Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacy - Year 2 > Infections JD + MAH > Flashcards

Infections JD + MAH Flashcards

1
Q

Epidemiology?

A

How often diseases occur in different people and why. Used for prevention strategies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Agent?

A

Substance (living/non-living) or force in excess which initiates disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Examples of agents?

A

Biological - bacteria/viruses
Nutrient - carbs
Physical - temperature
Chemical - uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Infection?

A

Entry + development/multiplication of infectious agent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Transmission (of infection)

A

Spread of inf agent through environment (from source)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Host?

A

Animal/human that affords lodgement for inf agent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Innate immunity?

A

immediate response to breach of barrier, causes swelling and redness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ex of barrier immunity

A

mucus, skin, acidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Adaptive immunity?

A

Delayed response, but specific to pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Barrier immunity?

A

Prevents pathogens entering body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T cells

A

kill pathogen infected cells, tell B cells to make antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

B cells

A

Make specific antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Antibodies

A

Bind to pathogens and make easy to kill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 major ways for pathogen transmission

A
  1. between humans
  2. via environment (soil/water)
  3. between humans and animals (vectors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

General transmission factors - abiotic

A

Wind, water, inhalation of spores, entry through skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

General transmission factors - animal vectors

A

Mosquitoes, fleas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Human to human transmission - direct contact

A

pathogen survives best in body through contact within skin, mucous, blood - HIV, ebola, herpes, chickenpox, ringworm, cold sores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Human to human transmission - indirect

A

path survives harsh environment - through surface or air - influenza, norovirus - objects called fomites - used tissue, handrails

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Human to human transmission - droplets

A

path in droplets - don’t survive long - ebola, bordatella pertussis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Human to human transmission - airborne

A

aerosolised + stay infective - influenza, TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Human to human transmission - faecal to oral

A

excreted from gut - eaten through contaminated food/water (fomite) - cholera, norovirus, shigella, hep a, rotavirus, intestinal worms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Human to human transmission - aerosol

A

via resp system - breathes, coughs, sneezes into air - another person inhales

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Human to human transmission - blood-borne path

A

unsafe injections. contaminated transfusions - (needles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Human to human transmission - vertical

A

mother to child - across placenta or milk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Environmental transmission

A

Natural reservoir that cause infection - soil + water - clostridium tetani - soil - produces spores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Environmental transmission - water

A

bacteria e.g or toxins/viruses survive and replicate within water (no host)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Environmental transmission - water - how to prevent? + examples of water-borne infection

A

sanitisation for safe water supply - cholera + legionnaires

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Can env transmission occur from inhaling?

A

yes - Pontiac fever, legionnaires

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Zoonoses?

A

Transmission from animal to human - ex are avian influenza (birds) + rabies (bite/scratch)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Vector-borne definition?

A

Part of life cycle in human host - part of cycle must take place in other species known as vector - mosquitoes, flies, ticks and lice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Spectrum of antibiotic activity

A
  1. measures how many organisms the antimicrobial targets - antibiotics + antifungals
  2. narrow - specific
  3. broad - wide range of organisms - typically target gram+ and gram-
33
Q

Penicillin V?

A

oral - narrow spectrum - mild infections (throat/skin)

34
Q

Penicillin G

A

unstable in acid - given IV /parenteral - severe infections - pneumonia, meningitis. syphilis

35
Q

flucloxacillin?

A

narrow spectrum - gram+

36
Q

amoxicillin?

A

broad spectrum

37
Q

Mechanisms of pathogen-host interaction

A

1, adherence (pili/fimbriae, adhesins.biofilms)
2. immune evasion (antigenic variation, intracellular survival, inhibition of phagocytosis)
3. tissue damage (toxins, inflammation, host cell death)

38
Q
A
39
Q
A
40
Q
A
41
Q

Infection pathogenesis

A
  1. colonisation (establish residence at site of infection)
  2. invasion (breach host barriers gaining access to deeper tissues)
  3. proliferation (path multiply and spread)
  4. dissemination (spread to other sites/or new hosts)
42
Q

Pathology ?

A

(medical) Term describing conditions observed in disease state. Describes abnormal or undesired condition.

43
Q

Physiology?

A

(Biological) term describing processes/mechanisms operating within an organism.

44
Q

Pathophysiology?

