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5th (Final year) > General Medicine > Flashcards

General Medicine Flashcards

1
Q

Causes of hepatitis? (VADAM)

A 
Viral - CMV/EBV/Hepatitis
Alcohol 
Drugs - Paracetamol, Phenytoin, Sulfonamides
Autoimmune hepatitis
Metabolic
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2
Q

Main electrolytes intracellularly?

A

Magnesium, Calcium and Potassium

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3
Q

Main electrolytes extracellularly?

A

Sodium and Chloride

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4
Q

Plasma level to be defined as hyperkalaemia?

A

> 5.5mmol/L

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5
Q

Causes of Hyperkalaemia?

A

Impaired kidney excretion

  • AKI/CKD
  • Drugs (ACEI, Spironolactone)
  • Hypoaldosteronism
  • Addison’s

Release from cells

  • Tumour-lysis syndrome
  • Rhabdomyolysis
  • Lactic acidosis
  • Massive haemolysis
  • DIgoxin
  • B Blockers
  • Insulin deficiency

DREAD

  • Drugs (ACEI, Spironolactone)
  • Renal failure
  • Endocrine (addisons)
  • Artefact
  • DKA
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6
Q

Hyperkalaemia presentation? (ECG findings)

A

Palpitations or chest pain.

ECG changes:

  1. Tall T waves
  2. Flattened p waves
  3. Prolonged PR
  4. Widened QRS
  5. idioventricular rhythms
  6. Sine waves
  7. VF/Asystole
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7
Q

Hyperkalaemia management?

A

ABCDE

Immediate ECG (any change then treat)

Treatment:

  1. Protect heart
  2. Lower serum K+
  3. Waste body K+
  4. Prevent future reoccurence
  5. Clacium Gluconate - 10ml 10% in 10mins
  6. Lower serum:
    - Insulin w/ Dextrose: 10-15units in 50ml@50%.
    - Nebulised salbutamol
  7. Waste:
    - Furosemide (Dialysis if no GFR)
    - Calcium resonium (bad compliance)
  8. Prevent
    - Monitor & repeat ECG
    - Low K+ diet
    - Treat cause
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8
Q

Serum level of potassium in hypokalaemia?

A

<3.5mmol/L

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9
Q

Calcium Gluconate dose in hyperkalaemia?

A

10 ml of 10% in 10 min

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10
Q

Presentation of hypokalaemia?

A

Lethargy and weakness
Muscle cramps
Palpitations

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11
Q

Causes of hypokalaemia?

A

Poor intake:

  • Anorexia Nervosa
  • Crohns

Increased gut loss:

  • Vomiting (Loss of H+ ions and alkalosis offset by bicarb excretion in the kidneys forces K+ excretion)
  • Diarrhoea (loss of bicarb)

Redistribution (into cell)

  • Insulin OD
  • Salbutamol
  • Theophylline

Renal losses

  • Furosemide
  • Renal tubular acidosis
  • Genetic renal pathologies

Endocrine (hyperaldosteronism)

  • Primary: Conns syndrome
  • Secondary: Kidney, renal, heart

Other:
- Hypomagnesaemia (can’t replace K+ without.)

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12
Q

Management of Hypokalaemia?

A
  1. ECG (flat t waves, U waves)
  2. Mild:
    - Oral Sando K for 3 days
  3. Severe:
    - IV 20-40mmol KCl in N saline over 6 hrs (no faster than 20mmol/hr)
    - Never as a bolus
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13
Q

What electrolyte disturbance is small cell lung cancer associated with?

A

SIADH (hyponatraemia)

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14
Q

Serum sodium in hyponatraemia?

A

<133 mmol/L (life threatening <120mmol/L)

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15
Q

Hyponatraemia presentation?

A 
Hallucinations
Headache 
Dizziness
N&amp;V
If more serious: fits, coma, death
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16
Q

Causes of hyponatraemia?

A

Have to consider hyponatraemia in relation to fluid status:

Hypovolaemic:
- Dehydration (Excess sweating, burns, fistulas)

  • D&V
  • Diuretic excess (Addison’s, osmotic diuresis)

Euvolaemic

  • SIADH
  • Hypothyroidism

Hypervolaemic:

  • HF, Kidney Failure, Liver failure
  • Nephrotic syndrome

Small cell Lung Ca.

DRugs
- SSRIs, TCAs, Antipsychotics, Antiepileptics, omeprazole

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17
Q

SIADH causes?

A

Hypoxia

  • Respiratory failure
  • COPD
  • Pneumonia
  • Small cell ung ca.

CNS diseases

  • Meningitis
  • Stroke
  • SAH
  • Trauma
  • Tumour
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18
Q

Hyponatraemia management?

