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PUBLIC EXAM Qs > Exam questions > Flashcards

Exam questions Flashcards

1
Q

Outline the common modes of action of antibiotics

A
  1. Cell wall synthesis inhibitors= inhibit PBP binding
    - penicillins
    - cephalosporins
    - monobactams
    - Carbapenems
    - B-lactam
  2. DNA protein synthesis inhibitors 50S ribosome
    - erythromycin
    - chloramphenicol
    - clindamycin
  3. DNA protein synthesis inhibitors 30S ribosome
    - tetracyclines
    - gentamicin
    - streptomycin
    - nitrofuran
  4. inhibitors of DNA-directed RNA polymerase= inhibits RNA synthesis
    - rifampicin
  5. Inhibitors of DNA gyrase
    - quinolones= nalidixic acid, ciprofloxacin
  6. folic acid metabolism inhibitors
    - trimethoprim
    - sulfonamides
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2
Q

What is varices?

A

Swollen veins in the lining of lower oesophagus near the stomach.

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3
Q

What causes varices?

A

Cirrhosis of the liver
Causes scarring nf slows blood flow through liver
Blood packs up into portal vein and increases portal pressure leading to portal hypertension
Portal hypertension occurs due to increased intrahepatic resistance and splanchnic arteriolar vasodilation
Liver cirrhosis also causes increased intrahepatic vascular resistance
This then leads to abnormal dilation of the collateral vessels

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4
Q

Why are varices clinically important?

A

They are a complication of portal hypertension
Indicate the risk of a variceal haemorrhage which ultimately leads to death
The size of the varices indicate the risk of bleeding- the larger the varices the higher the risk of variceal haemorrhage and bleeding

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5
Q

Why are INR and serum albumin more useful than conventional LFTs for assessing how well the liver is actually working?

A

INR measures how long blood take to clot
Conventional LFT do not tell us the function of the liver they detect the site of damage
Serum albumin tells us the how well liver is functioning as it detects how well liver is producing albumin
Conventional LFTs like y-glutamyl transferase, alkaline phosphatase, - Alanine transferase, - Aspartate transferase are useful in acute liver disease to track on a daily basis but they are not useful in assessing the severity of the disease in chronic liver disease
There could other causes for these abnormal liver enzyme results

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6
Q

Describe the hallmarks of cancer?

A
  1. Self sufficiency in growth signals
    - secrete GFs stimulating their own growth
    - mutation of cell surface receptor allowing constant cell growth and division
  2. Insensitivity to growth inhibitors
    - Growth inhibitors are inactivated in cancer leading to unregulated division and growth
  3. Apoptosis evasion
    - P53 mutation inactivates the apoptosis pathway
  4. Sustained angiogenesis
    - promote vascular development
    - induce angiogenic factors
    - induces VEGF
  5. limitless replicative potential
    - expression of telomerase to protect chromosomes and divide continuously
  6. tissue invasion and metastasis
    - decreased cell-cell adhesion
    - secrete proteases that digest surrounding barriers
  7. inflammatory microenvironment
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7
Q

Outline the main interventions that are used in the UK to reduce surgical site infections and explain how they work?

A
  1. Surveillance
  2. Infection control
    - hand washing
    - preoperative bathing with soap
  3. Prophylactic antibiotics
    - Give to patients before clean contaminated or contaminated surgery
    - Antibiotic choice depends on local antibiotic formulary
    - as single dose of antibiotic prophylaxis IV before operation
    - administration 2 hrs before surgery reduces risk the most
  4. asepsis
  5. preparing incision site
    - use Chlorhexidine alcohol or povidone iodine to decontaminate skin and reduce pathogens in clean contaminated surgery
  6. hair removal
    - improved view and access
    - Reduced infection rate
    - use clippers as recommended by WHO because razors damage skin and increase bacterial number
  7. oxygenation and glucose control
    - high oxygen and glucose provides bacteria with energy for survival and growth
  8. active warming to maintain normothermia
    - forced air warming, electrical blankets, radiant heaters
    - can lead to surgical hypothermia which increases SSI
    - Hypothermia= the blood vessels to constrict = reduce blood circulation and tissue perfusion= less effective wound healing
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8
Q

How are SSI’s classified?

