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FoM3 > week 2 > Flashcards

week 2 Flashcards

1
Q

if both parents have T2D; what is their child’s lifetime risk of developing T2D?

A

80%

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2
Q

what are the 5As of obesity intervention?

A

ASK: permission to discuss weight; explore readiness to change
ASSESS: obesity stage/BMI/comorbidities/factors
ADVISE: discuss treatment options and benefits
AGREE: expectations, goals, treatment plan
ASSIST: arrange follow up etc

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3
Q

what is tTG?

A

A tissue transglutaminase IgA (tTG-IgA) blood test measures the levels of antibodies in your blood that attack the enzyme tissue transglutaminase. It is not a clear diagnostic test for coeliac disease in adults. In children after expert assessment then can suffice.

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4
Q

obesity related skin conditions

A

acrochordons, acanthosis nigricans, intertrigo, skin infection/slower wound healing, increased acne severity, stretch marks, hirsutism, psoriasis, lymphoedema

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5
Q

what is use in place of normal formula for infants with cow’s milk intolerance?

A

an extensively hydrolysed infant formula

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6
Q

what conditions can result in impaired nutrient digestion or absorption (x5)

A

decompensated liver disease
pancreatic cancer
undiagnosed coeliac disease (Fe, calcium, B12)
Short bowel syndrome
Crohn’s disease

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7
Q

sepsis 6

A

TAKE 3 –> within one hour
1) Urine output (catheterise)
2) Serum lactate (>4) and Hb (and U&Es)
3) Blood cultures

GIVE 3 –> within one hour
1) High flow oxygen
2) IV fluids
3) Appropriate IV antibiotics

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8
Q

define sepsis vs septic shock

A

Sepsis is life threatening organ dysfunction caused by a dysregulated host response to infection

Septic shock is a subset of sepsis with circulatory and cellular/metabolic dysfunction associated with a higher risk of mortality

ie sepsis with persistent hypotension despite adequate fluid resus

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9
Q

describe the pathophysiology of sepsis

A

Release of cytokines result in massive vasodilation
- –> Hypovolaemia
- –> Leaky capillaries, microthrombis worsening circulation, not enough oxygen getting to tissues; particularly kidneys
–> Reduced urinary output, SOB, decreased sats and BP, tissue ischaemia leads to lactate rise

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10
Q

risk factors for sepsis (6)

A

1) Hospitalised over 48 hours (risk of hospital acquired infections)

2) Ventilatory infections

3) Time of year (winter impacting immune system)

4) Immunosuppression (chemotherapy, immunotherapy, HIV)

5) Chronic lung diseases (bronchiectasis, CF, COPD)

6) Epidemiological exposures and travel (MERS Co-V, SARS CO-V2, TB, legionella)

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11
Q

what tool is used to prompt sepsis suspicion?

A

NEWS above 5 for urgent review

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12
Q

what to give for septic shock to maintain MABP above 65mmHg

A

vasopressor; noradrenaline

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13
Q

describe how c diff infections can arise

A

C Difficile (gram positive) exists in the GIT normally. the following can lead to overgrowth:
taking PPIs which make the GIT less acidic which is favourable
taking antibiotics
age over 65, recent hospitalisation and co-morbidities are other risk factors.

faecal-oral route transmission

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14
Q

how to treat c diff

A

resistant spores so:
Give vancomycin orally to reach stomach directly (NG if needed)(not IV)

in addition infection control; use of soap and water for handwashing

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15
Q

symptoms of c diff infection

A

watery diarrhoea, fever, abdominal pain

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16
Q

e coli: symptoms, management

A

bloody diarrhoea, supportive treatment (IV fluids) –> avoid antibiotics

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17
Q

watery vs bloody diarrhoea pathogens

A

watery: norovirus, g. lamblia
bloody: e coli, salmonella, shigella, campylobacter

