair. What conditions (physiological/pathological) might be associated with regeneration/repair?
Injury!!
Regeneration
- renewing tissues (epidermis, GI tract)
- stable tissues (growth of liver)
Repair
- wound (healing; scar)
- chronic inflammation (fibrosis)
*Regeneration conditions:
- Physiological
- Liver regeneration after cancer
*Repair conditions:
- Pathological
- Would healing
- Deep injury
Regeneration and repair
i) Summarise the processes that regulate the mass of tissues (i.e. the baseline cell population).
- Baseline cell population
o Proliferation
o Differentiation
o Stem cells
o Cell death (apoptosis)
Regeneration and repair
ii) Provide an example of a tissue that experiences a change in the baseline cell population and two conditions/factors that might affect the baseline population.
Skin:
Growth factors – TGF-beta bind to receptors activate gene expression
Effects vary on tissue and type of damage
Growth inhibitor for most epithelial cells, loss fo receptor increases cancer cell proliferation
- Squamous epithelial cells (skin, oral)
- Columnar epithelial cells (GI tract)
- Transitional epithelial cells (urinary tract)
Consider the phenomenon of liver regeneration in a case study where an individual donates 60% of their liver to a recipient.
i) What process will occur in the donor, how is the process regulated?
Hyperplasia – excess cell production leads to increased cell number
Hepatocyte regeneration occurs by the activation of non-parenchymal cells (Kupffer cells) send signals to survived hepatocyte to proliferate
Regulated by IL-6 and TNF re-enters into G1 phase, DNA replication and mitosis
. Consider the phenomenon of liver regeneration in a case study where an individual donates 60% of their liver to a recipient.
ii) What will be the likely end result in the donor? (ie. how long would regeneration take, would the liver return to normal function?)
Liver regeneration = 3-6 months with 60% of the liver doubling of remaining 40% within 4 weeks
Hepatocytes are normally quiescent and require hours to re-enter the cell cycle and occurs by activation of non-parenchymal cells, Kupffer, endothelial and stellate cells
. Consider the phenomenon of liver regeneration in a case study where an individual donates 60% of their liver to a recipient.
iii) Speculate on the effect of the donor using excessive anti-inflammatory drug use.
Excessive use targets liver as drugs metabolised in the liver and affects regeneration
Also effects inflammatory response necessary for regeneration inflammation TNF suppression if anti-inflammatory drugs are taken growth is dampened as TNF is also involved in regeneration of liver
diagram indicating the components and distribution of ECM components within tissue.
Epithelium
integrins
fribriblast
integrins
endothelium
capillary
Clearly identify the main types of collagen and related molecules within the basement membrane and interstitial matrix.
Interstitial matrix: 1, 2, 3, 4, 5
Basement membrane: collagen 4
Related molecules: adhesive glycoproteins, proteoglycans, hyaluronan, elastin’s
Why is the type of collagen different in the basement membrane and matrix?
Type 4 acts as a barrier between epithelial and endothelial cells – nonfibrillar, joined by the laminin
ECF has both nonfibrillar and fibrillar laminin, provdes mechanical support and anchoring to surrounding cells
What is the difference between a primary and secondary union?
Primary:
Simple damage, surgical incision, re-approximated using suture. Limited death of cutaneous cells/basement membrane
Re-epithelialisation within thin scar
Secondary:
More complex in infected wounds, severe trauma where increased inflammation leads to extensive collagen/scar/wound contraction
Whats the time span of healing and cells involves in process
Inflammatory phase
- 4-6 days
Proliferative phase
- 2-24 days
Maturation phase
- 21 days - 2 years
Indicate the tensile strength of the scar at different times and any other important events that can determine the strength of scars as they mature.
Scar strength increases as collagen deposition increases – full restoration of strength may never occur
Scar strength
7 days healing = 10%
3 months healing = 70%
If injury is greater in size, lack of uniformity and greater exposure to bacteria – healing process will extend and greater degree of tissue degradation
Phases of scar healing:
• Inflammation
• Proliferation
• Maturation
Process
o Injury platelet aggregation blood clot inflammation
o Tissue granulation proliferation migration re-epithelialisation of wound
o Deposition of the extracellular matrix tissue remodelling wound contraction
What events could impair normal wound healing and how would they slow/interfere with the process?
System factors
• Nutrition – protein and vitamin c
• Metabolic status – diabetes
• Circulatory – decreased perfusion
Local factors
• Infection
• Mechanical – early motion delays healing
• Foreign bodies – steel, glass = inflammation
Define
Xenobiotic
– a substance, typically a synthetic chemical that’s foreign to the body
Define secondary malnutriton
arises when an individuals dietary intake is sufficient but energy is not absorbed by the body as result of infectious conditions e.g. diarrhoea, parasite, medical/surgical properties affecting the digestive system
Define laceration (soft tissue injuries)
a deep cut or tear in skin or flesh
Define insulin resistance
– an impaired response of the body to insulin, resulting in elevated levels of glucose in the blood
Define metablic syndrome
– biochemical and physiological abnormalities associated with the development of cardiovascular disease and T2DM
- Describe the different routes of exposure and metabolic pathways for toxin metabolism and excretion.
• Air, water or soil (carbon monoxide, metals, steels) = human exposure
• Skin, lungs and GI tract lead to absorption into blood stream
o Venous circulation
o Stomach to liver
• Distribution into tissues
o Toxicity or
o Metabolism = storage = excretion
- Lead toxicity remains a serious problem in industrialised countries, including Australia.
i) Describe the sources of toxic lead exposure and how lead usually enters the body
• Lead contaminates air, food and water
• The environmental contamination is mines, smelters (leaded petrol, paint, batteries, painted toys, paints)
• Maximum safe blood level is 10 micro/deci L
• Death at 100 micro/deci L
) Describe the pathophysiology of lead poisoning, where it accumulates, what effect it has in these organs and who it targets.
• 80-85% of absorbed lead deposits into teeth and bones
o Competes with calcium – synaptic transmission will get interrupted and cause neurological impairment – homeostasis in neurons (Calcium is needed for neurotransmitter release)
• Children are more susceptible absorbing 50 vs 15% of dose
o Blood brain barrier is less developed
• Clinical effects
o Bone remodelling
o Anaemia – inhibits enzymes in haem biosynthesis
How might one diagnose lead poisoning and what symptoms might you expect a patient to present with?
• Diagnosis
o Behaviour cognitive change
o Age
o Anaemia with basophilic stippling of RBCs
o Blood lead levels
- Thermal injury is responsible for a large number of hospitalisations in Australia each year.
i) How many hospitalisations and deaths occur each year to this avoidable condition?
~47,000 hospitalisations for burns
~25% in individuals less than 4 yrs
Males 88% burns from flammables
96% of admissions burns affecting <10% of body
Describe the different types of burn which may be encountered, the classification system, and the main reasons for which burns threaten life.
Superficial – epidermal injury 1st degree
Partial thickness – injury to dermis 2nd degree
Full thickness – subcutaneous tissue/muscle 3rd /4th degree
Burns more than 20% of BSA threaten life
• Fluid is redistributed to interstitial compartment
• Reduces blood volume and induces hypovolaemic shock
• Protein leaks into tissues causing systemic oedema
• Induce hypermetabolic state to heat loss
• Increases susceptibility to infection (sepsis)
• Injury to airways (nose, mouth, lungs)
- i) What is the difference between primary and secondary malnutrition?
Protein-energy malnutrition - resulting from deficiencies in any or all nutrients. Micronutrient deficiency diseases - resulting from a deficiency of specific micronutrients.
Describe two major diseases associated with primary malnutrition and which macronutrients are deficient in each.
Protein energy malnutrition (PEM)
• fatal affecting children, elderly, hospitalised
• underdeveloped countries
• famine, rapid cost increase, displacement (war)
• BMI less than 18.5-16
1. Marasmus – somatic and visceral protein content – subcutaneous fat and muscle serve as energy supplies and are depleted
2. Kwashiorkor – insufficient protein in diet – visceral protein depleted – leads to systemic oedema – masks weight loss by fluid retention
Provide the definition of obesity and the simplified causes of it.
Caloric imbalance when more consumption than expenditure = stored
• adipocytes specialised storage cells – humoral and neural mechanisms reguate hunger and satiety and nutritional, psychological genetic and environmental signals regulate metabolism – governed by hypothalamus
Provide an introduction describing appetite regulation and the neuro-hormonal mechanisms regulating it. In your answer, ensure that you cover the afferent, arcuate nucleus and efferent system.
• Afferent system generates signals
o Fats cells
o Ghrelin
o Peptide YY
o Insulin
• Arcuate nucleus
o Processes neuro-hormonal input/generates efferent output
First order neurons
• Efferent system
o Second order neurons regulate food intake/ energy expenditure
• Melanocyte stimulating hormone (MSH) stimulates MCR on second order neurons = lose weight, increase energy expenditrure
• Then NYP neurons produce orexigenic NTs = hungry – gain weight
• Leptin hormone synthesised by fat cells binds to receptor and can overeat stimulating increased MSH release and inhibits NYP neurons
• Stable weight = balanced output
• Reduced body fat = low leptin, increased hunger
• Mutations in MCR = no satiety
Define
Haemostasis
process of blood clotting
Define
Homeostasis
self-regulating process to maintain stability while adjusting to changing external conditions
Define
Cytopenia
condition of lower than normal number of blood cells
Define
Congestion
accumulation of excessive blood within blood vessels, localised or systemic
Define
Shock
state of cellular and tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption or inadequate oxygen utilisation
What are the functions of haemostasis? Describe some situations where haemostasis would be critical to life.
