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Medicine 2 > RCM Week 3 (pneumonia) > Flashcards

RCM Week 3 (pneumonia) Flashcards

1
Q

What is the volume of distribution and how do you calculate it

A

It is the apparent volume in which a drug is dissolved in the body

Vd = amount in body / conc
= dose / conc at t=0

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2
Q

What is clearance of a drug and how do you calculate it

A

The volume of plasma cleared of a drug in unit time

(Ml / min) , (L/h)

Clearance = renal clearance + hepatic clearance

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3
Q

What is first order kinetics

A

Rate of elimination is proportional to concentration of drug

Ct = C0e-kt

Where Ct = conc at t=t
C0 = conc at t=0
K = rate constant (per min or per hour)
T= time

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4
Q

How do you calculate half life

A

T1/2 = 0.693/ k

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5
Q

What is the steady state

A

The level that is the aim for the patients plasma concentration to be
Where
Administration rate = elimination rate

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6
Q

How do you calculate infusion rate

A

Clearance x Css (concentration steady state)

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7
Q

What is aminophylline

A

Used sometimes in severe asthmatic attacks
Is a bronchodilator
Given by IV infusion
(Is the salt of theophylline 80%)

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8
Q

How to calculate an oral dose

A

Dose - CL x CSS x tau / F

Tau is the dosage interval

  • double the dose = double the conc
  • F stands for bioavailability (fraction of the drug that is absorbed)
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9
Q

Describe the design of dosage regimens

A

1) the therapeutic window
- large TW ‘ maximal dose’ strategy
- small TW ‘target level’ strategy

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10
Q

What is the maximal dose strategy for dosage regimens

A

Give a large dose and give it frequently as you have a wide safety margin

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11
Q

What is the target level strategy for dosage regimens

A

Used for drugs with a small therapeutic window

IV infusion usually used so concentration is constant and avoids fluctuations

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12
Q

What is a strategy for reaching the plasma concentration more rapidly in the case of urgent medications

A

Loading dose = target Css x Vd / F

Then, maintenance dose = target Css x CL x tau / F

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13
Q

What is anti microbial chemotherapy

A

Using chemicals (antibacterials and antibiotics / anti microbials) drugs to selectively kill bacteria, viruses and fungi without affecting the host

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14
Q

What does antimicrobial chemotherapy target

A
  • bacterial cell wall
  • bacterial ribosomes
  • bacterial folate metabolism
  • bacterial DNA gyrase
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15
Q

What do all penicillins have in common

A

The beta lactam ring that can be broken down by bacteria

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16
Q

Describe the mode of action of penicillin

A

They target bacterial cell wall synthesis by binding irreversibly to a transpeptidase, which cross links peptidoglycan chains in the bacterial cell wall

  • only effective against dividing organisms as division requires cells wall synthesis, leading to lysis
  • penicillins are bactericidal : cause lysis of bacteria
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17
Q

What are beta-lactamases

A

Beta lactamases are secreted by resistant bacteria and can inactivate penicillin

To overcome this, clavulanic acid is included with some agents eg amoxicillin to inhibit the B-lactamases
And other penicillins eg flucloxacillin are resistant to B-lactamases

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18
Q

Advantages and disadvantages of clarithromycin

A

Advantages: very effective
Disadvantages: has lots of drug interactions.

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19
Q

Describe the action of tetracyclines

A

They inhibit protein synthesis by binding to the 30S subunit of the bacterial ribosome and prevent tRNA from binding at the acceptor (A) site

They actively accumulate in bacterial cells

They are bacteriostatic

Their use has decreased due to resistance

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20
Q

Describe how macrolides work eg clarithromycin, erythromycin

A

They prevent the translocation of the 50S subunit of the bacterial ribosome along the mRNA

  • prevent protein synthesis
  • bacteriostatic
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21
Q

Pros and cons of using macrolides (clarithromycin, erythromycin)

A

Pros: often used as an alternative to penicillin in patients with an allergy

Cons: macrolides are cytochrome P450 (liver- responsible for drug metabolism) inhibitors and associated with a range of drug interactions (increase concentrations of interacting drugs as they cant be broken down)

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22
Q

How do aminoglycosides work eg gentamicin, neomycin, tobramycin

A

Aminoglycosides bind irreversibly to the 30S subunit of bacterial ribosomes, leading to misreading of mRNA and interfere with protein synthesis

They are bactericidal and used to manage gram negative bacteria

Synergy with penicillins: breakdown of cell wall increases uptake of aminoglycosides

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23
Q

Describe how quinolones work eg ciprofloxacin, norfloxacin

A

These are inhibitors of bacterial DNA gyrase topoisomerase II and topoisomerase IV

Gram negative bacteria: dna gyrase is inhibited and quinolones inhibit the supercoiling of the bacterial DNA which is essential for DNA repair and replication

Gram positive bacteria: topoisomerase IV is the target and quinolones interfere with the separation of DNA strands on replication