A
  1. Assess fluid status
  2. Do Bloods
    - U&Es
    - 8am Cortisol
    - TFT
    - Serum osmolality
  3. Urine tests
    - Dip
    - Osmolality (w/ serum)
    - Sodium (off diuretics, if >40mmol/L then SIADH)

If Hypovolaemic:

  • Treat cause
  • Rehydrate w/ N saline

If Euvolaemic
- Treat cause

  • If SIADH :
    1. stop precipitating drug
    2. fluid restrict
    3. Tolvaptan
    4. Furosemide

If hypervolaemic:

  • Treat cause
  • Fluid restrict
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19
Q

Serum level of sodium in hypernatraemia?

A

> 145mmol/L

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20
Q

Presentation of hypernatraemia?

A

Headache, Nausea and Vomiting, Seizures, Confusion.

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21
Q

Causes of hypernatraemia?

A

Excess loss (fluid):

  • Diabetes insipidus**
  • Osmotic Diuresis** e.g. DKA, HHS
  • Diarrhoea
  • Vomiting
  • Sweating

Excessive hypertonic fluid

  • IV infusion
  • TPN
  • Enteral feeds

Decreased Thirst*

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22
Q

Management of hypernatraemia?

A
  1. If severe consider ITU
  2. Treat underlying cause
  3. If mild
    - Encourage oral intake of fluid
  4. If hypervolaemic from inappropriate IV fluid then IV 5% dextrose and furosemide.
  5. N saline if hypovolaemic
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23
Q

Features of Hyperparathyroidism, what’s the usual patient?

A

Bones, stones, abdominal groans and psychic moans:

  • Bone pain/fracture
  • Renal stones
  • Peptic ulceration/constipation/pancreatitis
  • Polydipsia, polyuria
  • Hypertension
  • Depression

Normally elderly female, with unquenchable thirst and raised or inappropriately normal PTH

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24
Q

Normal (most common) cause of Hyperparathyroidism

A

Solitary parathyroid adenoma

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25
Q

Investigations in Hyperparathyroidism?

A
  • Calcium - Raised (suppresses PTH)
  • Phosphate low
  • Pepperpot skull on XR
  • Technetium-MIBI subtraction scan
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26
Q

Management of hyperparathyroidism?

A

Parathyroidectomy

If low level disease could manage conservatively

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27
Q

U&E (and pH) changes associated with cushings syndrome?

A

Hypokalaemic metabolic alkalosis

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28
Q

What main two types of steroid hormone activity do exogenous corticosteroids have and what are their main activities?

A

Glucocorticoid
- Anti-inflammatory

Mineralocorticoid
- Fluid retention

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29
Q

A patient presents with lethargy, hyponatraemia and hyperkalaemia, what’s the most likely diagnosis?

A

Addison’s disease

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30
Q

How do you diagnose addison’s disease?

A

Short synacthen test (ACTH stimulation). It will show no rise in cortisol if the pt has Addison’s.

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31
Q

Two most common causes of hypercalcaemia?

A

Malignancy and primary hyperparathyroidism

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32
Q

Common presentation of primary hyperaldosteronism?

A

Hypernatraemia, Hypokalaemia and hypertension

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33
Q

Addison’s disease management?

A

Hydrocortisone and fludrocortisone

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34
Q

What are you looking for when ordering an ultrasound in urosepsis/UTI?

A

Rule out urinary obstruction or renal stone disease

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35
Q

Causes of pulmonary oedema?

A

Cariogenic
- Left sided HF

Non-cardiogenic

  • ARDS
  • Lymphatic insufficiency
  • Hypoalbinaemia
  • HAPE
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36
Q

What is gastroparesis?

A

Delayed gastric emptying, often caused by autonomic neuropathy in poorly controlled diabetes. Presents with persistent nausea and vomiting, feeling full quickly and loss of appetite.

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37
Q

Pathophysiological changes in AKI?

A

Abrupt decline in GFR

Often oliguria (<400ml/day)

Raised Urea & Creatinine

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38
Q

If a diabetic pt is going to theatre what blood sugars are you aiming for? What might you do to achieve this?

A

7-10 could use an insulin sliding scale

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39
Q

What Abx can you use to treat C diff?

A

Metronidazole or vancomycin

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40
Q

What is a tissued cannula?

A

When the cannula has been pulled out of a vein (or wasn’t in one in the first place) and fluid is collecting around the cannula site.

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41
Q

What test may you do to differentiate T1DM and T2DM?

A

C-Peptide

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42
Q

What is Bronchiectasis, what does it present with, what is it caused by?

A

Bronchiectasis is a permanent dilatation and thickening of the airways presenting with chronic cough, sputum production, recurrent infection, haemoptysis, SOB, chest pain, crackles & wheeze

Bronchiectasis is caused by chronic inflammation of the airways. It can be associated with lots of diseases causing inflammation.

  • Post lung infection
  • HIV
  • Connective tissue disorders such as RA, SLE.
  • Asthma
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43
Q

What is pemberton’s sign testing for? What is it?

A

SVC obstruction - red face when both arms held up

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44
Q

Treatment for SVC obstruction?

A

O2
Dexamethasone
Invasive - Stenting/radiotherapy

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45
Q

What is lambert eaton syndrome?

