Infectious diseases Flashcards
(67 cards)
what are 2 phases of the metabolic response to injury/sepsis
ebb + flow phase
separated by resuscitation
both can lead to multiple organ failure
ebb = hypometabolic, low core body temp, more catecholamines, poor tissue perfusion
flow = hypermetabolic, high core body temp, less catecholamine, no tissue perfusion
how do the 2 phases of metabolic response to injury differ
ebb = hypometabolic, low core body temp, more catecholamines, poor tissue perfusion
flow = hypermetabolic, high core body temp, less catecholamine, no tissue perfusion
both can lead to multiple organ failure
how does simple starvation + injure differ metabolically
starvation = metabolic adaptation to slower rate (so lower resting energy expenditure)
so lean tissue conserved - as body fuels/proteins conserved
injury (catabolic weight loss) = no adaptation, causing high metabolic rate spending lots of resting energy
so lean tissue breakdown (body fuels/proteins wasted) - even with nutrient intake
what is main fuel in starvation + stress
starvation = fat (ketosis - physiological response to alternative energy supply)
stress = fat + AA (causing muscle breakdown, occurs due to higher counter regulatory hormones to allow proteolysis)
why does ketosis occur
physiological response of body to need for alternative energy supply
brain needs glucose so adapts to ketones as they can cross BBB
what is serum analysis of starvation
high serum urea + ketones
high urea = protein/muscle breakdown, AKI
high ketone = alternative energy supply using TG-FFA breakdown
how does low glucose affect insulin + glucagon
low glucose = low insulin + high glucagon
causes degradation of glycogen, fat stores, protein
so muscle adapts to ketone to prevent protein breakdown
adipose tissue is sensitive to glucagon that stimulates lipase so more TG->FFA
what is insulin action
increase glucose uptake into skeletal muscle, adipose (by increasing sensitivity to more insulin)
suppress hepatic gluconeogenesis
directly inhibit lipolysis by ketones
how does DKA + alcohol ketoacidosis differ
DKA = high glucose + high ketones + metabolic acidosis
as glucose can’t be used, so ketones used instead as alternative energy supply
alcoholic ketoacidosis = not significant hyperglycaemia + high ketones + metabolic acidosis
when malnourished, ethanol metabolised to acetic acid (ketone) causing high ketones levels without high glucose
what hormones are involved in ketoacidosis
high glucagon + low insulin
ketosis occurs in liver
after prolonged starvation/fasting, when OAA depleted from gluconeogenesis
so acetyl-CoA can’t enter Kreb cycle
causes excess acetyl-CoA which is converted in liver mitochondria to ketones (acetone, acetoacetate, B-hydroxybutyrate)
what is major ketone in fasting ketosis
B-hydroxybutyrate
ketone = water-soluble, fat derived
physiological response to low glucose supply
what is SIRS criteria
2 or more:
temp <36 or >38
HR >90bpm
RR >20, PaCO2 <4.3/<32
WCC <4,000 or >12,000
how does severe sepsis + septic shock differ
severe sepsis = SIRS + associated organ failure, hypoperfusion, hypotension (SBP <90)
septic shock = severe sepsis + arterial hypotension unaffected by fluid resus
what is SEPSIS 6
take: lactate, urine output, blood culture
give: O2, IV fluids, IV antibiotics
why is glucose high in critical illness
stress mediators oppose anabolic actions of insulin = so more tissue lipolysis, skeletal muscle proteolysis + suppressed hepatic gluconeogenesis
high catecholamines (cortisol) has catabolic effect increasing gluconeogenesis (so more glycogen breakdown) = inhibits GLUT4 translocation in muscle/adipose so peripheral insulin resistance
what is immune system role in protein/lipid metabolism in illness
pro-inflammatory cytokines TNF reduces ability to use lipids as energy source
so skeletal muscle is major substrate for glucose (75%)
decrease in muscle -> insulin resistance
high catecholamines -> browning of fat (so hyper metabolic response + cachexia)
how does starvation effect endocrine system
sick euthyroid = low/N TSH, low/N T4, low T3
chronic undernutrition lowers metabolic rate so less T4 -> T3
HPO (ovarian) axis suppressed
hypogonadotrophic hypogonadism (low GnRH, low LH/FSH) = amenorrhoea, infertility
increased HPA axis
more stress so high cortisol (glucocorticoid)
breakdown protein - loss of collagen (osteopenia), loss of muscle (weakness)
what is sepsis
life-threatening organ dysfunction as dysregulated host response to infection
irrespective of organism/focus
how do SIRS + sepsis differ
sepsis = SIRS + infection
severe sepsis = sepsis + organ failure/hypoperfusion/hypotension (SBP <90)
septic shock = severe sepsis + arterial hypotension unaffected by fluid resuscitation + lactic acidosis
SIRS: 2 of
temp <36 or >38
WCC <4,000 or >12,000
HR >90
RR >20, PaCO2 <32
what is toxic shock syndrome
gram +ve bacteria release super antigens (antigens that cause immune response in 20% resting T cells + not restricted by antigen specificity)
staph aureus (burn) - TSS1
strep pyogenes (necrotising fasciitis)
how do gram +ve and -ve stain
-ve = pink stain as thin peptidoglycan + high lipopolysaccharide
e.coli, haemophilus influenza
lipopolysaccharides release ENDOtoxin (PAMP) recognised by TLR4 (PRR) that activate APC
+ve = purple stain as thick peptidoglycan layer + lipotechtic acid
less potent infection
staph aureus, strep pyogenes
forms super antigens (staph aureus, strep pyogenes) - protein EXOtoxin that stimulate immune response in 20% resting T cells, not restricted by antigen specificty
what are 3 shocks in sepsis
distributive = warm peripheries
hypovolaemic = cold peripheries + responds to fluid
cardiogenic = cold peripheries + not fluid responsive
how is sepsis severity determined
SOFA score:
RR >22
GCS <15
SBP <100
what causes malaria
protozoan parasite = plasmodium
p.falcifarum spread by bites of female anopheles mosquitoes (sub-Sahara)
p.falcifarum most common globally
p.vivax most common outside Africa
