Practicals Term I (+BP Prac) Flashcards Preview

Microbiology and Immunology > Practicals Term I (+BP Prac) > Flashcards

Flashcards in Practicals Term I (+BP Prac) Deck (74):
1

Gram +ve bacteria

  • have thick peptidoglycan cell walls
  • stain purple/blue
  • like dry environments

2

Gram +ve cocci on Gram stain suggest

normal flora

3

Gram -ve bacteria

  • have thin peptidoglycan cell walls and an outer membrane
  • do not stain (ie pink or red)
  • like moist environments

4

Gram +ve clusters are

Staphylococci

5

Gram +ve chains are

Streptococci

6

Green pus is likely caused by

Pseudomonas aeruginosa

7

Sulphur granules in pus indicate

Actinomyces israelii

8

Pus with an offensive odour is likely caused by

anaerobes

9

Thick, yellow pus is likely caused by

Staphylococcus aureus, etc.

10

Genetics account for what percent of BP variation in the population?

40%

11

What happens to systolic BP on sitting??

drops slightly; then restored (but not to lying pressure)

12

What happens to SV on sitting from lying?

  • decreases
  • perceived as a slight drop in BP by baroreceptors in carotids and aorta as decreased stretch
  • baroreceptors fire to activate medulla to increase SNS tone and decreased PNS tone
    • increased SNS and decreased PS increase HR and contractility to restore SV(but not to same level as lying)

13

What happens to systolic BP on standing from sitting?

initial drop in BP; restored

14

What happens to SV on standing from sitting?

drops; activates +SNS and -PNS via baroreceptor reflex to increase HR and restore SV

15

What happens to HR from lying to standing?

increases

16

What happens to diastolic BP from lying to standing?

decreases

17

What happens to cardiac output from lying to standing?

decreases

18

What happens to total peripheral resistance from lying to standing?

decreases

19

How does the body increase MAP from lying to standing?

by increasing TPR

(inc HR would compromise diastolic filling of coronaries)

20

Nicotine

increases BP, HR

21

Caffiene

initially increases blood pressure, long-term effects unknown

22

What are primary immunodeficiencies?

  • result of inherent congenital defects in the components of the immune system or their products

23

What are secondary immunodeficiencies?

  • result from effects of external agents or alterations in other body systems
  • more common than primary
  • associated with:
    • extremes of age
    • malnutrition
    • anatomic barrier dysfunction (incl medical devices)
    • non-infectious diseases (diabetes, tumours/cancer)
    • infections (malaria, HIV)
    • cytotoxic drugs/irradiation (chemo)
    • immunosuppresive drugs

24

Secondary immunodeficiencies are associated with

  • extremes of age
  • malnutrition
  • anatomic barrier dysfunction (incl medical devices)
  • non-infectious diseases (diabetes, tumours/cancer)
  • infections (malaria, HIV)
  • cytotoxic drugs/irradiation (chemo)









     












  • immunosuppresive drugs











     

 

 

25

Recessive gene defects that cause primary immunodeficiencies include

  • defects in development of primary lymphoid tissue (thymus, spleen)
  • defects in T cell development
  • MHC Class I or II deficiency
  • defects in B cell development and selected antibody deficiencies
  • phagocyte deficiencies
  • complement pathway deficiencies

26

What blood specimens are collected for immunodeficiency diagnosis?

  • blood - anticoagulant:
    • #s and function of immune cells
  • blood - plain tube:
    • clots; for complement and antibody estimations

27

What is the order of isotype switching?

IgM > IgG > IgE > IgA

28

How is blood analysed for populations of lymphocytes?

flow cytometry using anti-T (anti-CD3) and anti-B (anti-CD19) cell antibodies as markers

29

How are lymphocytes analysed in the blood?

  • flow cytometry for populations using anti-T (anti-CD3) and anti-B (anti-CD19) cell antibodies
  • antibody isotype analysis (IgG, IgM, IgE, IgA)
  • specific antibody analysis (tetanus, blood groups)
  • t-cell proliferation tests
  • flow cytometry of CD40L expression on activated lymphocytes

30

How is B-cell function analysed?

presence of antibodies made against immunisation antigens and blood group antigens

31

If B cell populations are normal but isotype switching is not occurring, where is the immunodeficiency?

T-cells; required for isotype switching

32

How is T-cell function analysed?

  • inducing T-cell proliferation by reacting them with anti-T/anti-CD3 antibodies
    • proliferation requires CD25 receptor for IL-2
  • expression of CD40L using flow cytometry on activated T cells

33

CD40L is on

T-cells

34

What is the function of CD40L?

  • required for activating B-cells
    • CD40L on T-cells binds to CD40 on B-cells to activate them
  • necessary for isotype switching of B cells
    • deficiency can cause hyper IgM (isotype cannot switch to IgG)
  • activates macrophages
    • deficiency means lack of inflammatory cytokine production (afebrile in infection), and defective respiratory burst
  • deficiency can also result in:
    • poor memory B cell production
    • inefficient induction of cyotoxic T-cells

35

The gene for CD40L is on which chromosome?