A

A paraneoplastic syndrome seen in lung cancer, consists of proximal muscle weakness, and difficulty contracting muscles initially (but getting better on repeated use)

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46
Q

How would you treat lambert eaton syndrome?

A

IV immunoglobulins, prednisolone, azothiaprine or pyridostigmine

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47
Q

Confusion bloods?

A 
FBC - (WCC, Neutrophils), anaemia
Us&amp;Es - Renal function
B12, Folate
TFTs
LFTs
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48
Q

SIADH treatment?

A 
Fluid restrict <1L
Demeclocycline if fluid restricting is not working
Hypertonic saline (1-2mmol/Hr) no more as risk of demyelination.
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49
Q

Common Lung Ca. symptoms?

A

Cough (present in 80%)

Haemoptysis, weight loss, lymphadenopathy

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50
Q

Causes of clubbing?

A

ABCDE

Abscesses
Bronchiectesis
Carcinoma 
Don't say COPD
Empyema
Fibrosis
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51
Q

Types of lung Ca?

A

Small cell

  • Rapid growing lesion
  • Associated with SIADH and cushings
  • Bad prognosis

Non-Small cell

  • Adenocarcinoma (non-smokers)
  • Squamous (raised calcium) - Smokers
  • Large (secrete B-HCG)
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52
Q

Types of drugs that affect coagulation?

A

Anticoagulants (Warfarin, Heparin, rivaroxaban, LMWH)

Fibrinolytics (streptokinase, alteplase)

Antiplatelet drugs (Aspirin, Clopidogrel)

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53
Q

Types of anticoagulants?

A

Vit K antagonist
- Warfarin

DOACs
- Xa inhibitors (Rivaroxaban, Apixaban)
Thrombin inhibitor:
- Dabigatran

Heparins (antithrombin activator)

  • Unfactionated Heparin
  • LMWH (dalteparin, enoxoparin)
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54
Q

Features of the heparins?

A

Heparins:

  • Must be given by injection (SC or IV)
  • Reversible with protamine

UFH (Heparin)

  • V short half life
  • Can cause thrombocytopaenia

LMWH e.g. enoxaparin

  • Longer half life
  • Less rate of thrombocyopenia
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55
Q

Features of Warfarin & the newer Factor inhibitors?

A

Warfarin

  • Can give orally
  • Full anticoagulant effect is delayed (4-5days)
  • Long half-life
  • Needs levels monitoring

Dabigatran (anti-thrombin), and Rivaroxaban (anti-Xa)

  • Oral
  • Acts rapidly
  • Does not require monitoring
  • Less reversibility available
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56
Q

In Liver disease what causes the pancytopenia?

A

Portal hypertension leads to splenomegaly and inhibits spleen function

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57
Q

What three veins contribute to the portal vein?

A

Superior and inferior mesenteric and splenic.

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58
Q

What is the function of the portal system? What is it’s pathway?

A

Drains blood from the GI tract, spleen, pancreas and gallbladder to the liver (to metabolise) then this is drained by the hepatic veins into the IVC.

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59
Q

What varices do you get in portal hypertension

Why do you get them in portal HTN?

A

Lower oesophageal
Anal wall
Caput medusa (on abdominal wall)

They are portal-systemic anastomoses and these engorge with increased pressure.

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60
Q

What are the different types of insulin and examples of them?

A

Rapid acting insulin analogues (act faster, and have shorter duration), often bolus in regimes:

  • Novorapid
  • Humalog

Short acting insulins: (can be bolus in regime)

  • Actrapid
  • Humulin S

Long acting insulins

  • Levemir
  • Lantus

There are also premix solutions available, e.g. Novomix

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61
Q

Relationship between steroids and insulin control?

A

Steroids induce hyperglycaemia and therefore insulin may need to be increased.

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62
Q

What is the difference in vertigo and dizziness?

A

Vertigo
- Experience of movement of self +/- the environment (especially rotation)

Dizziness
- Non-specific, light headed feeling, feeling faint (funny turns)

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63
Q

What are pleural plaques?

A

Plaques usually in the parietal pleura, caused by asbestos exposure, benign in themselves.

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64
Q

What is thyrotoxicosis?

A

Hyperthyroisim

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65
Q

What is diabetes insipidus? What are it’s causes?

A

Condition caused by hyposecretion or insensitivity of ADH:

  • Cranial: hyposecretion
  • Nephrogenic: resistance

Cranial: inherited or some kind of lesion

Nephrotoxic: acquired through metabolic disorders or congenital.

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66
Q

Acute alcoholic Tx?

A

Pabrinex, chlordiazepoxide

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67
Q

Paracetamol OD investigations and Tx?

A

Paracetamol levels

N-acetyl cystine

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68
Q

Pattern of spirometry changes in obstructive and restrictive lung disease?