Bactericidal

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24
Q

What is trimethoprim

A

A safe antibacterial used in UTIs

  • structurally related to folate
  • folate antagonist and inhibiting the bacterial dihydrofolate reductase, which converts folate to tetrahydrofolate

-trimethoprim is less potent against the human form of the enzyme

Bacteriostatic

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25
Q

What are sulphonamides

A

Analogues of p-aminobenzoic acid and inhibit the growth of bacteria by competitively inhibiting the enzyme dihydropteroate synthase, involved in the synthesis of folate from PABA

The availability of DNA and RNA precursors is therefore reduced

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26
Q

What is metronidazole

A

A pro drug which is activated by anaerobic bacteria to cytotoxic products which damages the helical structure of DNA, protein and the cell membrane

  • it is used against anaerobic bacteria and Protozoa
  • one of the only antibiotics that interferes with alcohol
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27
Q

What is croup

A

Inflammation around the epiglottis in young children

- inspiratory strider due to narrowed airways

28
Q

Describe the influenza virus

A

Segmented negative ssRNA genome

8 segments encode 11 proteins

29
Q

What are the high risk groups that would receive the flu vaccine

A 
Lung disease 
Cardiac disease 
Renal disease 
Endocrine disease 
Immunodeficiency 
Liver disease 
Anyone >65 
Pregnancy 
Young child
30
Q

What are the bacterium’s that cause tuberculosis

A

Mycobacterium tuberculosis mainly

Less commonly: M. Bovis (in cattle) M.africanum, M.microti

31
Q

Clinical features of TB

A

Non specific: fever, weight loss, night sweats

Respiratory symptoms:
Cough, shortness of breath, haemoptasis, chest pain

32
Q

What are the layers of blood vessels

A

Lumen
Tunica intima (internal elastic lamina)
Tunica media (external elastic lamina)
Tunica adventitia

33
Q

What type of cells line the lumen of blood vessels

A

Simple squamous endothelial

34
Q

Structure related to function of arteries and veins

A

Large T media in arteries for strength

Diameter of lumen is relatively smaller

Veins have thin walls and large lumen

35
Q

How are vessels adapted to allow blood flow

A

Endothelium is a smooth non stick surface which facilitates laminar flow

36
Q

When does turbulent flow in blood vessels occur

A

Turbulent flow occurs where vessels branch and when blood pressure is raised
This can eventually damage the endothelium which exposes the blood to collagen and other factors that cause the blood to clot

37
Q

What is a thrombus

A

Solid mass of blood constituents formed within the vascular system in life

38
Q

What is atherosclerosis

A

Fatty deposits in the Tunica intima harden the walls and narrow the lumen- this reduced blood flow to the tissues: ischaemia

39
Q

What causes varicose veins

A

Incorrect functioning of valves

40
Q

What are arterioles and venules

A

Arterioles are small vessels with muscular walls

Venules are the smallest vessels in the venous circulation

41
Q

What is the role of arterioles in resistance and blood pressure

A

Reduced blood flow leads to improper perfusion of tissues and lack of nutrients (ischaemia) which can lead to cell death

Too much flow damages delicate tissue structure

Arterioles control this by varying their diameter

42
Q

What are capillaries

A

Thin walled vessels to facilitate exchange of nutrients with the tissue:

  • endothelial cells ( 1 cell thick) + BM + collagen fibrils
  • occasional pericyte + BM
  • approx 5-8 microns in diameter
  • endothelial cells are joined by tight junctions and contain many vesicles
43
Q

What is the endothelial cell function

A

Permeability barrier

  • produces extracellular matrix
  • produces factors that modulate blood flow
  • produces anticoagulants and prothrombotics
  • regulates inflammation
  • cell growth
44
Q

3 types of capillaries

A

Continuous : found in nervous system, fat and muscle tissue

Fenestrated : have pores / holes (leaky capillaries) found in the glomerulus

Sinusoidal: much bigger holes to allow cells to move in and out found in liver, and bone marrow

45
Q

What is pneumonia

A

Infection and inflammation of the lung parenchyma

46
Q

How does pneumonia cause breathlessness

A

Fluid accumulates in the alveoli and impairs gaseous exchange

47
Q

How is the PCR test carried out for COVID 19

A

A nasal and throat swab done at the same time
Aim is to see if there’s any DNA and a machine then amplifies the DNA so even if there are only small amounts it can still be detected

48
Q

Difference between community and hospital acquired pneumonia

A

Any pneumonia (bacteria or viruses) acquired before being admitted to hospital is community acquired

Any pneumonia you get more than 48 hours after coming into hospital is hospital acquired

Important to classify properly as the pathogens involved are different and antibiotic treatment is different

49
Q

What is community acquired pneumonia

A

Acquired before or within the first 48 hours of coming into hospital

Acute illness with :
Cough
And
- new focal chest signs, or fever or dyspnoea/ tachypnoea
And
Radio graphic evidence of new lung infiltrates (X-ray)

50
Q

How does one get pneumonia

A

Failure of body’s own defence mechanisms against infectious agents:

