Shock and Hemorrhage; Aging Flashcards
definition of shock
when the heart is unable to perfuse the organs after hemorrhage caused by trauma
signs and symptoms of shock
Pallor (unhealthy paleness)
Cold Sweat
Weak or Undetectable Pulse
Loss of Sensibility
Muscular Collapse
Weakness of Cardiac Action
describe the initial response to hemorrhage in terms of what happens to the following:
venous return
central venous pressure
arterial pressure
cardiac output
vasculature (constriction or dilation)
What does your cardiac function curve look like? (i.e. areyou higher or lower on the curve for venous return/CO?)
Initial response to hemorrhage:
Vasoconstriction; mainly in the arteries than in the veins
The central venous pressure decreases as a result of blood loss, which decreases mean arterial pressure
Lower on curve for venous return; same curve for cardiac function
what’s the next response following the initial response to hemorrhage?
what happens to the following:
TPR
arterial pressure
CO
Increase in TPR
TPR goes up, which increases arterial pressure, but there’s still a decrease in cardiac output
what’s the effect of increasing cardiac contractility after hemorrhage?
is there a change in CVP?
Increasing contractility raises arterial pressure, which raises cardiac output
CVP doesn’t change
next response following increasing in cardiac contractility during hemorrhage
what happens to:
preload
arterial pressure
cardiac output
increasing venous tone
preload increases (more blood pushed into the heart)
arterial pressure increases
cardiac output increases
reflex response to hemorrhage:
blood loss and decreased blood pressure sensed by atrial stretch and baroreceptors. After sending signal to the brain, which 3 areas are impacted?
Sympathetic nervous system
Adrenal gland
Pituitary gland
Sympathetic nervous system response to hemorrhage (what happens to heart and sm ms in the blood vessels?)
Heart contraction; vasoconstriction
The Adrenal releases ___ which help in contractility and vasoconstriction; cortisol helps somehow (probably by increasing plasma osmolality)
catecholamines
The pituitary releases ACTH which promotes ___; and ___ which promotes free water retention and vasoconstriction
Proteolysis
Vasopressin
what’s the effect of decreased arterial pressure (on the kidney)?
Decreased arterial pressure: promotes Renin release and subsequent activation of the RAAS
which hormones are released from the following in response to hemorrhage?
Adrenomedullary (mine cats)
Pituitary (2)
Adrenocortical (2)
Kidney (rainin)
Pancreatic (G)
what’s the function of the hormones released?
Adrenomedullary – Catecholamines
Pituitary – ACTH and Vasopressin
Adrenocortical – Aldosterone and Cortisol
Kidney – Renin-Angiotensin
Pancreatic – Glucagon with Inadequate Insulin Secretion
net effects of hormonal response to hemorrhage (i.e. cardiovascular; conserving; metabolic)
Cardiovascular –Vasoconstriction & Cardiac contractility
Conserving – Antidiuresis & Sodium Retention
Metabolic – Catabolism leading to Hyperglycemia
Provides Glucose to Brain and Heart
Raises Extracellular Osmolality to Draw Fluid from the Intracellular to the Extracellular Compartment
metabolic response to hemorrhage:
what’s the function of the following/what happens in the following:
Cortisol
Liver
Adipose tissue
Sympathetic syst
Cortisol - proteolysis (muscle); proteins: broken down into aa’s >> osmolar solutes
Liver – increase gluconeogenesis and glycogenolysis
Adipose tissue – fatty acid oxidation; FFAs used for energy, glycerol for gluconeogenesis
Sympathetic syst – glucagon release in excess of insulin
what promotes the transcapillary refill? (think of the starling equation. what would increase plasma protein conc and thus water retention?)
Refill is reflected by changes in ___ and ___
Decreased Hydrostatic Capillary Pressure, Pc
Increased Hydrostatic Pressure in the Interstitium, Pi
Increased Capillary Oncotic Pressure, pc
how is blood volume restored during the transcapillary refill (what are the steps?)
- Blood loss from the intravascular space fluid causes decrease in hydrostatic pressure (increase in oncotic pressure); fluid enters from the interstitium into the intravascular space; hct goes down b/c increased fluid dilutes it out
- Hormonal and other responses start to kick in so that increases plasma osmolality, which in turn causes fluid to be drawn from the intracellular space
- At some point, convective movement of interstitial protein thru large pores >> increased lymphatic return
what happens to hct during transcapillary refill?
hct stays low because no blood added
Time course of compensation to hemorrhage (arrange the following:)
Movement of water
Hormonal response
Reflex vasoconstriction
Synthesis of new protein
Lymphatic return of protein
- Movement of water – a second
- Reflex vasoconstriction – seconds
- Hormonal response – minutes
–Increased vascular tone
–Glycogenolysis
- Lymphatic return of protein – hours
- Synthesis of new protein - day
stages of shock (and changes in blood loss %, pulse, bp and CO)
Stage 1: lose less than 2 units of blood; fairly normal everything
Stage 2: 2 units of blood loss
Stage 3: 3-4 loss; hypotensive, feel weak
Stage 4: lost more than 4 units of blood, everything is out of whack
factors that respond poorly to fluid resuscitation
- Failure of Cells to Maintain a Sodium Gradient
- Bacterial Translocation across the Gut
- Activation of Inflammatory Pathways
- Myocardial Depression
- Ischemia-Reperfusion Injury
Mitochondrial Dysfunction
therapies for hemorrhagic shock
Control the bleeding >> give IV fluids to get optimal cardiac output >> give blood transfusion for severe bleeding >> give adjuncts to prevent irreversible shock
what are the “adjuncts” used to prevent irreversible shock?