A

Obstructive

  • FEV1 reduced
  • FVC normal
  • Ratio reduced

Restrictive

  • FEV1 reduced
  • FVC reduced
  • Ratio Normal
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69
Q

Examples of obstructive and restrictive lung disease?

A

Obstructive (obstruct airways)

  • COPD
  • Asthma
  • Bronchiectasis

Restrictive (decrease lung vol.)

  • Pulmonary fibrosis (scarring, e.g. drug treatment/radiotherapy)
  • TB
  • ARDS
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70
Q

On an ECG If leads 1 and 3 are positive what does this show?

A

Normal axis

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71
Q

On an ECG if leads 1 and 3 are facing away from each other what does this mean?

A

Leaving = L for Left

Left axis deviation

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72
Q

On an ECG if leads 1 and 3 are facing towards each other what does this mean?

A

Returning = R for Right

Right axis deviation

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73
Q

Asthma exacerbation treatment?

A

O SHIT M

Oxygen hi-flo 100%
Salbutamol neb (if over 5y/o, 5mg)
Hydrocortisone - IV 200mg
Ipratropium bromide neb 500mg

Magnesium

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74
Q

Types of haematuria and their causes?

A

Visible (painful/not):

Painful
- Infection/stones/thrombosis/cysts/trauma

Painless
- Cancer/exercise induced

Non Visible

Glomerular (usually w/ protein)

  • IgA nephropathy/Glomerularnephritis
  • Hereditary Alports/benign/familial

Non-glomerular:
- Infection, BPH, Stones, Polyps, Ca., Cysts, sickle cell, necrosis

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75
Q

Normal fluid output for an adult?

A

0.5ml/kg/hr for an adult

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76
Q

Why is urinary retention such an emergency?

A

UTIs - urine hanging about

AKI - reflux of urine into the kidney

Bladder damage - stretch on the bladder itself

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77
Q

Points of anaphylaxis immediate management? (adult)

A
  1. Rapid A-E

A- Look for and relieve obstruction, remove any traces of allergen left

B- Look for and treat bronchospasm and signs of respiratory distress

C- Colour, pulse and BP

D- AVPU/GCS

E- Assess skin

  1. Give HiFlo oxygen
  2. Lay patient flat
  3. Give 0.5mg 1:1000 IM adrenaline
    - Repeat after 5 mins if no improvement
  4. Establish airway
  5. IV fluid challenge
    - Crystalloid (0.9% NaCl, Hartmans, plasmolyte)
  6. 10 mg IV Chlorphenamine
  7. 200mg IV/IM hydrocortisone
  8. If still needing respiratory resus then can use salbutamol, ipratropium, aminophylline or mag sulf
  9. Continue to monitor:
    - BP
    - ECG
    - Sats & Pulse
  10. Make sure you have removed allergen, recorded on the drug chart replace with alternative, do a tryptase to see if it was a true allergic reaction.
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78
Q

What are the reversible 4 H’s and T’s cause of cardiac arrest?

A

Hypoxia
Hypovolaemia (shock)
Hyperkalaemia (and other metabolic causes)
Hypothermia

Thrombosis
Tension pneumothorax
Tamponade
Toxins

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79
Q

Immediate treatment for MI? Mnemonic?

A

MONARCH

Morphine
O2
Nitrate - GTN
Aspirin
Reduced risk - Beta Blockers, ACEI, Statin
Clopidogrel
Heparin (LMW)
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80
Q

What are the different types of laxative?

A

Stimulants

  • Senna
  • Bisacodyl - dolculax
  • Docusate (also softener)
  • Glycerol

Bulk forming

  • Bran
  • Ispaghula - fybogel

Osmotic

  • Macrogol - movicol/laxido
  • Lactulose

Softener
Arachis oil (enema)
Docusate (also stimulant)

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81
Q

Risks of a fall in the elderly?

A

Long lie

  • Rhabdomyolysis - AKI
  • Pressure sores
  • Malnutrition etc

Bony fracture

  • NOF
  • Wrist
  • Clavicle
  • Vertebra
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82
Q

What level of protein:creatinine ratio would indicate nephrotic syndrome

A

> 300

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83
Q

How would you investigate HHS to confirm or refute your diagnosis?

A

Plasma Osmolarity - Usually above 300

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84
Q

What is ITP?

A

Immune thrombocytopenia

Autoimmune disorder causing reduced circulating platelets, due to increased destruction and decreased production. The most common presentation is petechiae or bruising, can cause larger bleeds, in children in normally occurs following a viral infection.

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85
Q

What is hepatorenal syndrome (HRS)?

A

A complication of end-stage liver disease, occurs in pts with :

  1. Chronic liver dysfunction
  2. Cirrhosis
  3. Ascites
  4. Acute liver failure

This leads to impaired RENAL function, often precipitated by lowered BP

About 35-40% of pts with end-stage liver failure will develop this.

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86
Q

What is the pathophysiology of hepatorenal syndrome?

What other hepatic failure complications is it associated with?