A

Convergence of pathology with physiology. explains functional changes occurring within an individual due to disease or pathologic state. The disordered physiological processes associated with disease or injury. Disruption of the body’s homeostasis; alteration in function, metabolism, organ systems and the mechanisms involved. (easy answer - combo of both - explains how boys normal processes are disrupted during disease leading to illness symptoms)

45
Q

Aetiology:

A
  1. Idiopathic
    - Don’t know what’s caused it – want to figure out
  2. Nosocomial (HAI e.g MRSA)
    - Healthcare or hospital acquired infections
  3. Iatrogenic
    - Caused by a doctor or healthcare professional
  4. Multifactorial
    - Pathogens, environment etc
46
Q

Risk Factor

A

presence of something increases the likelihood of disease

47
Q

Pathogenesis

A

development or evolution of the disease, from initial stimulus to manifestation of disease

48
Q

Pathogens

A

agent of disease: virus, bacteria, fungi, environmental, multifactorial

49
Q

Systems

A

affects systems i.e respiratory disorders etc complex thus look at pathophysiology of a disease state

50
Q
  1. Concept of disease
  2. Fundamental pathological process
  3. Systemic pathophysiology
  4. Pathophysiology of disease
A
  1. Concept of disease
  2. Fundamental pathological process
  3. Systemic pathophysiology
  4. Pathophysiology of disease
51
Q

Clinical course of a disease (biomedical perspective)

A
  1. Exposure to pathogen
  2. Biological onset of disease
    (Preclinical phase)
  3. Symptoms appear
    (Clinical phase)
  4. Diagnosis
    (Clinical phase)
  5. Therapy begun
    (Clinical phase)
  6. ‘Outcomes’ (cured; living with the disease; deteriorated; died)
  7. Diagnosis
    (Possible relapse and change in therapy)
52
Q

Symptoms?

A

Feeling: Headache, feeling hot, generally unwell

53
Q

Signs

A

Measurable: Temperature >38.9, Inflammatory markers, low blood pressure, low platelet count

54
Q

Syndrome

A

Diagnosis: Toxic shock syndrome

55
Q

Inflammatory markers of influenza

A
  • Sudden high temp
  • Tiredness and weakness
  • A headache
  • General aches and pains
  • A dry, chesty cough
  • Sore throat
  • Difficulty sleeping
  • Loss of appetite
  • Diarrhoea or tummy pain
  • Feeling sick and being sick
  • Chills
  • Runny or blocked nose
  • Sneezing
56
Q

inf markers Escherichia coli (E.coli)?

A
  • Diarrhoea (bloody in half of people)
  • Stomach cramps
  • Occasionally fever
  • Small number go on haemolytic uraemic syndrome (HUS)
  • Some people have no symptoms
57
Q

Staphylococcus aureus

A
  • Painful red lump or bump on skin (boil)
  • Hot, red and swollen skin (cellulitis)
  • Sores, crusts or blisters (impetigo)
  • Sore, red eyelids or eyes (stye or conjunctivitis)
  • Staph bacteria can also cause more serious infections, like blood poisoning and toxic shock syndrome. These are much less common than skin infections.
58
Q

3 Systemic effects of infection?

A

fever, sepsis, organ dysfunction

59
Q

Fever?

A

is the elevation of an individual’s core body temperature above a ‘set-point’ regulated by the body’s thermoregulatory centre in the hypothalamus.

60
Q

Elevated body temp >38 in response to infection, caused by the release of pyrogens?

A
  • Physiological process brought about by infectious causes or non-infectious causes such as inflammation, malignancy, or autoimmune processes
  • Fever is mediated by the pyrogenic activity of prostaglandins, specifically pge2
  • Pge2 stimulate endogenous pyrogens such as il-1, il-6, tumour necrosis factor (tnf), and interferon (ifn) to alter the hypothalamic set point
  • Endogenous pyrogens also act to trigger an immune and inflammatory response. The immune response includes leukocytosis, T cell activation, B cell proliferation, NK cell killing, and increased white blood cell adhesion
  • The inflammatory response includes increased acute phase reactants, increased muscle protein breakdown, and increased synthesis of collagen
61
Q

Sepsis?

A

a severe systemic response to infection, characterised by widespread inflammation and organ dysfunction.

62
Q

What happens during sepsis?

A
  • Infection triggers a dysregulated immune response, leading to a systemic inflammatory state.
  • Release of pro-inflammatory cytokines causes widespread endothelial dysfunction, coagulation abnormalities, and organ dysfunction
  • Understanding the cascade of events is crucial for early recognition and management of sepsis
  • …….. sepsis progressing to septic shock and multi-organ failure results from
    1. Circulatory insufficiency characterised by hypovolemia
    2. Myocardial depression
    3. Increased metabolic demands
    4. Vaso regulatory perfusion abnormalities
63
Q

SIRS?

