Haemdynamic disorders and inflamation and cell injury Flashcards Preview

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Flashcards in Haemdynamic disorders and inflamation and cell injury Deck (19):

Describe bodily fluids in human. How much is there? What is it? Where is it in the body

Water makes up around 60% of men weight and 50% of women.
Fluids can either be extracellular-45% of body water (19L)
made of Blood: 3L, Interstitial 1.5L and transcellular 1L
The other liquids are intraccellular-about 55% of body water-23L


What is oedoema? How can they be categorised? What are the causes? And consequences?

Oedema is abornmal increase in Interstitial fluid -normally hydrostatic pressure and plasma oncotic pressure balance - at the end of arteties, hydro>onco (fluid comes out), at veins, Onco>hdyro (fluid goes in). Endothelial permeability also plays a role
Usually categorised as localised (like cerebral or pulmonary) or generalised (fluid in serous cavities >5L)(caused by congestive heart failure, hypoproteinaneamia, Nutrition)
5 main causes of : Increased hydrostatic pressure-heart failure can lead to increases
Reduced plasma oncotic pressure (reduced protein/albumin)-albumin controls oncotic pressure-can cause generalised oedema-caused by proteins loss
Lymphatic obsutruction: Localised to where blocked-usually very protein rich oedema, (can be obstructed tumor, inflamation, etc)
Sodium retention-Reduced cardiac output can lead to sodium retention and generalised oedema
Inflamation-loss of epithelial permeability


What is thrombosis? Can you remember a triad in that? Remember main categories, causes and outcomes

thrombosis is abnormal blood clotting in ciruclation-usually categorised as veinous or aterial
3 causes: Endothelial injury, Statis/Turbulant blood flow, Blood hypercoagulability =>these are 3 of Virchows triad (2 should cause thrombosis)
Triad: Endothelial injury-Injury leads to platelet activation, which coagulate. arteries have high blood flow-therefore prone to injury with shear stress
Stasis/turbulant blood flow-Turbulant flow cause injury. Disruption of laminar blood flow-venous thrombi. Turbulant blow can cause arterial and veinous thrombi
Blood hypercoagulability-Blood disorder-can be primary (like Factor V, prot C deficiency)or secondary (like obesity, cancer, age, pill)
2 types of thrombus- pale (fibrin and platelets) and red (fibrin, platelets and rbc)
venous-occlusive thrombi due to sluggish blood flow. usually Rbc>platelets. can develop in healthy peeps-veins in leg most affected-characteristic appearence of lines of Zahn
Arterial-Occlusive-platelet, rbc, fibrin, leucocytes-mostly coronary > cerebral > femoral ateries-due to ruptures artherisclerotic plaques (enothelial injurt and abnormal blood flow)
Fate of Thrombi-Propagation-accumulate if semiocclusive (and spread), Embolisation (dislodge and move to anotherplace), dissolution (fibrinolysis), organisation and recanalisation (old thrombi are vascularised, have SMC and endothelial cells-cappilaries in them)


What is Embolism? How do they arise? What are risk factors? give Exemples of emboli consequences

Emboli is abnormal material in circulatory sysytem that is carried in blood to somewhere distant-90% are caused by thrombi. Others-vegetation (from artificial valves), Gas, Fat (fractures), tumour, amniotic fluid, foreign material
It is very linked with deep vei thrombosis-risk factors being immobility, trauma, contraceptive pill, tumours, obesity, past DVT, age, pregnancy
Pulmonary Emboli-can originate from DVT-can be silent (asymptomatic) or can cause suddent death
Systemic emboli (arise is arteries)-dislodged artheromatus or thrombi from within heart (caused by cardio death or arterial fibrillation
Arterial emboli-TIA, stroke, bowel, limb


What is infraction? What are the main causes? THe main types?

Infraction is the necrosis of tissue due to ischemia (no o2)-most commonly caused by thrombi or embolic occlusion
Can be red (occur in venous occlusion-loose tissue (lung), organs with dual circulation (lung, bowel), can reperfuse at site or previous occlusion
Or White (result of arterial occulsion, in DENSE organs
usually start sublte and increase with time-and usually wedge shaped
Myocardial infraction-most common cause if coronary artery occlusion (thrombus in coronary artery), but can be caused by Coronary artero vasoplas, emboli, vasculitis, heamotological abnormalities (like sickle cell)=> leads to cardiomycote death


What is haemorrage? What are the causes? What is shock?

