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302 review > Infectious diseases > Flashcards

Infectious diseases Flashcards

1
Q

what are 2 phases of the metabolic response to injury/sepsis

A

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

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2
Q

how do the 2 phases of metabolic response to injury differ

A

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

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3
Q

how does simple starvation + injure differ metabolically

A

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

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4
Q

what is main fuel in starvation + stress

A

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)

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5
Q

why does ketosis occur

A

physiological response of body to need for alternative energy supply

brain needs glucose so adapts to ketones as they can cross BBB

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6
Q

what is serum analysis of starvation

A

high serum urea + ketones

high urea = protein/muscle breakdown, AKI
high ketone = alternative energy supply using TG-FFA breakdown

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7
Q

how does low glucose affect insulin + glucagon

A

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

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8
Q

what is insulin action

A

increase glucose uptake into skeletal muscle, adipose (by increasing sensitivity to more insulin)
suppress hepatic gluconeogenesis
directly inhibit lipolysis by ketones

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9
Q

how does DKA + alcohol ketoacidosis differ

A

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

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10
Q

what hormones are involved in ketoacidosis

A

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)

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11
Q

what is major ketone in fasting ketosis

A

B-hydroxybutyrate

ketone = water-soluble, fat derived
physiological response to low glucose supply

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12
Q

what is SIRS criteria

A

2 or more:

temp <36 or >38
HR >90bpm
RR >20, PaCO2 <4.3/<32
WCC <4,000 or >12,000

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13
Q

how does severe sepsis + septic shock differ

A

severe sepsis = SIRS + associated organ failure, hypoperfusion, hypotension (SBP <90)

septic shock = severe sepsis + arterial hypotension unaffected by fluid resus

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14
Q

what is SEPSIS 6

A

take: lactate, urine output, blood culture
give: O2, IV fluids, IV antibiotics

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15
Q

why is glucose high in critical illness

A

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

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16
Q

what is immune system role in protein/lipid metabolism in illness

A

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)

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17
Q

how does starvation effect endocrine system

A

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)

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18
Q

what is sepsis

A

life-threatening organ dysfunction as dysregulated host response to infection

irrespective of organism/focus

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19
Q

how do SIRS + sepsis differ

A

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

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20
Q

what is toxic shock syndrome

A

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)

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21
Q

how do gram +ve and -ve stain

A

-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

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22
Q

what are 3 shocks in sepsis

A

distributive = warm peripheries
hypovolaemic = cold peripheries + responds to fluid
cardiogenic = cold peripheries + not fluid responsive

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23
Q

how is sepsis severity determined

A

SOFA score:

RR >22
GCS <15
SBP <100

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24
Q

what causes malaria

A

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

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25
Q

how do complicated + uncomplicated malaria differ

A

complicated = parasitaemia >2%
OR parasitaemia <2% + clinical signs

uncomplicated = parasitaemia <2% + no schizont + no clinical signs

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26
Q

what EIR (entomological inoculation rate) is stable + unstable

A

stable = EIR >10/yr
unstable = EIR <5/yr

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27
Q

how often do fever spikes occur in active malaria

A

every 48hr = fever spike corresponds with schizont rupture causing haemolytic anaemia

28
Q

how does malaria obstruct circulation + what is the impact

A

obstructs circulation by sequestering + rosetting
sequester = binding of 2 infected RBC
rosett = binding of uninfected + infected RBC

PfEMP proteins bind iRBC to vascular endothelium

causes hypoxia + cytokines release which damages tissue
so malaria can evade immune response

29
Q

what is protective against malaria

A

HbS sickle cell trait - common in africa

Duffy group + ve protective to p.vivax infection (common outside Africa)

30
Q

how does malaria present

A

recent travel to endemic country

pallor + jaundice = haemolytic anaemia
hepatomegaly

31
Q

how is malaria diagnosed

A

giema stain on blood film = RBC lyse appearing blue/purple

peripheral blood film = identify parasitaemia (how many schizonts to determine parasite stage)

32
Q

what are the main infective causes of headache

A

meningitis
encephalitis - inflamed brain parenchyma

33
Q

what is aseptic meningitis + meningococcal septicaemia

A

aseptic meningitis - meningitis not caused by pyogenic bacteria (doesn’t make pus)
meningococcal septicaemia - meningococcal bacteria infecting bloodstream

34
Q

what is main cause of community-acquired bacterial meningitis in
neonate
child
adult
60yr+ or immunocompromised

A

neonate - strep agalcteia group B (vertical transmission), e.coli
present with bulging fontanelle

child/adult (adolescent) - neisseria meningitidis group B
vaccine against haemophilus influenza type B

adult - strep pneumonia

immunocompromised - listeria monocytogenes (or TB)

35
Q

what is most common viral cause of meningitis

A

NPEV- non-polio human enterovirus

enterovirus species B, cocsackbe virus A9, echovirus A71

36
Q

how are viral meningitis pathogens spread

A

feacal-oral route

year-round in tropical/subtropic areas
seasonal in temperate climate

37
Q

how does bacterial + viral meningitis present

A

bacterial - sudden onset, systemic upset (sepsis)
viral - gradual onset, less severe

38
Q

what red-flag features indicate meningitis

A

headache, fever, neck stiff, photophobia
vomiting
altered conscious, seizures

if viral meningitis:
nuchal rigidity = resisting passive neck flexion
kerning sign = can’t extend knee when hip is flexed
brudinzski sign = when flexing neck, hip/knee spontaneously flex

39
Q

how do neisseria + strep pneumonia differ

A

neisseria.m = meningococcus (causes petechial rash)
gram -ve diplococci
commensal organism in URT

strep pneumonia = pneumococcus
gram +ve diplococci
meningitis occurs after pneumonia or ear infection