X; tf deficiency is x-linked

36

What is affinity maturation?

the process by which B cells produce antibodies with increased affinity for antigen during the course of an immune response

37

Monocyte function can be analysed by

  • assessing production of TNFa in response to stimulation by IFNy
    • TFNa stimulates granuloma formation, macrophage differentiation into giant cells etc.
    • tf deficiency in IFNy or IFNyR1 on macrophages results in decreased TNFa production and no granuloma formation where there should be (eg mycobacterium infections)
  • flow cytometric analysis for the expression of IFNyR1 (receptor) on monocytes

38

IFNy is produced by

activated CD4 T cells (particularly Th1)

CD8 T-cells

NK cells

39

IFNy activates

macrophages

40

What organisms are common in complicated UTI?

  • proteus
  • klebsiella
  • enterococci
  • pseudomonas

41

Complicated UTIs are associated with

  • anatomical abnormalities (including medical devices)
  • metabolic abnormalities (pregnancy, diabetes)
  • immunocompromise
  • unusual pathogens (yeasts)

42

What bacteria cause UTIs?

  • E coli (70-95%)
  • Staph saprophyticus (10-20% in sexually active females)
  • Proteus (GIT flora)
  • Klebsiella (GIT flora)
  • Enterococci (GIT flora)
  • Pseudomonas (environmental)

43

What laboratory investigations are undertaken for suspected UTI?

  • dip-stick for RBCs, leukocyte exterase, nitrites, protein
  • pyuria (pus) measured by counting WBC; >10^4-10^5/mL is abnormal
  • casts and crystals (microscopy)
  • culture; >10^8/L (>10^5/mL) organisms of a single type in MSU is significant, any grwoth from SPA is significant

44

What is an abnormal WBC count in urinalysis?

>10^4-10^5/mL

45

What culture count is significant in UTI?

>10^8/L (>10^5/mL)

46

What count of RBCs in urine is abnormal?

>2000/mL

47

Presence of RBC casts on urinalysis indicates

bleeding in the kidney

48

What media are used in urinalysis?

  • HBA (aerobic)
  • MAC (aerobic)
  • CLED (aerobic)
  • Lowenstein-Jensen if renal TB suspected
  • Selenite broth if suspected Salmonella Typhi carrier

49

Bactaeremia

  • bacteria in blood
  • transient (not uncommon), intermittent, or continuous
  • not necessarily associated with clinical features
  • requires a mode of entry

50

Septicaemia

  • bacteraemia causing symptoms
    • fever, increased CO and RR, changes to body systems/perfusion of organs
  • serious
  • systemic - sepsis or septic shock

51

Sepsis

  • septicaemia infection
  • fever or hypothermia
  • tachypnoea or tachycardia
  • high or low white cell counts

52

Septic shock

  • severe sepsis
  • potentially fatal drop in BP

53

Bacteria and septicaemia result from

  • infection
  • massive traua
  • inflammatory disease

54

Systemic inflammatory response syndrome

two or more of:

  • temperature >38C or <36C
  • resp rate >20/min
  • HR >90/min
  • WBC >12x10^9/L or <4x10^9/L or >10% immature cells

55

What are the common gram positive causes of septicaemia?

  • staph aureus
  • strep pyogenes
  • staph epidermidis
  • viridans strep
  • strep pneumoniae
  • enterococcus spp

56

What are common gram negative causes of septicaemia?

  • E. coli
  • pseudomonas aurigenosa (environmental)
  • klebsiella
  • enterobacter spp
  • nisseria meningitidis

57

What are other common causes of septicaemia?

  • Candida
  • rickettsiae

58

What are some of the risk factors for septicaemia?

  • impaired immunity
    • breached integument, neutropenia
  • hospitalization
  • indwelling (bladder) catheterization
  • overseas travel
  • occupational
  • contact with animals, contaminated food, water
  • infection by a virulent pathogen

59

Sources of septicaemia bacteria are

  • skin
  • URT
  • genito-urinary tract
  • GI/biliary tract

60

GPC are either

staph or strep

61

Staph is catalase

+ve

62

Strep is catalase

negative

(as is enterococci)

63

Staph aureus is coagulase

+ve

64

Coagulase negative staph are likely

epidermidis (susceptible to novobiocin)

saprophyticius (resisitant to novobiocin)

65

URTIs are commonly caused by

viruses

66

sore throat is predominaly

viral infection

67

sinusitis is predominantly

bacterial infection (often post-viral)

68

otitis media is often

bacterial infection

69

LRTIs include

  • croup (laryngotracheobronchitis)
  • whooping cough
  • bronchiolitis
  • bronchitis (acute and acute exacerbation of chronic)
  • pneumonia

70

What number of microorganisms in sputum suggest infection?

>10^7/mL

especially of one type

71

Small numbers of small pink colonies on MAC suggest

growth of normal microbiota (eg e. coli)

72

How do conjugate vaccines work?

  • polysaccharide of capsule conjugated to protein = antigen
  • protein antigen presented by APCs to T cells activates them to express CD40L
  • polysaccharide antigen recognized by Ig on B cells internalized the conjugate
    • peptide portion presented on MHC class II of B cell
  • activated T cell binds MHC class II peptide on B cell, CD40 on B cell ligates CD40L
  • induces isotype switching, affinity maturation, memory cell secretion
  • polysacch on its own cannot activate T cells; can activate some (CD5) B cells (T-indep) but regardless only get IgM and no secondary immune response
  • tf peptide conjugate is vital to generating isotype switch and secondary immune response

A image thumb
73

What is haemolytic uremic syndrome?

  • haemolytic anaemia +
  • acute kidney failure (uremia) +
  • low platelet count (thrombocytopoenia)

74