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18
Q

raw veg bacterium

A

shigella

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19
Q

infective endocarditis: most common bacterium, risk factors, detection

A

S aureus the most common cause. Cardiac devices or IV drug use. If suspected then do repeat blood cultures; ideally 3 sets 6 hours apart (if sepsis suspected then 2 sets over the first hour)

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20
Q

treatment of infective endocarditis

A

GIVE FLUCLOXICILIN 2 grams 4 hourly minimum (high dose)

If MRSA then give vancomycin

Identify source:
Remove device if that is the cause; then exchange for different device. Washout if septic arthiritis is the cause. Drain any abscesses/debride necrotic bone in osteomyelitis/replaced infected vascular catheter/relieve urinary or biliary obstruction

Venous catheter = central line

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21
Q

DUKE criteria for diagnosing infective endocarditis

A

Major Criteria (Mnemonic: BE)
Blood Culture POSITIVE > 2 times 12 hrs apart.
Echocardiographic evidence of Endocardial Involvement

Minor Criteria (Mnemonic: TIMER)
Temperature > 38°C (Fever)
Immunological Phenomena (Osler’s nodes, Roth spots)
Microbiological Evidence (Positive blood culture not meeting a major criterion)
Embolic Phenomenon (Arterial emboli, septic emboli, conjunctival hemorrhage, & painless skin lesions)
Risk Factors - (Congenital heart condition or IV drug use)

Diagnostic Criteria:
Definitive Diagnosis: Two major criteria OR one major and three minor criteria OR five minor criteria.

Possible Diagnosis: One major and one minor criteria OR three minor criteria.

22
Q

pneumonia pathogens x3

A

Streptococcus pneumonia, haemophilus influenza, legionella (especially with travel)

1&2 have vaccines!

23
Q

CURB-65 is for

A

pneumonia severity

24
Q

treatment for pneumonia

A

amoxicilin
doxycycline
co-amoxiclav

etc

25
Q

what are the main 3 families of antibiotics

A

beta lactams (37.5%)
tetracyclines
macrolides

26
Q

how do beta lactam antibiotics function?

A

Beta-lactams target the cell wall of the target bacteria. Penicilin binding proteins (PBPs) are a group of enzymes key to synthesising bacterial cell walls. Beta-lactams resemble the target protein of this enzyme and bind to the PBPs, inactivating them.
-cilin drugs

27
Q

how do glycopeptide antibiotics work?

A

Non-beta lactam antibiotic; ex vancomycin

These target the cell wall by binding to the peptide side chains (D-alanine D alanine) and thereby preventing PBP from binding to them and incorporating them into the cell wall.

28
Q

natural antibiotic resistance (x4 modes)

A

Natural resistance refers to features that bacteria have that make them resistant to certain antibiotics; before any prior exposure to the drugs

- The bacteria lacks the target of the antibiotic (ex mycoplasma has no cell wall)

- The bacteria have a permeability barrier to the antibiotics (ex gram negative bacteria's outer membrane is a barrier to many drugs)

- The bacteria can be metabolically inert (dormant state where the antibiotics that target active cellular processes are less effective, ex. the spores of c. diff)

- The bacteria is able to produce enzymes that inactivate the antibiotics (beta lactamase)
29
Q

acquired resistance (x5 modes)

A

Acquired resistance refers to resistance that develops due to genetic changes, either through mutations or the acquisition of resistance genes from other bacteria via horizontal gene transfer

- Impaired influx: the bacteria acquires mutations that reduce the uptake of antibiotics

- Increased efflux: vice cersa

- Target modified or altered (vancomycin-resistant enterococci (VRE) have cell walls that prevent vancomycin binding)

- Insensitive target (MRSA have PBP2a that does not bind to beta lactams)

Degradation/inactivation (beta lactamase)

30
Q

common antibiotics for UTIs 2

A

Nitrofurantoin
Trimethoprim

31
Q

beta lactamase inhibitors x2

A

clavulanic acid, tazobactam

32
Q

persister cells

A

When antibiotics hit their target, they initiate a chain reaction of damage that ultimately kills the bacteria. However, this process relies on the bacteria being metabolically active and growing.