40
Q

what are the different rashes in menigitis

A

petechial/purpuric rash - from meningococcal infection (neisseria)

non-blanching rash - meningococcal septicaemia (when pathogens enter bloodstream)

41
Q

why does a non-blanching rash occur in meningococcal septicaemia

A

DIC + subcutaneous haemorrhage

42
Q

how to investigate meningitis

A

bacterial = CSF sample from LP
viral = PCR

43
Q

what causes aseptic meningitis

A

usually viral pathogen

drug - amoxicillin, NSAID, trimethoprim+sulfamethoxazole

malignancy, SLE, Kawasaki disease

44
Q

what is seen on bacterial + viral meningitis CSF sample

A

viral - all normal other than high WCC

bacterial - cloudy CSF
high opening pressure, high protein
high neutrophil (polymorphic leukocytes)
LOW glucose

45
Q

how do HSV1 + HSV2 differ

A

HSV1 = most common cause of sporadic encephalitis globally

HSV2 = causes benign recurrent aseptic/lymphocitic meningitis

46
Q

how is meningitis managed

A

if bacterial = inform PHE

<3months = IV amoxicilline + IV ceftriaxone
3+ months = IV ceftriaxone

if penicillin allergy, chloramphenicol instead

steroids used as adjunct to prevent hearing loss, cerebral palsy

47
Q

what signs are seen with viral meningitis

A

nuchal rigidity = resisting passive neck flexion

kerning sign = can’t extend knee when hip is flexed

brudinzski sign = when flexing neck, hip/knee spontaneously flex

48
Q

what is measles virus

A

non-segmented, negative sense RNA
only encodes 1 type of antigen (unlike other RNA viruses)

transmitted via resp route (droplets/aeresols suspended in air last for 2hr)
incubation period 12.5 days

morobillus genus, paramyxoviridae family

49
Q

what gene of measles encodes the 2 non-structural proteins

A

protein V + C (non-structural proteins of measles)
within phosphoprotein gene

50
Q

how does measles differ from other RNA viruses

A

antigenically monotypic
despite its genotypic diversity and that RNA viruses have high mutation rates

51
Q

how long is the infectious period for measles

A

begins several days before and lasts several days after rash onset

coincides with peak viraemia, cough/corozya

52
Q

what rash occurs in measles

A

macropapular rash - initially face + behind ears, then spreads down trunk

occurs 3-4 days before fever onset

53
Q

what vitamin deficiency makes children susceptible to measles

A

Vitamin A

54
Q

how is measles diagnosed

A

PCR assay for measles virus RNA
measles-specific IgM in blood

55
Q

what is HIV incidence

A

highest in East/South Africa
most new HIV infections in sub-Saharan Africa

56
Q

how is HIV characterised + how does it present

A

characterised - high viral load, high risk of transmission
high inflammatory response causes systemic responses

present - fever, sore throat, macropapular rash (similar to EBV)
but symptoms improve few wks later (asymptomatic phase)

57
Q

what is AIDS

A

when CD4 count <200cells (marked rebound in HIV viral load)

causes onset of opportunistic infections, malignancy

58
Q

what is HIV virology

A

genus - lentivirus
family - retrovirus

made of 2 identical ssRNA molecules
so needs reverse transcriptase RT to form DNA + intergrase IN to combine this viral DNA with the host’s

enclosed in viral capsid

59
Q

how do HIV 1 + 2 differ

A

both are zoonotic in origin

HIV1M most common globally (other HIV1 types confined to west/central Africa)
HIV2 rare outside west-Africa

HIV1 (chimp, gorilla) - 4 groups M,N,O,P
HIV2 (sooty mangabey) - 9 groups A-H, J, K

60
Q

where is the highest HIV1 genetic diversity

A

central africa

61
Q

what is structure of HIV1

A

viral capsid containing 2 identical ssRNA molecules + RT/IN enzymes

glycoprotein GP-120 + GP-41
viral envelope proteins

these attach to CD4-Tcells
with coreceptors: CCR5 (if R5 virus) + CXCR4 (if X4 virus)

62
Q

how is HIV transmitted

A

blood Bourne virus
parenteral exposure (sharing needle), sexual exposure, vertical transmission

63
Q

why can ART antiretroviral treatment not eliminate HIV infection

A

ART can suppress viral replication but not residual replication

ART can’t eliminate HIV integrated viral DNA from infected host cells
so residual replication can still occur to maintain HIV reservoir

64
Q

why can host immune response not contain HIV infection

A

CTL (CD8 cytotoxic T lymphocyte) escape mutants
HIV viral capsid is glycosylated to evade immune system + cellular restriction factors like APOBEC3

65
Q

what occurs in AIDS stage

A

CD4 <200cells, causes immunosuppression, opportunistic infections, AIDS-malignancy

more pro-inflammatory cytokines (type 1 IFN, IL6, IL1)
low CD4/CD8 ratio
exhaustion/sensescence of T cells + macrophages

pro-inflammatory state causes premature ageing, multi-organ disease

66
Q

what is PJP

A

AIDS related infection, when CD4 <200cells

presents: oral candidiasis
2wk hx of fever, SOB, non-productive cough
9 month of weight loss

if HIV +ve, confirmed PJP (fungal infection)
Cotrimoxazole, prednisolone, fluconazole

67
Q

how does HIV alter lymphoid structure

A

changes intestinal lymphoid structure so disturbed gut barrier, causes more microbial translocation

more plasma lipopolysaccharide circulation, so enhanced persistent immune activation

302 review (14 decks)

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