HOMEOSTASIS Flashcards
Total body mass of water between males and females? Why do we see a difference?
55% is fluid in females. 60% in males. We see a difference based on lean muscle mass. Muscles contain lots of water.
What are the two main compartments of fluid in the body?
intracellular (2/3 body fluid) and extracellular (1/3) comprised of interstitial fluid 80% and plasma 20%
What are the two barriers that seperate the intracellular, interstitial and blood plasma
the plasma membrane and blood vessel walls
How does aerobic respiration assisst with water regulation or gain?
metabolic synthesis- water is produced as a by product through glycolysis, krebs cycle and electron transport system. Up to 200mls per day
Where is the thirst centre found and how does it regulate body water.
hypothalamus. detects via thirst signals –> decrease in bp secondary to decreased blood volume.
neurons in mouth detect dryness
baroreceptors detect hypotension
triggered after a 2% reduction in volume
Hormones that regulate renal sodium and chloride reabsorption
macular densar cells release prostaglandins
juxtglomerular cells (kidney) relase Renin –> secondary to reduction in GFR
stimulates angiotensinogen from liver
converts to angiotensin 1
this acts on endothelial cells
angiotensin 2 –> primary role is to act on smooth muscle cells and cause vasoconstriction (^resistance) and stimulate thirst centre in hypothalamus
kidneys increase volume through decreased excretion = ^ SV
Pituitary gland releases ADH –> smooth muscle contraction and acts on kidneys
Adrenal glands release aldosterone –> acts on kidneys
What is atrial natriuretic peptide (ANP)
Myocytes begin to stretch due to increased volume and this send signals to stop releasing aldosterone. This promotes natruresis = elevated urinary excretion of Na and CI accompanied by water. = increased loss of water in urine. Helps maintain homeostasis.
4 functions of electrolytes in the body
-control the osmosis of water between fluid compartments
-helps maintain acid base balance
-carries electrical current
-serves as cofactors
Sodium- normal level and roles
-135 to 145
-maintains osmolarity, where sodium goes water follows
-transmits nerve impulses
Hyper vs hyponatremia
Hyper >145
Hypo <135
Potassium normal levels and roles
-3.5-5.5
-most abdundant in ICF
-mostly controlled by aldosterone
Hypo vs HyperK
HyperK >5.5, look for flatterned p wave and widened QRS
Hypo <3.5
Acid vs base vs buffer
acid = proton (h+) donor
base = proton acceptor
buffer = solution that can maintain a nearly constant pH even if it is diluted
Removal of H+ ions from the body relies on what 3 mechanisms
-exhalation co2
- buffer system
- kidney excretion of H+
what are the 3 buffer systems of body fluids
-protein buffer system (albumin)
-phosphate buffer system
-carbonic acid buffer system
Describe the carbonic acid buffering system
CO2 + H20 <- -> H2CO3 <–> H+ + HC03-
When CO2 increases the reaction is driven to the right
when CO2 decreases the reaction is driven to the left
Compensation mechanisms for changes in blood pH
Resp increase or decrease- occurs within mins.