A

Associated with GI bleeds, Spontaneous bacterial peritonitis other infection e.g. Pneumonia

Splanchnic vasodilatation leading to system circulatory dysfunction and intrarenal arterial vasoconstriction - renal dysfunction.

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87
Q

Differing symptoms of Crohns and UC? What symptoms are common between the two?

A

UC:

  • Bloody diarrhoea more common
  • Abdominal pain in the left lower quadrant
  • Tenesmus

Crohns

  • Diarrhoea usually non-bloody
  • Weight loss more prominent
  • Upper gastrointestinal symptoms, mouth ulcers, perianal disease
  • Abdominal mass palpable in the right iliac fossa
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88
Q

UC pharmacological management?

A

Aminosalicylates such as messalizine good for induction and maintenance of remission in UC

Corticosteroids for flare ups

Azathioprine
- when corticosteroids don’t cut it

Infliximab and other biologics to treat flare ups and induce remission

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89
Q

Crohns pharmacological management?

A

Initially glucocorticosteroid

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90
Q

What is the AFP tumour marker for?

A

Hepatocellular carcinoma and testicular ca.

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91
Q

What is a PTC procedure (gastro) and why would you perform it

A

Percutaneous transhepatic cholangiogram

Interventional radiological technique where cotrast is injected into the biliary tree to visualise it and can also be used to stent the biliary tree (Mr Cooms)

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92
Q

What is the proportion of inheritance in Dominant, recessive and X-linked disorders?

A

Autosomal dominant

  • 50% affected
  • 50% unaffected

Autosomal Recessive

  • 25% affected
  • 25% unaffected
  • 50% carrier

X-Linked recessive disorders

  • Only affect males
  • Inherited from mother
  • 50% chance males will be affected, 50% chance unaffected
  • 50% chance females carrier, 50% unaffected
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93
Q

What is the relationship between gout and furosemide?

A

Furosemide may increase levels of uric acid to rise, and could lead to gout.

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94
Q

When do you measure troponin?

A

At presentation and at 10-12 hours after.

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95
Q

What are the types of atrial fibrillation and how long do they last?

A

Paroxysmal <1 week

Persistent >1 week (self terminates or cardioverted)

Permanent - can’t be terminated

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96
Q

What are the different classifications of diverticular disease?

A

Diverticulosis - Asymptomatic diverticulae

Diverticular disease - intermittent problems occurring due to diverticulosis - Intermittent abdo pain

Diverticulitis - Inflammation due to lodged stool and possible infection - Constant abdominal pain and fever

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97
Q

What are the Z and T scores in osteoporosis? What do the values mean for diagnosis?

A

T - In comparison to healthy population

Z - In comparison to age matched population

Osteopenia - T score of less than -1

Osteoporosis is a T score

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98
Q

What area of the body do DEXA scans generally measure?

A

The hip and spine

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99
Q

Management of osteoporosis?

A

Lifestyle advice:

  • Nutrition
  • Exercise
  • Smoking
  • Alcohol

Adcal if necessary

If postmenopausal and no #

  1. Bisphosphonates, first line is alendronate. Only recommended in postmenopausal women < 65 w/ confirmed osteoporosis and no fragility fractures.
    - Second line includes risedronate and may be considered if >65 and unable to take alendronate
  2. Denosumab reduces osteoclast activity, 6 monthly SC injections
  3. Strontium ranelate only if all other options fail

If Postmenopausal and ##

  1. Bisphosphonates - alendronate
  2. Raloxifen
  3. Strontium, Denosumab or Teriparatide

Some combination for premenopausal/Men - but should investigate why osteoporotic first

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100
Q

Features of liver failure as opposed to stable chronic liver disease?

A

Liver failure (acute or decompensated chronic disease) is characterised by:

  • Raised PT time (coagulopathy)
  • High bilirubin
  • Hepatic encephalopathy

Also, may have ascites and jaundice

Chronic cirrhosis is often asymptomatic, and may present with vague lethargy e.t.c. AST/ALT rise, portal hypertension, ascites, hepatomegaly, jaundice e.t.c.

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101
Q

For breath/stool H.Pylori test to be most effective what can’t you have taken, and for how long?

A

PPI for past 2 weeks and Abx for past 4 weeks

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102
Q

Criteria for diagnosis of malnutrition?

A

BMI <18.5
BMI <20 and unintended Weight loss of >5% for last 3-6Months
Unintended Weight loss >10% in last 3-6Months

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103
Q

What are the types of bowel ischaemia, and the features of each?

A

Mesenteric ischaemia

  • Small bowel
  • Abdo pain
  • Embolism
  • Sudden onset & severe
  • High mortality - needs urgent surgery

Ischaemic colitis

  • Large bowel
  • Abdo pain
  • Multifactorial
  • transient, less severe symptoms
  • ‘Thumbprinting’
  • Conservative management
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104
Q

What is achalasia?

A

Lower oesophageal sphincter dysfunction (stays contracted) shown on barium swallow with dilated upper oesophagus and very small lower oesophagus

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105
Q

How does achalasia present?