Extravasation of blood due to vessel rupture
can be due to trauma or intrisic disease (amyloid, collagen vascular diseases)-rupture of major vessel cause acute heamorrhage with risk of hypovaleamia (low blood pressure) shock and death
Shock is systemic hypotension due to reduced cirulatory volume or reduced cardiac output-results in hypoxia and ischemia
Cadiogenic shock (heart isnt working properly-many causes
Hypovaleamic shock- loss of blood due to traumaor hemmorrhage
Septic shock-infection activates immune system-vasodilation and pooling of blood
Neurogenic shock-loss of vascular tone, cord injury, aneastetic medication


What is inflammation? What can cause it? What are the 3 main types of inflamation? Why is it important?

Inflammation is a complex cellular reaction in viable vascularised tissue in response to injury-its a protective response geared towards clearing the cause and repairing damage. very tighly regulated by the immune system
Its caused by damage, which activates numerous cells of the immune system, namely-Neutrophils, macrophages, lymphocytes, eosinophils, mast cells, and soluble factors like AB, cytokines, Complement and coagulation
3 main types are acute, chronic and granulomous
Acute-rapid non specific, orchestrated by mediators released by injured cells, leukocytes and vascular response
Chronic-long term persistant inflammation-cycle of inflamation and repair at the same time-can arise from acute
granulomous is a speficic type of chronic-subset
Its important because many diseases can cause it, and can underlie many disease states (innaporpirate response, innadapted, chronic, granulomous) and diseases (infection, AID, allergy, trauma, chronic diseases)


What are signs of acute inflammation? What is the pathophysiology behind acute inflammation?

Signs of acute inflamation are: Rubor (redness), Calor (heat), tumor (swelling) and dolor (pain) -4 ors and they appear quickly
Acute inflammation has rapid delivet of leukocytes and proteins to site of injury-and main features and alteration of blood vessels to increase flow, structural changes of blood vessels to allow passage and activation of leukocytes at injury


Explain vasodilation and increased permeability in acute inflammation. Describe exudate and Transudate

Vasodilation is earliest sign of inflammation-cause heat and redness. Mostly induced by histamine (mast cells), NO (endothelial at damage), and complement system (C3a/C5a and IL1/IL8-quickly followed by increased permeability (leads to stasis by increasing fluid slow down and fluid loss)-dysregulation is what leads to allergy
Permeability-endothelial contract, increasing spacing-immediate response to injury. Can also be caused by toxin damage (smoking), leukocytes and VEGF
Inflammation caused Exudate-result of increased permeability-rich in protein (fibrin, AB), contains cell and cell debris, can be leukocyte rich
Transudate is caused by imbalance between hydrostatic and oncostatic -low protein content, low cell content (usually oedema)
The role of exudate is to dilute pathogens, wall them off, allow spread of mediators, provide substrate for inflamatory cell migration-but fluid loss can be dangerous


Describe the leukocyte response in acute inflammation. Describe how they enter the injury, what they do and the main mediators of inflammation
Describe termination of the response

Main leukocytes are neutrophils and macrophages-kill bacteria, eliminate foreign and dead material, produce factors for inflammation-harmful in long term
Neutrophils are BM produced, and circulate in blood normally-first one to response, main role is to kill bacteria and recruit other cells (degranulate)
Neutrophils enter the injury similarly to HEV-Margination, bind slelectin, roll, bind integring, adhere, then diapedesis
Phagocytosis is the first main defence-needs attachment, englufment and degradation/killing-O2 dependent (ROS, RNS, NOO-,) or O2 independent (enzymes)
Key mediators-Histamine (vasodilation and permeability_, prostaglandins (vaso, pain, fever), cytokines (endothelial activation, leuko active, systemic response), chemokine (recruiting other cells), complement (activate, opsionise, kill, inflamation, etc)
Termination-mediators and neutrophils have short half life, macrophages M2 release anti-inflammatory products, mast cells and lymphocytes also stop it (tReg, lipoxin)-need cause of injury to be removed


What is chonic inflammation? Describe its characteristics, the main cell type acting

Chronic inflammation-prolonged duration during which inflammation, injurt and repair all coexist-can follow from inflammation, but can arise from low grade smouldering inflammation (persistent (mycobacteria), prolonged exposure to toxin (pollution, etc), AID, foreign body (implant)
Very different from acute-usually mononuclear cells in injury (macrophage and lymphocytes), tissue destruction induced by cells or inflammatory agents-and attemps at healing cause replacement tissue (granulation tissue, of fribrosis and angiogenesis-loss of function)
Main cell type is macrophages-normally not much as monocytes-become different types of macro in tissue
Role as phagocytosis, Amplification of inflam (M1), repair and anti inflam (M2)
In chronic, M1 persist and cause significant destruction, and cascade can also cause M2 to also try and repair, and also can lead to acute inflam (chronic and acute can coexist)
Other cells types-T and B cells act (usually CD4 and plasma), eaosinophils, mast cells, neutrophils (if acute also), and lots of angiogenesis (VEGF)


