HOMEOSTASIS Flashcards

Question

where does all lymph drain into

Answer 1

our l and r subclavian veins

Answer 2

one way movement due to valves. *Sequence of flow blood/capillaries-interstitial spaces0lymphatic capillaries (lymph) - lymphatic vessels (lymph) -lymphatic ducts (lymph) -junction of the internal jugular and subclavian veins (blood)-back into the venous system

Answer 3

-skeletal muscle pump -respiratory pump, changes with ventilation and smooth muscle contraction

Answer 4

red bone marrow thymus - located in mediastinum. comprised of t cells which flow into our lymph to assisst with immune response

Answer 5

lymph nodes - approx 600, contain t and b cells. filters lymph spleen- contains white pulp (b and t cell production) and red pulp (removes defective blood cells) lymphatic nodules- found in connective tissue of mucous membranes, participates in immune response

Answer 6

non specific with nil memory component 1st line - skin, mucous membranes and flora 2nd line - innate immune cells, inflammation, complement and antimicrobial substances

Answer 7

neutrophils - engulf and destroy microbes and then die "phagocytosis" macrophages- 2nd line, also engluf however they "spit out" meaning they are able to do more than neutrophils

Answer 8

5/10% of lymphocytes are NKC present in spleen, lymph nodes and bone marrow target specific cells and cause apoptosis

Answer 9

redness = blood accumulation pain = injury to neurons and toxic chemicals release by microbes heat = increased blood to area of injury swelling = interstitial fluid that has leaked out of capillaries

Answer 10

* Tissue injury  histamine is released from mast cells, basophils and platelets  vasodilation and increased blood vessel permeability  increased blood flow to area and permits antibodies and clot forming chemicals to enter area from the blood * The increased tissue permeability  clotting proteins leaked into tissues  fibrin network traps invading organisms and prevents their spread  resulting clot isolates the invading microbes and their toxins * Chemotaxis phagocytes attracted to site  immigration of neutrophils  hours pass  monocytes arrive at injury site transform into macrophages  damaged tissue, worn out neutrophils and invading microbes engulfed * Macrophages die pocket dead macrophages and damaged tissue forms pussdays

Answer 11

interleukin 1 (cytokine) are released from macrophages (monocytes)

Answer 12

production of specific cells or antibodies

Answer 13

antigen = any substance that the immune system recognises as foreign antibody (t cells) a protein produced by b cells in presence of a specific antigen, the antibody combines with the antigen to destroy it

Answer 14

made in the thymus cell mediated response attaches to cells and splits into different types * Helper t cells(regulatory): stimulate t and b cells “hurry up and mature” to incompetent or naïve b and t cells * Cytotoxic (killer) t cells kill and engulf and cause “death” * Memory t cells remembers antigen for future encounters * Suppressor t cells : inhibits once the job done

Answer 15

produced in bone marrow float around in lymphatic and interstitial space until activated response to specific antigens then become plasma cells and secrete different antibodies (plasma proteins the immunoglobins)

Answer 16

SEPSIS- Life threatening organ dysfunction* caused by dysregulated host response to infection SEPTIC SHOCK - Sepsis and vasopressor therapy needed to increase MAP greater than or equal to 65mmhg and lactate >3mm/L despite adequate fluid resuscitation. Associated with mortality in excess of 40%

Answer 17

* Lowered SVR – leads to hypotension with normal or increased cardiac output, this is due to endothelial nitric oxide production (in response to TF, by product of inflammatory processes) * Pulmonary vascular resistance rises later in infective process, causes increased right heart workload (why?) * Increased venous capacitance (holds more blood due to relaxed lumen), secondary to nitric oxide, relative hypovolemia * Increased capillary permeability, both systemic and pulmonary, fluid and albumin (maintains oncotic pressure) is lost * Clotting- TF is released, activation of the clotting cascade, both clotting and anti-clotting factors are released (clotting vs lysis ongoing), decrease in antithrombin III (anti-coagulant), inhibition of fibrinolytic system, proliferation of thrombin, lots of micro clots and/or diffuse bleeding * Hypovolemia: occurs because of increased capacitance, lowered SVR, capillary leakage, increased cellular permeability to sodium, decreased oral intake, polyuria * Cardiomyopathy: bi ventricular systolic and diastolic failure due to increased end systolic and diastolic volume, onset within 24hours, myocardium is depressed, impacts ability to compensate

Answer 18

* ARF * Oliguria * Inappropriate polyuria * Increased serum creatine and urea

Answer 19

* Hb falls * Red blood cell life span decreases * Decreased RBC production * Neutropenia occurs (low WBC count) * Thrombocytopenia(low platelet count) with or without DIC

Answer 20

* Hyperglycaemia (secondary to sympathetic drive) * Insulin resistance

Answer 21

Inflammatory agents cause vasodilation  small arterioles unable to constrict  blood pools in dilated vessels  concurrently neutrophils adhere to endothelial walls  increased capillary membrane permeability  profound hypovolemia  reduction in tissue perfusion  activation of extrinsic clotting system clotting cascade and platelet activity  release of plasminogen activator inhibitor 1  decreased fibrinolytic response DIC  increased clotting and Vaso regulatory dysfunction  decreased blood flow  decreased oxygen delivery to tissues  tissue hypoxia  anaerobic metabolism  lactic acidosis metabolic acidosis  increased respiratory rate

Answer 22

heat redness swelling pain loss of function

Answer 23

* Vasodilation (increased blood flow) * Increased vascular permeability (plasma leakage) * Diapedesis – migration of WBC to injury site