A

Difficulty swallowing solids and liquids equally
Some heartburn
Some regurgitation of food

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106
Q

How does haemochromatosis classically present?

A 
Fatigue, erectile dysfunction and arthralgia
Bronze skin
Diabetes
Liver pathology e.g. hepatomegaly
Hypogonaodism 
Arthritis
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107
Q

What does Gamma GT bloods test for?

A

Raised GGT in chronic alcohol use, bile duct scarring and non-alcoholic liver disease.

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108
Q

How does autoimmune hepatitis present (inc. bloods)

A

Young females
- Raised antinuclear/anti smooth-muscle antibodies

Children
- LKM1 raised

Middle aged adults
- Soluble liver-kidney antigen

Generally:

  • May present with signs of chronic liver disease
  • Acute hepatitis: fever, jaundice etc (only 25% present in this way)
  • Amenorrhoea (common)
  • ANA/SMA/LKM1 antibodies, raised IgG levels
  • liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
  • ALT/AST rise
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109
Q

How do you interpret Hep B antigen/antibody bloods?

A

Previous immunisation: anti-HBs positive, all others negative

Previous hepatitis B (> 6 months ago), not a carrier: anti-HBc positive, HBsAg negative

Previous hepatitis B, now a carrier: anti-HBc positive, HBsAg positive

Way to remember:
HBsAg = ongoing infection, either acute or chronic if present > 6 months, OR prev. infection, now a carrier

anti-HBc = caught, i.e. negative if immunized OR IgM Anti-HBc - chronic

110
Q

What is cardiomyopathy and what are the types?

A

Definition:
- ‘myocardial disorder in which heart muscle is structurally and functionally abnormal without coronary artery disease, hypertension, valvular or congenital heart diseases’.

Dilated cardiomyopathy:

  • Most common
  • Left or both ventricles are dilated
  • Reduced ejection fraction
  • Causes: ischaemic, alcoholic, genetic, idiopathic

Hypertrophic cardiomyopathy:

  • Usually familial
  • Preserved ejection fraction
111
Q

Normal LVEF (L ventricular Ejection fraction)?

A

55-70%

112
Q

What are the dose conversion rates for the different steroids?

A

20 - 5 - 4 - 1

Hydrocortisone - Prednisolone - Methylprednisolone - Dexamethasone

113
Q

How do you calculate the CURB 65 score, what is it used for?

A

Pneumonia

Confusion
Urea (>7)
RR >30
BP <90 Systolic
Above 65 age ?
114
Q

What is a transudate and exudate pleural effusion? What can cause each?

A

Transudate is fluid pushed through capillary beds due to high pressure (oncotic or hydrostatic)

  • Heart failure
  • Cirrhosis
  • Hypoalbuminaemia

Exudate is when fluid as leaked around cells in inflammation

  • Pneumonia
  • Malignancy
115
Q

Sound of a fourth heart sound?

A

Le Lub dub

116
Q

What causes a fourth heart sound?

A

HF, MI Cardiomyopathy, HTN (pressure overload)

117
Q

Pressure overload causes what in terms of apex beat?

A

Powerful, non-displaced beat

118
Q

Volume overload causes what in terms of apex beat?

A

Displaced beat (dilated heart)

119
Q

Sound of a third heart sound?

A

Lub de dub

120
Q

Causes of a third heart sound?

A

Normal in children and young adults (up to 30)

HF, MI, Cardiomyopathy and Hypertension

Mitral and aortic regurgitation (in volume overload)
Constrictive pericarditis

121
Q

Signs of infective endocarditis?

A

2 in the hands (clubbing and splinters)
Rare: Oslers nodes, Roth spots and Janeway lesions
1 in the heart (changing murmurs)
2 in the abdomen (Splenomegaly, microscopic haematuria)

122
Q

Types of tremor, and their findings on examination?

A
  1. Parkinsonian:
    - Most obvious at rest.
    - Usually unilateral
    - Pill rolling quality
    - Cog wheeling (on rapid flexion and extension)
    - Better on movement
  2. Fine tremor (Physiological)
    - Thyrotoxicosis. anxiety, alcohol withdrawal
    - Fine tremor
    - Bilateral, symmetrical and non-progressive over time
  3. Benign essential tremor
    - Most obvious when doing something (although present at rest)
    - Head nodding
    - Symmetrical
    - Amplitude is highly variable depending on emotional and physiological state.
  4. Cerebellar (intention tremor)
    - Most obvious at the end of an inaccurate movement (finger to nose)

Essentially

  • Rest tremor - parkinsons
  • Action tremor - benign essential
  • Fine tremor, the same - physiological
  • Intention tremor - cerebellar
123
Q

How would you examine a tremor?