To reduce blood loss and maintain blood in fluid state within the vessels
• prevention of blood loss from intact vessels (sound vessel walls and platelets)
• arrest of bleeding from damaged vessels by
o blood vessel reaction to injury
o platelet plug formation
o plasma protein = coagulation
What is the relationship between primary and secondary haemostasis?
Primary:
Initiation of coagulation cascade mediated by the interaction of platelets and blood vessels
• depends on vascular integrity and platelet reactivity
Secondary:
Formation and stabilisation of fibrin clot
• dependant on adequate procoagulants and appropriate natural anticoagulants
Primary formation of platelet plug
Secondary (coagulation) clotting factors proteolytically activated activation of fibrin (factor Ia)
- Describe the complete coagulation cascade from endothelial disruption to stable clot formation with a full diagram showing intrinsic, extrinsic and common pathways with the regulatory mechanism (natural anticoagulants).
Vascular injury exposure to negatively charged surfaces including phospholipids and collagen triggers contact initiation and activates Factor 9 after significant injury tissue factor and Factor 7a stimulate activation of Factor 9 & 10 through calcium and phospholipid signalling
Factor 10 then at end of intrinsic and extrinsic pathway Factor X, V and calcium bind form prothrombinase complex prothrombin thrombin cleaves fibrinogen fibrin clot thrombin activating platelets
- What is oedema and explain the process of oedema development in relation to hydrostatic and interstitial fluid pressure at capillary bed level for the two categories of oedema formation
Oedema is:
An abnormal increased in interstitial fluid within tissues water and solutes movement between intravascular and interstitial spaces
Increased capillary pressure = decreased colloid osmotic pressure = increased interstitial fluid
Process:
• Exudate
o Inflammatory oedema with high specific gravity
o Due to increased vascular permeability
o High protein and cellular debris
• Transudate
o Non-inflammatory oedema with low specific gravity
o Due to increased hydrostatic pressure (heart, kidney, liver failure) decreased osmotic pressure (low proteins in blood)
o Increased salt
o Lymphatic obstruction
- What is the difference between thrombus and embolus? What are the five most common types of emboli? Give an example of each type of emboli.
Thrombosis = blood clot in veins
Embolus = a mobile clot that moves through blood vessels until reaching a vessel that is too small to pass through
Five common types:
1. Pulmonary embolism
2. Systemic thromboembolism – emboli through arterial circulation (smoking, surgery)
3. Fat and marrow embolism – severe skeletal injuries
4. Liquid – amniotic fluid embolism
5. Air embolism – gas bubbles within skeletal muscles
- Endothelial cells have both antithrombotic and prothrombotic properties. Briefly explain these properties giving examples where relevant.
Antithrombotic**
Anti-platelet effect – prostacyclin and nitric oxide prevent platelet adhesion to endothelial cells
Anti-coagulant effect – thrombomodulin and tissue factor pathway inhibitor, a cell surface protein, inhibits TF (tissue factor – an initiator of blood coagulation) and factor VIIIa and factor Xa activity
Fibrinolytic effect – tissue type plasminogen activator (tPA) promotes fibrinolytic activity
**Prothrombotic**
Platelets adhere to endothelium after injury by interacting with vWF (Von Willebrand factor) which is produced by normal endothelial cells
Has a procoagulant effect from exposure to cytokines or bacterial endotoxins, endothelial cells produce TF (extrinsic pathway)
Antifibrinolytic effect by secretion of plasminogen activator inhibitor from endothelial cells which limits fibrinolysis
- What is an embolus?
a. An intravascular mass that forms in one anatomic site
b. A freely movable, intravascular mass that is carried from one anatomic site to another by the blood
c. An intravascular mass that forms in the legs
d. An intravascular mass that forms in the brain
e. An intravascular mass that forms in the foramen ovale
b. A freely movable, intravascular mass that is carried from one anatomic site to another by the blood
- Exudate in oedema is defined by:
a. Protein rich fluid
b. Protein poor fluid
c. Decreased vascular permeability
d. All of the above
e. None of the above
a. Protein rich fluid
- What is the most likely fate of venous emboli from deep leg veins?
a. Pulmonary embolism
b. Myocardial infarction
c. Stroke
d. b&c above
e. None of the above
a. Pulmonary embolism
- In the formation of a thrombus _______ is polymerized into _______ forming a meshwork of thin filaments that bind together cellular elements of blood forming a clot.