A
  1. Deep incisional
    - involves skin, SC, deep soft tissue fascia and muscle
  2. Superficial incisional
    - involves skin and subcutaneous tissue
  3. organ/space
    - Involves all other parts that are opened or manipulated other than incision
    - intra abdominal
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9
Q

Describe the types of operative procedures including examples of each type?

A
  1. Clean procedure/wound
    - risk from contaminants form environment, surgical team, skin colonists
    - Example= elective inguinal hernia repair
  2. Clean-contaminated procedure/wound
    - Operative procedures that enter into colonised viscus or cavity of body
    - Contaminants= endogenous bacteria from within patient
    - Examples
    Elective intestinal resection
    Pulmonary resection
    Gynaecological procedures
    Head-neck cancer op involving oropharynx
  3. Contaminated wound/procedure
    - Examples
    Laparotomy for penetrating injury with intestinal spillage
    Elective intestinal procedures with gross contamination of surgical site
    - Contaminants= bacteria introduced by gross soilage of surgical field
    - absence of active infection
  4. Dirty wound/procedure
    - presence of active infection
    - Examples
    Intra-Abdominal abscesses
    Abdominal exploration for acute bacterial peritonitis
    - contaminants = from the active infection
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10
Q

What is the risk of SSI for each type of procedure?

A
  1. clean= <2%
  2. clean-contam= 5-15%
  3. contam= 15-30%
  4. dirty= >30%
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11
Q

What is NNHS risk index?

A

risk index system= hospitals report cumulative wound infection data
compares different patient populations from different hospitals and areas
score system 0-3
0-1= low risk
2-3 high risk

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12
Q

Describe the virulence factors of staphylococcus aureus?

A

Protein A= interacts with IgG Fc region and inactivates it to evade phagocytosis
Elastic, collagen and fibronectin binding proteins= allow cell adhesion
Superantigens= enterotoxin B and alpha toxin= stimulate excessive t cells= increased cytokines= uncontrolled inflammation
Coagulase= catalyses fibrinogen to fibrin, activates prothrombin and coagulation
Haemolysin= forms pores in host cell= cytotoxic to tissue cells and leukocytes
Proteases= degrade and inactivate proteins
Forms biofilms= adheres to polymer surface like catheters= evades immune response
Clumping factor= clots blood plasma
PVL= break down WBC so inflammatory contents released into host and inflammation occurs

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13
Q

Describe morphology of staphylococcus aureus?

A
  • Gram +ve
  • Spherical
  • Non-motile
  • Colonises skin and upper respiratory tract(oral cavity and nose)
  • Can infect surface due to shedding skin
  • Opportunistic pathogen
  • Golden grape like appearance
  • Aerobic or facultative anaerobe
  • Transmission= aerosol like cough droplets or direct contact- droplets and shed skin
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14
Q

Compare and contrast the types of S.aureus strains-MRSA and MSSA?

A

• MRSA= methicillin resistant staphylococcus aureus
• MSSA= methicillin sensitive staphylococcus aureus
Same golden spherical shape and appearance
Different antibiotic susceptibilities
MRSA resistant to
1. Methicillin
2. Penicillin’s- penams and beta lactams
3. Cephalosporins- 1st, 2nd, 3rd, 4th generations
4. Carbapenems
MRSA is more virulent and easily transmitted
MRSA higher mortality rates than MSSA
MRSA is acquired in community and hospital = HA-MRSA AND CA- MRSA

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15
Q

Compare and contrast HA-MRSA and CA-MRSA?

A

HA infects UT but CA infects skin and soft tissue
HA strains rarely possess PVL virulence factor but CA do
Both show b-lactam resistance
HA more resistant to different types of antibiotics
HA risk mainly for elderly, hospitalized and surgery patients but CA mainly children, homeless, jail, younger adults

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16
Q

Describe morphology of streptococcus pyogenes?