A
  1. Inspect
    - Resting tremor?
    - parkinsonian features
    - Hyperthyroidism features
    - Head nodding (benign essential)
    - Tardive dyskinesia (e.g. lip smacking)
  2. Arms outstretched - fingers spread
    - Fine tremor (thyroid, anxiety, alcohol)
    - Clubbing (acropachy)
    - Sweating
    - Pulse for tachycardia and fibrillation
  3. Arms outstretched, wrists cocked back
    - CO2 retention, hepatic encephalopathy
  4. Finger-nose test
    - Intention tremor (at end of movement - cerebellar)
    - Tremor worse on movement (benign essential tremor)
124
Q

Features of Renal bone disease, pathophysiology?

A

Osteoporosis
Hyperparathyroidism
Osteomalacia (not common)
Osteosclerosis

Renal damage leads to reduced activation of Vit D (loss of 1-alpha enzyme) and therefore less Ca++ absorption from the gut. Renal damage also leads to phosphate retention.

Decreased Ca++ leads to increased PTH

Increased PTH increases Osteoclast activity - resorbing bone

Increased PTH also increases Osteoblast activity causing increased sclerotic lesion laid down at bone end plates.

125
Q

What are the three groups of thyroid antibodies and in what conditions are they raised?

A

Antithyroid peroxidase (TPA Ab) - raised in Hashimoto’s (thyroid cells destroyed) - Hypothyroidism.

Antithyroglobulin (TG Ab) - Raised in Hashimotos’s too.

Thyroid stimulating immunoglobulin Ab (TSI Ab) - Activate TSH receptors in the thyroid - Causing Graves disease - Hyperthyroidism.

126
Q

What are the characteristics of small cell lung Ca., what medical pathologies is it associated with?

A

Rapid growing lesion with bad prognosis

Associated with Cushing’s disease and SIADH

127
Q

Do smokers or non smokers get Adenocarcinoma of the lung?

A

Non-smokers

128
Q

What medical abnormalities is squamous lung cancer associated with?

A

Raised calcium

129
Q

What medical abnormality is large cell lung cancer associated with?

A

B-HCG raised

130
Q

What is Interstitial lung disease what causes it?

A

Term for restrictive lung diseases caused by damage to the pulmonary interstitium (Connective tissue surrounding the alveoli and other structures).

Caused by many things, including idiopathic pulmonary fibrosis, inhalation of asbestos, Systemic inflammatory disorders, reactions to drugs (e.g. Amiodarone and methotrexate) and infections.

131
Q

What is polymyalgia rheumatica? How does it present?

A

Inflammatory condition

Severe bilateral pain and morning stiffness (>45mins) of:

  • Shoulder
  • Neck
  • Pelvic girdle

Raised CRP/ESR and Over 50, lasting for >2 weeks

132
Q

What is Lichen Planus and Lichen Sclerosus?

A

Lichen Planus

  • T cell mediated autoimmune disease
  • Purple Polygonal Papules and Plaques
  • All over body including mouth (often wrist ankles and back

Lichen sclerosus:

  • Genital and perianal areas
  • More common in women
  • May be autoimmune - unknown
  • in women can cause itching, bleeding (from microtrauma) and loss of vulval architecture
  • In men penis may become white, firm and scarred.
  • Can be extragenital (rare) - firm white plaques
133
Q

How is B12 absorbed and what is pernicious anaemia?

A

B12 is mostly absorbed in terminal ileum and requires Intrinsic Factor (IF), secreted by parietal cells.

Pernicious anaemia is an autoimmune condition that causes loss of the mucosa of the body and fundus of the stomach resulting in the loss of parietal cells and therefore IF - B12 deficiency.

134
Q

What type of anaemia does B12 deficiency cause?

A

Megaloblastic anaemia (macrocytic) - High MCV

135
Q

What are the causes of megaloblastic (macrocytic anaemia)?

A

Deficiency of:

  • Folate
  • Folic acid
  • B12
136
Q

What are the causes of B12 deficiency?

A
  • Gastrectomy, H-Pylori, congenital deficiency
  • Inadequate intake e.g. Vegan/Vegetarian
  • Malabsorption e.g. coeliac/crohns
  • Drugs e.g. colchicine
137
Q

Presentation of B12 deficiency?

A 
Fatigue
Lethargy
SOB 
Faintness 
Headache
Palpitations

Neurology

  • Parasthesia
  • Peripheral neuropathy
138
Q

How does cauda equina syndrome present?

A

Variable clinical presentation, can be sudden onset or more insidious.

Typically :

  • Bladder/bowel dysfunction
  • Saddle anaesthesia
  • Sexual dysfunction
  • Motor or sensory dysfunction of the lower limb
139
Q

What causes type 1 respiratory failure and type 2 resp failure?

A

Type 1

  • COPD (both)
  • Pneumonia
  • Pulmonary fibrosis
  • PE
  • Pneumothorax

Type 2

  • COPD (both)
  • Severe asthma (getting very bad here)
  • Myasthenia gravis
  • Poly neuropathy
  • Polio
  • muscle disorders/skeletal abnormalities
140
Q

What is cyclical vomiting syndrome?

