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FOUNDATIONS > HOMEOSTASIS > Flashcards

HOMEOSTASIS Flashcards

1
Q

Total body mass of water between males and females? Why do we see a difference?

A

55% is fluid in females. 60% in males. We see a difference based on lean muscle mass. Muscles contain lots of water.

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2
Q

What are the two main compartments of fluid in the body?

A

intracellular (2/3 body fluid) and extracellular (1/3) comprised of interstitial fluid 80% and plasma 20%

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3
Q

What are the two barriers that seperate the intracellular, interstitial and blood plasma

A

the plasma membrane and blood vessel walls

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4
Q

How does aerobic respiration assisst with water regulation or gain?

A

metabolic synthesis- water is produced as a by product through glycolysis, krebs cycle and electron transport system. Up to 200mls per day

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5
Q

Where is the thirst centre found and how does it regulate body water.

A

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

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6
Q

Hormones that regulate renal sodium and chloride reabsorption

A

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

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7
Q

What is atrial natriuretic peptide (ANP)

A

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.

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8
Q

4 functions of electrolytes in the body

A

-control the osmosis of water between fluid compartments
-helps maintain acid base balance
-carries electrical current
-serves as cofactors

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9
Q

Sodium- normal level and roles

A

-135 to 145
-maintains osmolarity, where sodium goes water follows
-transmits nerve impulses

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10
Q

Hyper vs hyponatremia

A

Hyper >145
Hypo <135

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11
Q

Potassium normal levels and roles

A

-3.5-5.5
-most abdundant in ICF
-mostly controlled by aldosterone

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12
Q

Hypo vs HyperK

A

HyperK >5.5, look for flatterned p wave and widened QRS
Hypo <3.5

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13
Q

Acid vs base vs buffer

A

acid = proton (h+) donor
base = proton acceptor
buffer = solution that can maintain a nearly constant pH even if it is diluted

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14
Q

Removal of H+ ions from the body relies on what 3 mechanisms

A

-exhalation co2
- buffer system
- kidney excretion of H+

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15
Q

what are the 3 buffer systems of body fluids

A

-protein buffer system (albumin)
-phosphate buffer system
-carbonic acid buffer system

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16
Q

Describe the carbonic acid buffering system

A

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

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17
Q

Compensation mechanisms for changes in blood pH

A

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

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18
Q

Respiratory acidosis

ABGl level
conditions that cause it

A

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

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19
Q

respiratory alkalosis

AGB
Conditions

A

pCO2 <35mmhg
hyperventilation is main cause
(high altititude/CVA/anxiety/pulmonary disease)

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20
Q

Metabolic acidosis

A

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+

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21
Q

Metabolic Alkalosis

A

pH >7.45, and elevated ABG HCO3 (>26mEq/l)
excessive vomitting/severe dehydration, diuretics, endocrine disrupters, increased intake of antacids

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22
Q

define lymph

A

interstitial fluid that has passed into lymphatic vessels

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23
Q

functions of lymphatic system (3)

A

-drains interstitial fluid
-transports dietary lipids
-carries out immune response

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24
Q

what is a lymph trunk

A

where lymphatic vessels and lymph nodes unite, this is where we see drainage into our venous system

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25
Q

where does all lymph drain into

A

our l and r subclavian veins

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26
Q

describe flow of lymph

A

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

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27
Q

two main pumps to assisst with flow of lymph

A

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

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28
Q

primary lymphatic organs

A

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

29
Q

secondary lymphatic organs

A

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

30
Q

describe innate immunity

A

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

31
Q

describe two types of phagocytes

A

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

32
Q

natural killer cells

A

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

33
Q

describe 4 parts of inflammation

A

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

34
Q

describe 4 stages of inflammation

ie patho

A
  • 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
35
Q

what causes a fever

A

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

36
Q

what is adapative immunity

A

production of specific cells or antibodies

37
Q

antigen vs antibody

A

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

38
Q

what are t cells

where are they made
types of t cells

A

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

39
Q

what are b cells

produced where
found where

A

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)

40
Q

Sepsis vs septic shock

A

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%

41
Q

cardiovascular patho of sepsis

A
  • 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
42
Q

Renal issues in sepsis

A
  • ARF
  • Oliguria
  • Inappropriate polyuria
  • Increased serum creatine and urea
43
Q

Haematologic issues in sepsis

A
  • Hb falls
  • Red blood cell life span decreases
  • Decreased RBC production
  • Neutropenia occurs (low WBC count)
  • Thrombocytopenia(low platelet count) with or without DIC
44
Q

Endocrine issues in sepsis

ie issues with blood sugars and insulin

A
  • Hyperglycaemia (secondary to sympathetic drive)
  • Insulin resistance
45
Q

Septic shock patho

A

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

46
Q

5 cardinal signs of inflammation

A

heat
redness
swelling
pain
loss of function

47
Q

3 important processed for the vascular response of inflammation

A
  • Vasodilation (increased blood flow)
  • Increased vascular permeability (plasma leakage)
  • Diapedesis – migration of WBC to injury site
48
Q

Plasma proteins and healing - 3 interrelated systems
THE COMPLEMENT SYSTEM

A
  • 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
49
Q

Plasma proteins and healing - 3 interrelated systems
THE CLOTTING SYSTEM

A
  • 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
50
Q

Plasma proteins and healing - 3 interrelated systems
THE KININ SYSTEM

A

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

51
Q

How does histamine contribute to the inflammatory response

A

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

52
Q

Define chronic inflammation

A

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

53
Q

Define anaphalaxis

A

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

54
Q

what is an opsonin

A

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

55
Q

what is a type II or III hypersensitivity reaction

A

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

56
Q

what is a type I or IV sensitive or hypersensitive reaction

A

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

57
Q

Anaphalaxis patho

A

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

58
Q

Glucagon use in anaphalaxis

A

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

59
Q

Hypovolemic shock

A
  • 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
60
Q

cardiogenic shock

A
  • 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
61
Q

distributive shock

A
  • 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
62
Q

Neurogenic shock

A

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

63
Q

Obstructive shock

A
  • 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
64
Q

Stages of shock

A

-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

65
Q

Compensatory mechanisms for shock

A
  • 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
66
Q

complications of shock - ARDS

A
  • 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
67
Q

complications of shock - ARF

A

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

68
Q

Complications of shock - GI

A

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

69
Q

what is MODS

A

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

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