If a bacterium is slow-growing or in a metabolically inactive state, the antibiotic might not be able to initiate or sustain this damage cascade effectively. This is particularly relevant for persister cells, which are in a dormant state where their metabolic activities are minimized.

Persister cells are a specialised subpopulation of bacteria that can survive antibiotic treatment without having genetic resistance. They have tolerance not resistance.

Persister cells are not permanently in this state. They are transient between being active and dormant; making them challenging to target.

33
Q

biofilms and planktonic cells

A

Planktonic cells are bacteria that float in a liquid environment (ex blood).
A biofilm is a community of bacteria that adhere to surfaces and are protected by a matrix. Persister cells can be either of these, but especially biofilms.

Biofilms form over surfaces like medical devises, tissues or teeth. The matrix can prevent antibiotics or immune cells from penetrating. Associated with chronic or recurring infections and being challenging to treat.

34
Q

what drug type is contraindicated with sildenafil?

A

Sildenafil (Viagra, a PDE-5 inhibitor) used to treat erectile dysfunction. It works by dilating blood vessels, which can lower blood pressure.
Isosorbide mononitrate is a nitrate, also used to dilate blood vessels and reduce chest pain (angina).
When taken together, sildenafil and nitrates can cause a significant and potentially life-threatening drop in blood pressure, leading to collapse or even death.

35
Q

what medication used for CHF can also exacerbate gout?

A

furosemide can increase serum uric acid

36
Q

which drugs should grapefruit be avoided with?

A

statins and calcium channel blockers

37
Q

colchicine use and contraindication

A

acute gout exacerbations. renal impairment.

38
Q

pain killer to use with warfarin

A

paracetamol (aspirin, diclofenax, ibuprofen etc are NSAIDs and can increase risk of bleeding when combined with warfarin)

39
Q

how long in advance of surgery should warfarin be stopped?

A

5 days

40
Q

Mechanism by which spinal anaesthesia most commonly causes hypotension

A

Blockade of sympathetic transmission to blood vessels, causing vasodilation

41
Q

Clonidine

A

centrally acting alpha-2 agonist - lowers blood pressure

42
Q

anti-emetic for Parkinson’s Disease patients

A

Domperidone is often preferred in patients with Parkinson’s disease because it does not cross the blood-brain barrier, meaning it does not worsen Parkinson’s symptoms. Other antiemetics like metoclopramide and chlorpromazine are dopamine antagonists that can exacerbate Parkinson’s symptoms by blocking dopamine receptors in the brain.

43
Q

ARB and potassium

A

ARBs can cause hyperkalaemia –> as aldosterone normally promotes K excretion

44
Q

pharmacokinetics vs pharmacodyamics

A

pharmacokinetics is what the body does to the drug, and Pharmacodynamics is what the drug does to the body.

45
Q

mechanism of furosemide induced gout exacerbation

A

urinate more. lowers fluid in the body. remaining fluid is more concentrated. can make the crystals that cause gout more likely to form.

also decreases uric acid secretion

46
Q

why no grapefruit and statin?

A

Grapefruit contains a compound known as furanocoumarin, which deactivates an enzyme that breaks down certain drugs, including statins. As a result, the drug concentration increases dramatically. This can cause a rare but serious condition that causes breakdown of muscle tissue and can lead to kidney failure.
pharmacokinetic result

47
Q

naproxen

A

NSAID for gout
decreases prostaglandins
can be good but contraindicated if renal issues as can be toxic in these cases.

48
Q

when to take a sample for measurement of drug levels?

A

at trough levels of steady state - ie just before next dose

49
Q

parkinson’s first line therapy

A

Co-careldopa
Combination of Levodopa + Carbidopa
One of the first line therapy

due to side effects may need an anti-emetic

49
Q
A
50
Q
A

FoM3 (9 decks)

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