What is granulomous inflammation? What are the causes

Distinct pattern of chronic inflam, showing granuloma formation-granuloma is aggrgate of macrophages trying to eliminate an agent-triggered usually by Tcell response
Caused by-infection (low grade-TB, syphilis), foreign material, tumour, granulomous disease (chrons)


What are long term sequelae of inflammation? List positive and undersirable outcomes

Positive-removal of agent, cease reponse and repair tissue without loss of function. undesirable-excessive damage-loss of function and scar, systemic involvment and multiorgan failure (shock)


Describe wound healing and what are the possible outcomes? Also mention complications and impairments of wound healing

Wound healing always finishes in scarring or resolution-resolution is regeneration of parenchymal cells (main cells). Scarring invloves remaking tissue-angiogenesus, fibroblast repair (cant remake original cell type-loss of function)
can also get resolution with some scarring-the outside of the injury where not much damaged is repaired-and if large damage-not even same cell types-no function
Impaired wound healing can be due to-poor nutrition (energy, vitamics C,A, Minerals (zInc), supressed inflam (steroids, age), poor local blood supply, persistant foreing body, movement)
Complication include keyloid scars, healing in the wrong position (especially with bone), or necrosis of tissue and scarring at wrong places (like heart)


Recall the triad of cell survival, describe the 2 types of cell injury, and list the main causes of cell injury

The triad starts with a normal cell-with stress/increased demand, try to adapt. if cannot, cell death. And injurious stimulus can lead a cell directly to death
Injuries can be lethal-induce cell death, or sublethal-injury not result in death, can be reversible or progess to death
Main sources are: Oxygen depravation, chemical agents, infectious agents, Immune reaction, Genetic defects, Nutrition, Physical agents, age


Recall and explain the mechanism of cell injury, and the main adaptation methods

Cellular response will depend to type of injury, duration and severity, and the consequences will depend on the type of cell and its status
4 intracellular systems are particularly vulnerable-cell membrane integrity, ATP generation, protein synthesis, integrity of genomes-not vulnerable but so very important-any changes can be lethal
Because biochemisty is fast and so interconnected, secondary effects are rapid-function loss before cell death cause morpholigical changes


List the main adaptation methods of cells to injury

Atrophy: Shrinkage of cell or organ due to loss of cell substance-happens in dementia, or muscle after denervation
Hypertrophy-increase of the cell or organ size-can be physio or pathological => caused weither by increased functional demand or hormonal stimulation eg:Uterus during pregancy, atrophy of myocytes after blockage/increased load
Hyperplasia-increase of the amount of cells in organ-can be physio (compensationy or hormonal) or patho (excessive hormone or GF stimulation) eg: normal-proliferative endometrium, pathological-carcinoma
Dysplasia-precancerous growth-genetic or cytological features of malignancy-but non invading. eg cells that start invaginating, or barrets oesophagus
Metaplasia-reversible change of differentiation of adult cell-can be physio or patho-in cervix, or damaged Barrets oesophagus (lose epithelium)


What are the light microscopic feature changes associated with reversible injury? And irreversible injury?

Fatty acid change-alcoholic fatty change cause small white holes in microscope; cellular swelling-balloning degenration (larger holes)
irreversible: Coagulative necrosis, liquefactive necrosis, caseous necrosis, fat necrosis
Coagulative necro: achitecture preserved for a bit (usually due to oxygen lack)-lighter tissue and no nucleus
Liquefactive necrosis-transformation into liquid mass-complete lack or archi or even cells-show as big black mass on MRI (brain infact)-fungi and stuff
Caseous Necrosis: cells forms a dense cell mass-ressembling cheese/bread-soft and white mass. -Histology-pink anuclear, granuloma around -TB, low smouldering infection (chronic inflam)
Fat necrosis: dead cells release lipase that eat TAG and release fatty acids-become large white foamy wholes


What is the difference between apoptosis and necrosis? List the main causes of each and their features

Apoptosis-cell collapses on itself, not disseminating its content-then eaten by macrophages. necrosis-cell explodes, enzymatic digestion to clear by release inside
Apop causes:-embryogenesis, deletion of autoreactive t cells, homrones dependent involution, cell deletion in proliferating pops, variety of small stimule that cause irreperable DNA damage and trigger suicude pathway
Apotosis can be physiological-and is an active energy process. Also NOT associated with inflammation
Necrosis-confluent cell death associated with inflammation
AND ANOTHER ONE EXISTS: Necroptosis: programmed cell death associated with inflammation-many caused (like viral infetion, CTL cells, etc)