a. Fibrinogen; fibrin
b. Fibrin; fibrinogen
c. Plasminogen; plasmin
d. Plasmin; Plasminogen
e. All of the above
a. Fibrinogen; fibrin
- An infraction is typically caused by:
a. Overexhaustion
b. Liver failure
c. Occlusion by an embolus
d. Respiratory failure
e. Stroke
c. Occlusion by an embolus
- A red infarct is often found in solid tissues occluding arteries and is anaemic.
a. True
b. False
True
- Congestion is a passive process due to decreased outflow of blood from a tissue.
a. True
b. False
True
- Oedema is caused by:
a. Increased colloid osmotic pressure
b. Decreased interstitial fluid
c. Decreased capillary pressure
d. Decreased colloid osmotic pressure
e. When outflow from arteriolar end is less than inflow into venular end
d. Decreased colloid osmotic pressure
- Which statement is NOT true about transudate?
a. It is protein poor fluid without cells
b. It is non inflammatory oedema
c. It is caused by increased hydrostatic pressure
d. Plasma osmotic pressure proteins are increased
e. Kidney problems with increased salt intake may cause transudate oedema
c. It is caused by increased hydrostatic pressure
- Which of the following is NOT an active system of haemostasis?
a. Vascular system
b. Lymphatic system
c. Coagulation system
d. Fibrinolytic system
e. Platelet system
b. Lymphatic system
- Hyperaemia is:
a. Decreased volume of blood in an effected tissue
b. A process where arteriolar constriction decreases blood flow
c. Increased volume of blood in an effected tissue
d. A process where arteriolar constriction increases blood flow
e. None of the above
d. A process where arteriolar constriction increases blood flow
Define
B cell
Plasma cell
Antibody
Allergen
Definitions
B cell – lymphocyte responsible for antibodies
Plasma cell – type of immune cell that secretes immunoglobulin
Antibody – a blood protein produced in response to and counteracting a specific antigen
Allergen – substance causing IgE mediated defensive against allergen
What are the main features of Type I, Hypersensitivity? What antibodies and cells are involved and provide examples and details of clinical conditions induced by each type of reaction.
Type 1
- Immediate after exposure to antigen
- IgE mediated
- Hay fever, anaphylaxis
What are the main features of Type II,Hypersensitivity? What antibodies and cells are involved and provide examples and details of clinical conditions induced by each type of reaction.
Type 2
- Antibody-mediated immune reaction where antibodies IgG or IgM cytotoxic are directed against cellular or extracellular matrix antigens cellular destruction, functional loss or damage to tissues
- Drug allergy
What are the main features of Type III, Hypersensitivity? What antibodies and cells are involved and provide examples and details of clinical conditions induced by each type of reaction.
Type 3
- Immune complex mediated disease, serum disease, transfusion reaction inadequate immune response to harmless soluble antigens IgG antibody response
- immune complex diseases RA or SLE
What are the main features of Type , IV Hypersensitivity? What antibodies and cells are involved and provide examples and details of clinical conditions induced by each type of reaction.
Type 4
- T cell mediated secrete cytokines activating machrophages and cytotoxic T cells macrophage accumulation at site Delayed type hypersensitivity
- Contact allergy – diabetes, RA, MS
Provide 3 examples how to diagnose a hypersensitivity reaction and detail how the tests are conducted. Use images/a video from the web to demonstrate one of the tests.
Prick test – Type 1 hypersensitivity – skin is pricked with comb like tool with allergens added to it
Specific IgE testing – type 2/3 – blood test for IgE antibodies against specific allergen (anaphylaxis)
HLA Tetramers – type 4 - reagent used to detect antigen specific auto-reactive T cells in tissue biopsy
) What is the mechanism that leads to tissue damage in type II hypersensitivity?
Type 2 hypersensitivity is an antibody mediated immune reaction where IgG/IgM are directed to attack cellular or extracellular antigens leading to cellular destruction, functional loss and tissue damage
Cause self reactive lymphocytes released from bone marrow supposed to be destroyed release IgG or IgM bind to antigens on target cell surface activate complement cascade
What is the difference in antigen recognition between B cells and T cells? Draw a diagram to summarise the difference. Can you find and present a video to support your explanation?
B Cells
• involved in binary complex of membrane Ig and Ag
• they bind to soluble antigen
• not required in MHC molecules
• contain protein, polysaccharide, lipid
• hydrophilic, mobile peptides containing sequential or nonsequential amino acids
T cells
• involves ternary complex of T-cell receptor, Ag and MHC molecule
• they don’t bind to soluble antigen
• required to display processed antigen in MHC molecules
• mostly made of proteins, lipids and glycolipids
• internal linear peptides produced by processing of antigen and bound to MHC molecules