A
  • Gram +ve cocci in chains
  • Facultative anaerobe
  • Lancefield grouping- in group A streptococcus GAS
  • Non-motile
  • Colonises upper respiratory tract
  • Causes invasive infections
17
Q

Describe the virulence factors of streptococcus pyogenes?

A

M protein= evade phagocytosis, immune evasion
Protein F= fimbriae= cell adherence and attachment
Hyaluronic acid Capsule= prevents phagocytosis
Lipoteichoic acid= adheres to molecules on host epithelial cell
pyrogenic exotoxin

18
Q

What infections are caused by streptococcus pyogenes?

A 
scarlet fever
impetigo
sore throat
cellulitis
necrotising fasciitis
19
Q

Describe the virulence factors of streptococcus pneumoniae?

A

polysaccharide capsule= antiphagocytic, prevents mucopolysaccharide binding
pneumolysin= pore forming toxin, induces cytokine release, membrane damaging, inhibits phagocytic cell oxidative burst
hydrogen peroxide= evades host defenses, forms oxygen radicals
surface protein adhesin= helps cell adherence and colonization
cell wall teichoic acid and peptidoglycan= induces inflammation, activates alternative complement pathway
Secretory IgA protease= disrupts IgA mediated clearance

20
Q

What infections are caused by streptococcus pneumoniae?

A

CAP

21
Q

Describe morphology of streptococcus pneumoniae?

A

 Gram positive coccus
 >90 capsular types
 Non-infectious forms are non-capsulated
 Non motile
 Inhabits upper respiratory tract including nasal cavity, pharynx, and nasopharynx
 Affects children more than adults

22
Q

Explain how dental caries and periodontitis arise and how, as a pharmacist you would advise your patients to prevent these diseases (15).

A

Dental caries arises on a susceptible tooth surface where dietary sugars are present in the oral cavity meaning there is a reduced flow of saliva and reduced fluoride exposure
White spots present on the surface of the enamel also make the tooth susceptible
Aciduric and acidogenic bacteria for example mutans streptococci and lactobacilli form a biofilm on the surface of the tooth and produce acid leading to the formation of plaque
The sugar ferments and increases the presence of organic acids and reduces ph causing an ecological shift in minerals
This leads to demineralisation of the tooth and eventually formation of caries
Periodontal disease arises from the inflammation of the gingival crevice and the wasting of bone around the tooth
gingivitis is the initial stage in the development of periodontitis and it is the inflammation of the gums and the presence of redness and bleeding
When alveolar bone and tissue loss starts to occur and the loss of attachment is initiated this leads to chronic periodontitis
This then leads to necrotising periodontal disease as more bone and tissue is lost and there is presence of pain, bad breath, grey-pseudomembrane on the gingivae
The final stage in the progression of periodontal disease is aggressive or severe periodontitis leading to rapid loss of attachment
The disruption of the microflora leads to periodontal disease and arises when plaque accumulates as it causes an inflammatory response
This leads to an increase in the flow of gingival crevicular fluid allowing nutrients to reach bacteria aiding the growth and survival of proteolytic bacteria
Bacteria presence can also be increased due to risk factors such as smoking, tongue piercings, hormonal disturbances in pregnancy, certain drugs and medications such as drugs used in chemotherapy, immunosuppression such as HIV/AIDS, low salivary flow and dry mouth
As a pharmacist the following prevention advice should be initiated
Brush teeth twice a day once at night and once in the morning
Reduce sugar intake and if using medications especially for children use sugar free alternatives
Use interdental brushes and floss between teeth and below the gumline to reduce the risk of plaque formation
For people who smoke smoking cessation service should be adviced and signpost
If it is linked to certain medications involve the patients GP to discuss alternative drugs that could be used
Use dental products that contain fluoride
If the above methods of maintaining dental hygiene is inadequate in controlling plaque advise on the use of antimicrobials such as mouthwashes containing chlorhexidine

PUBLIC EXAM Qs (1 decks)

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