renal - if pH is abnormal secondary to respiratory causes. Renal tubules will change either excretion of H+ or HCO3-. Begins in minutes but takes days to reach max
Respiratory acidosis
ABGl level
conditions that cause it
pCO2 >45MMHG
Any condition that DECREASES the movement of co2 from the blood to the atmosphere, causes increase in co2, H2CO3 and H+
(not breathing enough/hypoxic/build up co2)
emphysema/APO/injury to medulla oblongata/AO/pneumonia
respiratory alkalosis
AGB
Conditions
pCO2 <35mmhg
hyperventilation is main cause
(high altititude/CVA/anxiety/pulmonary disease)
Metabolic acidosis
pH <7.35 and low HC03 (<22mEq/L)
causes: loss of HCO3 (diarrhoea/renal dysfunction), accumulation of an acid (DKA), failure of kidneys to remove H+
Metabolic Alkalosis
pH >7.45, and elevated ABG HCO3 (>26mEq/l)
excessive vomitting/severe dehydration, diuretics, endocrine disrupters, increased intake of antacids
define lymph
interstitial fluid that has passed into lymphatic vessels
functions of lymphatic system (3)
-drains interstitial fluid
-transports dietary lipids
-carries out immune response
what is a lymph trunk
where lymphatic vessels and lymph nodes unite, this is where we see drainage into our venous system
where does all lymph drain into
our l and r subclavian veins
describe flow of lymph
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
two main pumps to assisst with flow of lymph
-skeletal muscle pump
-respiratory pump, changes with ventilation and smooth muscle contraction
primary lymphatic organs
red bone marrow
thymus - located in mediastinum. comprised of t cells which flow into our lymph to assisst with immune response
secondary lymphatic organs
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
describe innate immunity
non specific with nil memory component
1st line - skin, mucous membranes and flora
2nd line - innate immune cells, inflammation, complement and antimicrobial substances
describe two types of phagocytes
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
natural killer cells
5/10% of lymphocytes are NKC
present in spleen, lymph nodes and bone marrow
target specific cells and cause apoptosis
describe 4 parts of inflammation
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
describe 4 stages of inflammation
ie patho
- 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 pussdays
what causes a fever
interleukin 1 (cytokine) are released from macrophages (monocytes)
what is adapative immunity
production of specific cells or antibodies
antigen vs antibody
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
what are t cells
where are they made
types of t cells
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
what are b cells
produced where
found where
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)
Sepsis vs septic shock
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%
cardiovascular patho of sepsis
- 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
Renal issues in sepsis
- ARF
- Oliguria
- Inappropriate polyuria
- Increased serum creatine and urea
Haematologic issues in sepsis
- Hb falls
- Red blood cell life span decreases
- Decreased RBC production
- Neutropenia occurs (low WBC count)
- Thrombocytopenia(low platelet count) with or without DIC
Endocrine issues in sepsis
ie issues with blood sugars and insulin
- Hyperglycaemia (secondary to sympathetic drive)
- Insulin resistance
Septic shock patho
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
5 cardinal signs of inflammation
heat
redness
swelling
pain
loss of function
3 important processed for the vascular response of inflammation
- Vasodilation (increased blood flow)
- Increased vascular permeability (plasma leakage)
- Diapedesis – migration of WBC to injury site
Plasma proteins and healing - 3 interrelated systems
THE COMPLEMENT SYSTEM
- 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
Plasma proteins and healing - 3 interrelated systems
THE CLOTTING SYSTEM
- 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
Plasma proteins and healing - 3 interrelated systems
THE KININ SYSTEM
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
How does histamine contribute to the inflammatory response
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
Define chronic inflammation
must be 2 weeks or longer
follows unsuccessful acute inflammatory response
characterised by dense infiltration of lymphocytes and macrophages
causes granulomas
Define anaphalaxis
Acute systemic inflammatory response reaction to a previously exposed antigen resulting in an exaggerated immune response and eventual cardiovascular collapse
what is an opsonin
a protein that helps reduce the immune response
binds to an antigen and promotes phagocytosis
what is a type II or III hypersensitivity reaction
initiated when a circulating antibody (IgE or IgM) combines with foreign antigen
what is a type I or IV sensitive or hypersensitive reaction
IgE antibodies bind to mast cells or basophils resulting in mild reaction to anaphalaxis
Anaphalaxis patho
First exposure antigen enters via skin/GIT/airway/IVstimulation 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 hypotensionrelative 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
Glucagon use in anaphalaxis
increased cAMP production which stabilises mast cells leading to decreased inflammatory mediator release
activates an alternate pathway (if BBLOCKED) via g coupled proteins
Hypovolemic shock
- 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
cardiogenic shock
- Failure to eject blood from hearthypotension 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
distributive shock
- 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
Neurogenic shock
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
Obstructive shock
- 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
Stages of shock
-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
Compensatory mechanisms for shock
- 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
complications of shock - ARDS
- 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
complications of shock - ARF
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
Complications of shock - GI
results from redistribution of blood flow resulting in diminished mucosal perfusion… vulnrable to ischaemia
what is MODS
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