A

systemic inflammatory response syndrome describes the inflammatory response, independent of cause, based on a combination of vital signs and blood work.

64
Q

SIRS includes 2 or more of the following?

A
  • Temp greater than 38C or less than 36C
  • HR greater than 90bpm
  • Tachypnoea greater than 20 breaths per minute or PaCO2 less than 32mmHg
  • WBC count greater than 12,000 per cubic millimetre or fewer than 4000 per cubic millimetre, or greater than 10% immature (band) forms
65
Q

Severe Sepsis?

A
  • Sepsis associated with organ dysfunction (1 or more), hypo-perfusion abnormality, or sepsis-induced hypotension
  • Hypo-perfusion abnormalities may include but are not limited to lactic acidosis, oliguria, or acute change in mental status
66
Q

Septic shock?

A
  • Sepsis induced hypotension despite adequate fluid resuscitation ?
67
Q

Organ dysfunction ?

A

infections can directly impact various organs, leading to impaired function or failure.

68
Q

What happens during organ dysfunction?

A
  • Organ dysfunction is an integral part of sepsis, and the presence of unexplained organ dysfunction in a patient who is acutely ill should raise suspicion of the possible presence of sepsis and encourage an appropriate diagnostic examination.
  • The pathophysiology of organ dysfunction in sepsis is similar for all organs and involves complex haemodynamic and cellular mechanisms.
  • First goal in prevention of organ dysfunction in sepsis is to restore and maintain adequate oxygen delivery to cells.
  • Single-organ dysfunction in sepsis is rare, and several organs are usually affected; mortality in patients with sepsis correlates with the number of organs that are affected
  • Most organ dysfunction in sepsis is reversible
  • Current treatment for sepsis aims to limit the development of organ dysfunction by providing rapid control of infection, haemodynamic stabilisation and organ support when possible to ensure recovery of organ function
69
Q

Pathogenesis of UTI?

A
  1. Colonisation
    - Pathogen colonises the periureteral area and ascends through the urethra upwards towards the bladder.
  2. Uroepithelium penetration
    - Fimbria allow bladder epithelial cell attachment and penetration.
    - Following penetration, bacteria continue to replicate and may form biofilms.
  3. Ascension
    - Once sufficient bacterial colonisation occurs, bacteria may ascend on the ureter towards the kidney.
    - Fimbria may aid in the ascension process.
    - Bacterial toxins may also play a role by inhibiting peristalsis (reducing the flow of urine).
  4. Pyelonephritis
    - Infection of the renal parenchyma causes an inflammatory response called pyelonephritis.
    - While infection of the renal parenchyma is usually the result of bacterial ascension, it can also occur from hematogenous spread.
  5. AKI
    - If the inflammatory cascade continues, tubular obstruction and damage occur, leading to interstitial oedema.
    - This may lead to interstitial nephritis, causing acute kidney injury.
70
Q

Chronic renal failure?

A

look at slide in lecture because its starred?

71
Q

Pneumonia? signs and symptoms? - look back at lecture - starred slide for development of it?

A
  • Chest pain when breathing or coughing
  • Cough, which may produce phlegm
  • Fatigue
  • Fever, sweating and shaking chills
  • Confusion or changes in mental awareness (65+)
72
Q

Clinical course of a disease: 4 prevention stages?

A
  1. Primordial Prevention
    - Alter societal structures and thereby underlying determinants
  2. Primary prevention (direct action)
    - Alter exposures that lead to disease
    (etiological phase – social + environmental determinants, risk + protective factors)
  3. Secondary prevention (early detection)
    - Detect and treat pathological process at an earlier stage when treatment can be more effective
    (preclinical phase)
    (clinical phase)
  4. Tertiary prevention (treatment and rehabilitation)
    - Prevent relapses and further deterioration via follow-up care and rehabilitation
    (post-clinical phase)
73
Q

Accurate diagnosis?

A

understanding mechanisms of infection aids in accurate diagnosis

74
Q

Effective management?

A

Knowledge of pathophysiology guides interventions and treatment strategies

75
Q

Prognostic indicators

A

recognise systemic effects can provide insights into prognosis and potential complications

76
Q

Epidemiology?

A

study of diseases within a population

77
Q

to look up:

A

diagnosis, prognosis, morbidity, mortality, incidence, prevalence, endemic, epidemic, pandemic

78
Q
A

Pharmacy - Year 2 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions