Shock and Hemorrhage; Aging

Question 1

definition of shock

Answer 1

when the heart is unable to perfuse the organs after hemorrhage caused by trauma

Question 2

signs and symptoms of shock

Answer 2

Pallor (unhealthy paleness)

Cold Sweat

Weak or Undetectable Pulse

Loss of Sensibility

Muscular Collapse

Weakness of Cardiac Action

Question 3

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?)

Answer 3

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

Question 4

what’s the next response following the initial response to hemorrhage?

what happens to the following:

TPR

arterial pressure

CO

Answer 4

Increase in TPR

TPR goes up, which increases arterial pressure, but there’s still a decrease in cardiac output

Question 5

what’s the effect of increasing cardiac contractility after hemorrhage?

is there a change in CVP?

Answer 5

Increasing contractility raises arterial pressure, which raises cardiac output

CVP doesn’t change

Question 6

next response following increasing in cardiac contractility during hemorrhage

what happens to:

preload

arterial pressure

cardiac output

Answer 6

increasing venous tone

preload increases (more blood pushed into the heart)

arterial pressure increases

cardiac output increases

Question 7

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?

Answer 7

Sympathetic nervous system

Adrenal gland

Pituitary gland

Question 8

Sympathetic nervous system response to hemorrhage (what happens to heart and sm ms in the blood vessels?)

Answer 8

Heart contraction; vasoconstriction

Question 9

The Adrenal releases ___ which help in contractility and vasoconstriction; cortisol helps somehow (probably by increasing plasma osmolality)

Answer 9

catecholamines

Question 10

The pituitary releases ACTH which promotes ___; and ___ which promotes free water retention and vasoconstriction

Answer 10

Proteolysis

Vasopressin

Question 11

what’s the effect of decreased arterial pressure (on the kidney)?

Answer 11

Decreased arterial pressure: promotes Renin release and subsequent activation of the RAAS

Question 12

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?

Answer 12

Adrenomedullary – Catecholamines

Pituitary – ACTH and Vasopressin

Adrenocortical – Aldosterone and Cortisol

Kidney – Renin-Angiotensin

Pancreatic – Glucagon with Inadequate Insulin Secretion

Question 13

net effects of hormonal response to hemorrhage (i.e. cardiovascular; conserving; metabolic)

Answer 13

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

Question 14

metabolic response to hemorrhage:

what’s the function of the following/what happens in the following:

Cortisol
Liver
Adipose tissue
Sympathetic syst

Answer 14

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

Question 15

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 ___

Answer 15

Decreased Hydrostatic Capillary Pressure, Pc

Increased Hydrostatic Pressure in the Interstitium, Pi

Increased Capillary Oncotic Pressure, pc

Question 16

how is blood volume restored during the transcapillary refill (what are the steps?)

Answer 16

1. 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
2. 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
3. At some point, convective movement of interstitial protein thru large pores >> increased lymphatic return

Question 17

what happens to hct during transcapillary refill?

Answer 17

hct stays low because no blood added

Question 18

Time course of compensation
 to hemorrhage (arrange the following:)

Movement of water

Hormonal response

Reflex vasoconstriction

Synthesis of new protein

Lymphatic return of protein

Answer 18

• 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

Question 19

stages of shock (and changes in blood loss %, pulse, bp and CO)

Answer 19

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

Question 20

factors that respond poorly to fluid resuscitation

Answer 20

• Failure of Cells to Maintain a Sodium Gradient
• Bacterial Translocation across the Gut
• Activation of Inflammatory Pathways
• Myocardial Depression
• Ischemia-Reperfusion Injury

Mitochondrial Dysfunction

Question 21

therapies for hemorrhagic shock

Answer 21

Control the bleeding >> give IV fluids to get optimal cardiac output >> give blood transfusion for severe bleeding >> give adjuncts to prevent irreversible shock

Question 22

what are the “adjuncts” used to prevent irreversible shock?

Answer 22

Promoters of Sodium Transport
Anti-Inflammatory Rxs
Anti-Oxidants
Cooling and cardiopulmonary bypass

Question 23

define “popping the clot”

Answer 23

Normal blood pressure but no control of the bleeding causes someone in hemorrhage to bleed more

Question 24

what’s the effect of hypothermia (induced by shock) on clotting?

effect of pH on clotting?

Answer 24

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

Question 25

define functional physiological reserve/functional reserve capacity

Answer 25

Functional physiological reserve/functional reserve capacity: difference between maximum functionality and the minimum functional effort required to keep you alive

Question 26

define primary vs secondary vs tertiary aging

Answer 26

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

Question 27

effects of aging on body systems (which ones decline quicker? which ones decline faster?)

Answer 27

Reproductive system declines the quickest with increasing age

GI system declines the least with increasing age

Question 28

2 main characteristics of aging

These can be due to increased allostatic load and homeostenosis. define them.

Answer 28

loss of physiologic reserve and homeostatic control

Allostatic load is overactivation of neuroendocrine, immune and autonomic systems)

Homeostenosis = altered responseto physiologic stresses

Question 29

impact of homeostenosis

Answer 29

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

Question 30

impact of age on death rate and clinical presentations of disease

Answer 30

death rate increases with age; clinical presentation may also vary w/ age

Question 31

explain te following theories of aging:

anatagonistic pleiotropy

mutation accumulation

what is senescence?

Answer 31

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

Question 32

aging mechanisms (what are they?); ticking cells damage DNA stems; cells with EPIc genes die coz they’re on fire)

Answer 32

Biological clock

(decrease in) stem cells

DNA damage (via free radical; repair defects)

Epigenetic changes

Apoptosis

Inflammaging

Question 33

define inflammaging

Answer 33

when you have an increase in proinflammatory mediators but the immune system is not responsive)

Question 34

biomolecular markers of aging (what’s that all about?)

Answer 34

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)

Question 35

define the following in terms of cross sectional studies of aging:

Cohort or generational effects
Selective mortality

Answer 35

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

Question 36

explain what happens to the following with declining renal function and increasing age:

Answer 36

↓ 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

Question 37

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?

Answer 37

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

Question 38

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

Answer 38

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

Question 39

Fill in the blank

Answer 39

Question 40

Fill in the blanks

Answer 40

Question 41

Frailty definition

Markers of frailty (what happens to lean body mass, endurance and balance, physical perfomance?)

Answer 41

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

Question 42

sarcopenia definition

myopenia vs dynapenia

Answer 42

loss of skeletal muscle mass or sarcopenia

myopenia (a decline in muscle mass) and dynapenia (a decline in muscle strength)

Question 43

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

Answer 43

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

Question 44

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?)

Answer 44

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)