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Year 3 Workbook > Medicine day case > Flashcards

Medicine day case Flashcards

1
Q

What are the different types of vasculitis and why are there different types

A

c- ANCA -> WG (granulomatosis + polyangitis)

p-ANCA -> CSD (eosinophilic granulomatosis + polyangitis

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2
Q
  1. What is Gilberts syndrome?
A
  1. Higher amounts of bilirubin

Think its because of a gene/ familial -> less UGT enzyme UDP-glucuronosyltransferases

Not harmful

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3
Q
  1. Parapneumonic effusion causes:
  2. How does GTN cause a cough?
  3. Tazocin:

What is it, Indications

  1. Citalopram
A
  1. penumonia, lung abscess, bronchiectasis
  2. Bradykinin -> vasodilator (ACE inhibitors 2nd effect dec bradykinin breakdown vs ARB does not effect it)
  3. pipercillin with tazobactam

HAP, Sepsis, complicated UTI, skin inf, soft tissue

IV: 4.5g every 8hrs

s/e: thrombocytopenia

pregnancy: only in B> risk
4. MOA: SSRI

Indication: depression

Adult 20mg-40mg/day (PO) tablets

Indication: panic disorder

10mg-40mg/day PO tablets

s/e: prolonged QT interval, acute angle closure glaucoma

; 4.

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4
Q
  1. What is Ventalin?
  2. What is the normal range for eosinophils
  3. What is Fostair 100/6
  4. With ACE-I what should we check?
  5. What do HF patients bring up?
  6. S/e of Haemodialysis
A
  1. B2 agonist (blue SABA)
  2. Adult 0.04 – 4.00 x 109/L
  3. 100 micrograms of beclometasone dipropionate and 6 micrograms of formoterol fumarate dihydrate. (LABA)
  4. Kidney monitoring, potassium (hyperkalaemia)
  5. pinkish phlegm
  6. cramps due to volume changes (?poor perfusion)
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5
Q
  1. What are you suspecting with a pansystolic murmur
  2. What is Becks triad
  3. In fluid overloaded patients what may you see in fluid overload
  4. What is nicorandil and its indications
A
  1. mitral regurgitation
  2. Associated with cardiac tamponade

Low arterial BP, distended neck veins, and distant, muffled heart sounds.

  1. kerley k lines, batwing sign in PO, enlarged upper lung veins
  2. Nicorandil is a vasodilatory drug used to treat angina

Prophylaxis and treatment of stable angina (second-line)

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6
Q
  1. What can happen with iron infusions
  2. Why should we give transfusions to HD patients
  3. What is urokinase?
  4. What is Augumentin?
A
  1. anaphylaxis
  2. have HLA, Ab form to blood products which can cause rejection of a kidney in the future
  3. A plasmin activator, thrombolytic enzyme

It works by converting plasminogen to plasmin, which then catalyses the breakdown of fibrin

Administered intra-arterially and intravenously

Clearance of a thrombosis can take from 4-18 hour

4. AUGMENTIN (brand name) is an oral antibacterial combination consisting of amoxicillin and the beta lactamase inhibitor, clavulanate potassium (the potassium salt of clavulanic acid).

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7
Q

Sarcoidosis

  1. What is it
  2. PC
  3. What is LOFGREN syndrome
  4. Ix
  5. Prognosis
  6. Epidemiology
A
  1. Granulomas: lung 90%, skin, lymph nodes (painful red lumps)
  2. Lung: wheeze, persistant dry cough, SOB, chest pain

red sore eyes

  1. fever, lymphadenopathy, arthritis, erythema nodosum
  2. CXR: perihilar lymphadenopathy

Bloods: hypercalcaemia & normal PTH, ACE inc in blood

CT

Bronchoscopy + biopsy

  1. Majority: symptoms improve months - years

Otherwise: ibuprofen/paracetomol

Otherwise: Steroids (weight gain, mood swings, osteoporosis)

  1. 30-40yo

W>M

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8
Q
  1. What is Personal Independence Payment (PIP)?
A
  1. A benefit for people who may need help with daily activities or getting around because of a long-term illness or disability.

PIP has two parts - a daily living component and a mobility component.

PIP has replaced Disability Living Allowance for anyone making a new claim.

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9
Q
  1. When should I offer lipid-modification therapy for primary prevention of cardiovascular disease|?
  2. What interventions and tests should I implement before starting lipid-modification treatment for the primary prevention of cardiovascular disease?
A
  1. QRISK2
    * =84yo if their estimated 10-year risk of developing cardiovascular disease (CVD) using the QRISK®2 >/= 10%

Offer lipid-modification therapy (without the need for a formal risk assessment) to people with:

  • T1DM
  • CKD
  • Familial hypercholesterolaemia
  • > 85yo
  1. FULL LIPID PROFILE
  • Reduce the risk of CVD: smoking, high blood pressure, and obesity
  • Managing secondary causes: excess alcohol consumption, uncontrolled diabetes mellitus, hypothyroidism, liver disease, and nephrotic syndrome.
  • Full lipid profile: TC, HDL, non-HDL, triglycerides

TC >7.5 mmol/L & FHx of CHD -> think familial hypercholesterolaemia

TG > 20mmol/L -> urgent specialist review

TG conc 10-20 mmol/L:

TG 10- 20 mmol/L:

  • Repeat TG within 2 weeks
  • Review for secondary causes
  • Lipid clinic if the TG conc remains elevated
  • TG 4.5 - 9.9 mmol/L, optimize the management of other CVD risk factors present. Seek specialist advice if non-HDL cholesterol concentration is more than 7.5 mmol/L in this group of people.