  • cough
  • mucociliary escalator
  • macrophages

Could be due to virulent organism or immune dysfunction / dysregulation

51
Q

Clinical presentation of pneumonia

A

Chest infection often complicates a ‘cold’ especially in more elderly patients
- green sputum - consistent with infection
- crackles heard on chest - indicating fluid
- resp rate 30 breaths per min normally 13-15 per min
Body’s response to poor O2 saturation:
- chest pains on breathing - pleuritic pain?
- pyrexia at 39c - infection
- patient very confused due to hypoxia and / or systemic infection

52
Q

Summary of the clinical respiratory and non respiratory features of pneumonia

A

Respiratory: cough, breathlessness, chest pain

Non respiratory: fever, confusion, drowsiness, lethargy / tiredness

53
Q

Clinical signs of pneumonia

A

General examination:

  • temperature
  • high respiratory rate
  • low O2 levels
  • low BP

Auscultation of the chest

  • decreased air entry
  • crackles
54
Q

Investigations to test for pneumonia

A

1) blood tests :
- markers of infection
- markers of dehydration

2) microbiology: to identify causative organisms
- blood cultures
- sputum cultures
- urine samples

3) other tests: not always required unless diagnostic uncertainty or failure to respond to treatment
- CT scan of chest
- bronchoscopy

55
Q

How is arterial O2 levels linked to pneumonia

A

Arterial O2 levels should be >95% <92% patient is likely to have symptoms of hypoxia

It is measured by pulse oximetry with a non invasive device on the finger

56
Q

What is the CURB 65 severity assessment

A
  • confusion
  • urea >7mmol/l
  • resp rate >30/min
  • blood pressure, SBP <90 or DBP <60 mmHg
    Age >65

0-1 points = 1.5% mortality
2 points = 9.2% mortality
3-5 points = 22% mortality

57
Q

What is enoxaparin.

A

An injectable anticoagulant to prevent thrombosis

  • patients who are immobile in hospital are at risk of DVT due to poor venous return and the blood stagnates
  • DVT poses a risk for a life threatening pulmonary embolism
58
Q

How can pneumonia be treated with antibiotics

A

Co-amoxiclav and clarithromycin

Blind: the best guess: the concept of using broad spectrum agents in the absence of microbiological evidence

59
Q

3 different types of treatment for pneumonia

A

1) antimicrobial therapy:
- broad spectrum antibiotics initially narrow spectrum antibiotics antivirals

2) supportive measures
- oxygen
- IV fluids

3) symptomatic treatment
- paracetamol
- painkillers

60
Q

What is co-amoxiclav

A

Amoxicillin and clavulanic acid

- clavulanic acid is a beta lactamase inhibitor to prevent bacterial beta-lactamases degrading the beta-lactam ring

61
Q

Why are antibiotics administered intravenously

A

The patient is severely unwell and a rapid response is needed
Swallowing may also be different
- once afebrile for 24 hours then aim to switch to oral (easier and not complicated by a risk of line infection)

62
Q

Explain the 4 stages of pneumonia : consolidation, red hepatization, grey hepatization, resolution

A

1) consolidation:
- 1st 24 hours
- cellular exudate comprising neutrophils, lymphocytes etc replace alveolar air
- congestion of surrounding capillaries

2) red hepatization
- occurs within 1st 3 days
- hyperaemic lung with engorged capillaries
- fibrinous exudates fill alveoli along with RBCs

3) grey hepatization
- occurs after the above
- lung appears ‘grey’ because of disintegration of red cells; persistence of fibrin exudate

4) resolution
- phagocytosis / enzymatic digestion of bacteria / exudates by leucocytes
- restoration of lung architecture

63
Q

What is treatment failure

A

Clinical deterioration:

  • persistence or reappearance of fever
  • respiratory failure (increasing oxygen requirement)
  • radiographic progression
  • need for mechanical ventilation
  • shock
  • death
64
Q

What are cephalosporins

A

Eg cefaclor, cefalexin, cefotaxime, cefuroxime
- B-lactam antibiotics
Act in a similar way to penicillins
- they show cross reactivity with penicillins and approximately 0.5-6.5% of penicillin-allergic patients will also be allergic to cephalosporins

65
Q

What are glycopeptides

A

Eg teicoplanin, vancomycin

  • these also inhibit bacterial cell wall synthesis by inhibiting the growth of the peptidoglycan chain
  • they are often used to manage severe infections due to ‘superbugs’ such as methicillin-resistance staphylococcus aureus (MRSA)
  • largely bactericidal
66
Q

What are aminoglycosides eg gentamicin, neomycin, tobramycin

A

Aminoglycosides bind irreversibly to the 30S subunit of bacterial ribosomes leading to misreading of mRNA and interfere with protein synthesis

They are bactericidal and used to manage gram-negative bacteria
Synergy with penicillins: breakdown of cell wall, increases uptake of aminoglycosides

Medicine 2 (16 decks)

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