Promoters of Sodium Transport
Anti-Inflammatory Rxs
Anti-Oxidants
Cooling and cardiopulmonary bypass
define “popping the clot”
Normal blood pressure but no control of the bleeding causes someone in hemorrhage to bleed more
what’s the effect of hypothermia (induced by shock) on clotting?
effect of pH on clotting?
Shock induces hypothermia, which is probably what impairs clotting because platelets and other clotting factors don’t like cold
seems like pH also negatively impacts clotting
define functional physiological reserve/functional reserve capacity
Functional physiological reserve/functional reserve capacity: difference between maximum functionality and the minimum functional effort required to keep you alive
define primary vs secondary vs tertiary aging
Primary (biologic)
Secondary (lifestyle): Sedentary, Obesity, Poor diet, Smoking, Psychological and social factors
Tertiary (disease): Coronary heart disease, Atherosclerosis, Osteoporosis, Arthritis, Cancer, Neurologic disease, Other chronic diseases
effects of aging on body systems (which ones decline quicker? which ones decline faster?)
Reproductive system declines the quickest with increasing age
GI system declines the least with increasing age
2 main characteristics of aging
These can be due to increased allostatic load and homeostenosis. define them.
loss of physiologic reserve and homeostatic control
Allostatic load is overactivation of neuroendocrine, immune and autonomic systems)
Homeostenosis = altered responseto physiologic stresses
impact of homeostenosis
Effect of homeostenosis: some stressor that one might be able to manage at a younger age pushes one beyond their functional capacity, which can cause problems, like disease or death
impact of age on death rate and clinical presentations of disease
death rate increases with age; clinical presentation may also vary w/ age
explain te following theories of aging:
anatagonistic pleiotropy
mutation accumulation
what is senescence?
Antagonistic pleiotropy:
(pleiotropic alleles) that promote benefits in survival/reproduction early in life, even if they will reduce those same factors later in life, will accumulate b/c the early benefits outweigh the later-in-life disadvantages (e.g. Apolipoprotein E mutation)
Mutation accumulation theory:
Mutations that may have deleterious effects accumulate over time but don’t appear until later on in life
Senescence: decline in organismal fitness and performance with age
aging mechanisms (what are they?); ticking cells damage DNA stems; cells with EPIc genes die coz they’re on fire)
Biological clock
(decrease in) stem cells
DNA damage (via free radical; repair defects)
Epigenetic changes
Apoptosis
Inflammaging
define inflammaging
when you have an increase in proinflammatory mediators but the immune system is not responsive)
biomolecular markers of aging (what’s that all about?)
you can basically use DNA methylation levels w/in a given tissue to estimate the age of that tissue (specifically: cytosine-5-methylation w/ CpG nucleotides)
define the following in terms of cross sectional studies of aging:
Cohort or generational effects
Selective mortality
Cohort/generational effects: some change in the group that’s occurred over time (so people who were kids back, say 50 years ago, aren’t the same of course because maybe there were nutritional deficits in certain things back then but they have them now when they’re 80, so that affect the outcomes of the study)
Selective mortality: people who are older/dying are no longer being studied so that can also affect your data
explain what happens to the following with declining renal function and increasing age:
↓ Cr clearance & GFR (10mL/decade) → ↓ excretion of drugs, toxins
↓ concentrating and diluting capacity
↓ serum renin and aldosterone (30-50%)
→ fluid and electrolyte abnormalities - ↑ volume depletion and dehydration
→ ↑ risk of hyperkalemia
→ ↓ Na & K excretion and conservation
↓ vitamin D activation
changes in renal structure w/ declining renal function
(when your kidneys are shot, they lose blood, weight and mass)
if you have excessive protein intake (relates to which aging type?), how does that affect renal function?
how does that affect tertiary aging?
Loss of vasculature
decreased cortical renal mass
decreased renal weight
excessive protein intake promotes decline in renal function
all kinds of diseases, e.g. hypertension
effect of age on pulmonary function
what happens to our alveoli as we age?
what 2 main things contribute to decline in pulmonary function?
main effects of decline in pulmonary function
pulmonary function declines with age
alveoli get larger as we age
decreased elasticity and # of alveolie and capillaries
decrease in FEV1, FVC and ventilation-perfusion mismatches
Fill in the blank
Fill in the blanks
Frailty definition
Markers of frailty (what happens to lean body mass, endurance and balance, physical perfomance?)
Decreased physical reserve and resistance to stressors
Markers of frailty include age-associated declines in:
–Lean body mass
–Decreased ability to respond to stressors
–Endurance
–Balance
–Walking performance/physical activity
sarcopenia definition
myopenia vs dynapenia
loss of skeletal muscle mass or sarcopenia
myopenia (a decline in muscle mass) and dynapenia (a decline in muscle strength)
what happens to the following w/ increasing age:
motor units
muscle fibers *type 2 fast twitch vs type 1 fibers*
fatigability
basal metabolic rate
T/F: fat starts to infiltrate muscle as one gets older
greater loss of type II fast twitch than type I
Loss of motor units (progressive denervation of muscle fibers)
Truth. There’s infiltration of fat into muscle bundles
↑ Fatigability
↓ Basal metabolic rate
define anabolic resistance that occurs with age
which pathway that’s responsible for building muscle mass and protein synthesis is blunted in elderly patients following bed rest? what stimulates this pathway (specifically which one of these?)
Older people need increased amount of aa for protein synthesis: suggests metabolic (anabolic) resistance that occurs with age
MTORC1 pathway; stimulated by essential amino acids; leucine (seems to be involved in mRNA translation for muscle protein synthesis)