CREATINE KINASE (Do not measure CK in asymptomatic people being considered for statin treatment.)

LFT

RENAL FUNCTION

HBA1C

HbA1c of 48 mmol/mol is recommended as the cut point for diagnosing diabetes mellitus

TSH

Hypothyroidism causes dyslipidaemia

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10
Q

Which first-line lipid modification therapy should I offer for primary prevention of CVD?

A
  • High-intensity atorvastatin 20mg/day unless this is contraindicated (for example in pregnancy)
  • Discuss risks and benefits: cardiprotective, s/e: myopathy and rhabdomyolysis
  • follow up (repeat bloods)
  • if statins CI then

Ezetimibe

  • Mechanism = cholesterol lipase inhibitor which selectively inhibits intestinal cholesterol absorption
  • Side effects = headache, abdominal pain, diarrhoea
  • Dose = 10mg
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11
Q

What follow up is recommended after initiation of statin therapy for primary prevention?

A
  • Measure TC, HDL, and non-HDL cholesterol levels after 3 months of atorvastatin treatment. The aim of treatment is to achieve a greater than 40% reduction in baseline non-HDL cholesterol levels.

If a greater than 40% reduction in non-HDL cholesterol is not achieved:

Discuss adherence and timing of dose.

Reinforce adherence to diet and lifestyle measures.

Consider increasing the dose of atorvastatin if the person is judged to be at higher risk of cardiovascular disease (CVD) because of comorbidities or risk score, or using clinical judgement.

If a greater than 40% reduction in non-HDL cholesterol is still not achieved after appropriate dose titrations of atorvastatin, or because dose titration is limited by adverse effects:

Ezetimibe, co-administered with atorvastatin, can be considered for people with primary hypercholesterolaemia (consider seeking specialist advice).

  • Recheck liver function tests (LFTs) within 3 months of starting treatment, and again at 12 months.
  • Review statin treatment annually.
  • Routinely monitor for adverse effects of lipid-modification therapy.
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12
Q

Lipid therapy - secondary prevention of CVD

  1. When should I advise lipid-modification therapy for secondary prevention of cardiovascular disease?
  2. What interventions and tests should I implement before starting lipid-modification treatment for the secondary prevention of cardiovascular disease?
A
  1. Established CVD (e.g. past/ current Hx of MI, angina, stroke, TIA, or peripheral arterial disease)

2.

  • Reduce the risk of CVD-smoking, HTN, obesity
  • Managing secondary causes
  • Baseline bloods: full lipid profile, CK, LF, renal function, HbA1c, TSH (hypo)
  • atorvastatin 80 mg
  • same for primary prevention
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13
Q

Clinical features of emphysema and bronchitis

complications

MRC dyspnoea score explain

Ix

A
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14
Q

Managing stable COPD

A
  1. Smoking cessation (offer nicotine replacement therapy e.g. varenicline or bupropion + support programme
  2. Inhaled therapy: SABA or SAMA
  3. Offer LAMA+LABA to:
  • spirometrically confirmed COPD and
  • do not have asthmatic features

OR Consider LABA+ICS to:

  • have spirometrically confirmed COPD and
  • have asthmatic features/features suggesting steroid responsiveness
  1. LAMA+LABA+ICS: COPD with asthmatic features/features suggesting steroid responsiveness who remain breathless or have exacerbations despite taking LABA+ICS.
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15
Q

How do you rate control AF?

A
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16
Q

How do you rhythm control?

Amiodarone

  1. Indications
  2. S/E
A
  1. VF or pulseless VT refractory to defibrillation (for cardiopulmonary resuscitation)

paroxysmal supraventricular, nodal and ventricular tachycardias, atrial fibrillation and flutter, ventricular fibrillation, and tachyarrhythmias associated with Wolff-Parkinson-White syndrome

  1. Arrhythmias; hepatic disorders; hyperthyroidism; nausea; respiratory disorders; skin reactions

constipation; vomiting, hypothyroidism

17
Q

What determines if we anticoagulate a patient?

A
18
Q

How do we treat PO

A
19
Q

Digoxin

  1. Indications
  2. S/e
  3. MOA
A
  1. Rapid digitalisation/maintenance, for atrial fibrillation or flutter

HF

  1. Arrhythmias; cerebral impairment; diarrhoea; dizziness; eosinophilia; nausea; skin reactions; vision disorders; vomiting

Reverse tick

- Down-sloping ST depression

- T wave inversion

  1. Inhibits Na-K-ATPase, inc in intracellular sodium. The NCX in turn tries to extrude the sodium and in so doing, pumps in more calcium. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Digoxin also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.
20
Q

Adenosine

MOA

SEs

Relative CIs

Interactions

A

Adenosine

+ MOA: temporary AVN block

+ SEs: Transient chest tightness, dyspnoea, flushing, headache

+ Relative CIs: asthma, 2nd/3rd degree block

+ fx ↑d by dipyridimole􏰁 fx ↓d by theophylline

21
Q
  1. Signs of left and right HF
  2. FAML
  3. TAILS
A
  1. FOLATE/B12 DEFICIENCY

APLASTIC ANAEMIA

MYELODYSPLASTIC SYNDROME

LIVER DISEASE

  1. THALASSEMIA

ANAEMIA OF CHRONIC DISEASE

IRON DEFICIENCY

LEAD

SIDEROBLASTIC DISEASE: body has enough iron but cannot use it to make Hb, iron accumulates in the mito

22
Q
A
23
Q

What is scleroderma

A

Year 3 Workbook (21 decks)

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