Answer 24

- part of innate immunity - a group of plasma proteins that opsonise pathogens and create inflammatory response - Inactive until injury or infection occurs - Attacking chemical compounds via MAC (kills things via cell lysis) Has 3 different pathways for how it works Classic pathway- antigen and antibody complex and then triggers off the cascade working towards cell lysis Lectin pathway Alternative pathway

Answer 25

- Activated when exposed to damaged tissue(damage to endothelium and sub-endothelial layer (Hageman factor) which then releases Factor 12a - Factor 12 and 12a causes cascade of kinin system - Prevents spread of infection - Traps micro-organisms in damaged area via clot formation - Framework for repair and healing - Main substance is fibrin (mesh that holds clot together) - Fibrinopeptides are chemotaxic, increased permeability to area and also enhances the effects of bradykinin

Answer 26

Release of Bradykinin….causes more dilation of blood vessels, stimulates nerve endings causing pain, causes smooth muscle contraction, Increases vascular permeability and increases leukocyte chemotaxis

Answer 27

released from mast cells causes temporary rapid constriction of large vessel walls but dilates post capillary venules, causing increased blood flow into the microcirculation, this then causes retraction of endothelial cells lining capillaries increasing permeability. This creates a swollen and leaky area primed for inflammatory response and movement of factors of inflammation into the area

Answer 28

must be 2 weeks or longer follows unsuccessful acute inflammatory response characterised by dense infiltration of lymphocytes and macrophages causes granulomas

Answer 29

Acute systemic inflammatory response reaction to a previously exposed antigen resulting in an exaggerated immune response and eventual cardiovascular collapse

Answer 30

a protein that helps reduce the immune response binds to an antigen and promotes phagocytosis

Answer 31

initiated when a circulating antibody (IgE or IgM) combines with foreign antigen

Answer 32

IgE antibodies bind to mast cells or basophils resulting in mild reaction to anaphalaxis

Answer 33

First exposure  antigen enters via skin/GIT/airway/IVstimulation of B lymphocytes to produce IgE antibodies  igE will attach to mast cells and basophil membranes  mast cell destabilisation  release of inflammatory mediators  increased capillary membrane permeability intravascular fluid leakage oedema/angioedema/stridor (laryngeal oedema)/wheeze (bronchial oedema)/urticaria  vasodilation of capillaries and venules  hypotensionrelative hypovolemia reduced preload and SV  decreased CO  decreased tissue perfusion  anaerobic metabolism  contraction of vascular smooth muscle (especially in GIT and bronchial tree)  bronchospasm/laryngospasm/cramps/N/V/D

Answer 34

increased cAMP production which stabilises mast cells leading to decreased inflammatory mediator release activates an alternate pathway (if BBLOCKED) via g coupled proteins

Answer 35

* Loss of 15-20% circulating blood volume before we start to see signs and symptoms * Causes external loss, plasma (burns, also distributive shock), extracellular (GIT loss/dehydration) * Sympathetic mediated ^HR and vasoconstriction to maintain BP

Answer 36

* Failure to eject blood from hearthypotension and decreased cardiac output * Occurs rapidly most common cause is AMI * Can follow other types of shock or occur secondary to substances released into blood stream * Causes: inadequate filling, poor contractility, obstruction of blood flow from heart to central circulation  AMI/Arrthymia/tamponade/contusion/TPT/severe vascular disease/cardiomyopathy/PE/AA

Answer 37

* Loss of blood pressure tone, enlargement of vascular compartment, displacement of vascular volume away from systemic circulation * You’ve got good volume its just sitting in the wrong areas and poor return back to the heart * Causes of tone reduction: decreased sympathetic control of vasomotor tone, vasodilators, vessel damage * 3 shocked states share the umbrella term  septic, anaphylactic and neurogenic

Answer 38

caused by decreased sympathetic control of blood vessel tone (brain injury, anaesthetic agents, hypoxia, hypoglycaemia)  defect in sympathetic outflow to blood vessels = Bradycardia (decreased force of contraction), warm dry skin

Answer 39

* Obstruction outside of the cardiac tissue * Mechanical obstruction of the outflow of blood * Causes: tamponade, TPT, PE * Physiological effects: increased r sided heart pressure(trying to pump against pressure in pulmonary circulation or backflow of blood into LV) decreased preload * Increase central venous pressure and JVD

Answer 40

-initial stage -compensatory stage (think sympathetic stimulation) -progressive stage, starting to fail, fluid is leaving capillaries, sluggish blood flow, cells and enzymes becoming damaged -irreversible stage - vital organ failure and cellular death

Answer 41

* Sympathetic mediated response (HR BP vasoconstriction) * RAAS (ADH released from pituitary gland, triggers salt and water retention, peripheral vasoconstriction) * Adrenaline and nor adrenaline released from adrenal glands

Answer 42

- Fluid leakage from intravascular, into interstitial into alveolar space = surfactant wash out and impaired gas exchange - Decrease oxygenation then further compounds shock process - Neutrophils thought to play key role - Cytokine mediated activation and accumulation of neutrophils in pulmonary vasculature

Answer 43

Acute tubular necrosis/ischemia: renal lesion most frequently seen in post severe shock, usually reversible, weeks to months duration - Can be reversible but depends on duration and severity

Answer 44

results from redistribution of blood flow resulting in diminished mucosal perfusion... vulnrable to ischaemia

Answer 45

Progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to severe injury or illness - Progresses to organ failure and death - Causes sepsis/septic shock/major surgery/ acute pancreatitis/ any disease initiating inflammatory response