A

Repeated episodes of severe nausea, vomiting and physical exhaustion.

No known cause, associated with migraines.

Severe nausea and sudden vomiting lasting from hours to days. Typically after a warm shower. Can be cannabis induced.

141
Q

What is the Glasgow-Blatchford Score used for, what does a score above 6 indicate?

A

Used for Upper GI bleeds, above 6 needs an endoscopy.

142
Q

Where are the three common regions of the bowel that Crohns affects?

A

40% in terminal ileum
30% in colon
20% have small and large disease

143
Q

Management of decompensated liver disease?

A

Drain ascites - rule out spontaneous bacterial peritonitis

Aggressively treat issues that arise

144
Q

Two cardinal features of osteoporosis?

A

Reduced bone mass

Disrupted bone architecture

145
Q

Osteoporosis R/Fs?

A 
White and Asian women
Old
Early menopause
Smoking
Reduced Ca++ intake
146
Q

What are the risks associated with bisphosphonates?

A

Atypical fractures

  • Often wrist
  • Due to over-strengthened brittle bone
  • Only a small risk, 130 fractures saved for every one it causes
  • Reduce risk by having breaks in taking it

OsteoNECROSIS of the jaw

147
Q

What is Teriperatide how does it work?

A

Most effective way of building bone

  • Raises PTH
  • Expensive, and only used in risky pts
148
Q

What is the cardinal feature of osteomalacia

A

Loss of calcification (e.g. low Vit D)

Rickets in young

149
Q

Management of Osteomalacia?

A

Diet, sunlight, Vit D/Ca++ supplements, treatment of underlying cause.

150
Q

How does Denosumab work in the treatment of osteoporosis?

A

Inhibits osteoclasts

151
Q

How long should you put a blood transfusion on for?

A

90mins - 4 hours

152
Q

What is TACO?

A

Transfusion associated Circulatory Overload

153
Q

How can you prevent the occurrence of TACO in infusions?

A

Take Hx and Exam - for R/Fs

  • Low Albumin
  • CVD
  • GFR
  • SIze of pt
154
Q

Lifestyle advice for the management of reflux disease?

A

Quit smoking
Stop drinking Alcohol

Dietary changes:

  • Less spicy foods
  • Less fatty foods
  • Eat smaller meals
  • Eat meals earlier
155
Q

Long term risks of Omeprazole?

A

Hyponatraemia
Glomerulonephritis
Gastroenteritis
Osteoporosis

156
Q

What level of faecal calprotectin suggests pathology?

A

150 more convincing, but can be NSAIDS/Small bowel disease

157
Q

What tests should you run before starting azothioprine?

A

HIV, EBV, CMV, Hep B and C

TPNT - enzyme that breaks it down

158
Q

Differentials for pulmonary cavity?

A

CAVITY

Cancer
- SCC

Autoimmune
- GPA (granulomatosis with polyangiitis)

Vascular
- Pulmonary embolus/infarction

Infection
- Abscess (TB, Staph A)

Trauma

Youth
- Bronchogenic cysts

159
Q

Who gets pseudomonas chest infections?

A

Immunocompromised pts only.

160
Q

What sats do you aim for in a CO2 retainer?

A

88-92

161
Q

Features of parkinsonism?

A

Cardinal:

TRAP

Tremor.
Rigidity.
Akinesia (bradykinesia).
Postural instability.

Also (less important)

  1. Asymmetric onset
  2. One side predominant
  3. Dyskinesia
  4. Fine tremor
  5. COgwheeling
162
Q

Causes of parkinsonism?

A

80% - parkinsons disease

Others

  • CVD
  • Parkinsons plus
  • Other brain disorders: post-HIV etc.
163
Q

Symptoms of autonomic neuropathy?

A

Dry Skin
Dry mouth/Excessive
Bowels - constipated
Postural hypotension

164
Q

Non-motor symptoms of Parkinsonism?

A 
Depression/Anxiety 
Behavioural problems 
Sleep disarrangement/REM disorders 
Hallucinations 
Anosmia 
Anergia
165
Q

What causes the first and second heart sound?

A

First is the Atrio-Ventricular valves closing at the end of atrial systole (diastole) = Lub

Second is the Aortic and pulmonary valves closing at the end of ventricular systole/start of diastole - Dub

166
Q

Common causes of splinter haemorrhages?

A

Most common - Microtrauma

Can also be

  • Vasculitis
  • Infective Endocarditis§
167
Q

What are the five common signs of endocarditis?

A

2 in the hands

  • Clubbing
  • Splinter haemorrhages

1 in the heart
- Changing murmurs

2 in the abdomen

  • Splenomegaly
  • Microscopic haematuria

Also rare: oslers nodes, janeway lesions, roth spots

168
Q

Why do ventricular ectopics disappear when exercising?

A

They occur in diastole, when exercising daistole is shorter and so there is less of a window of opportunity.

169
Q

How do ventricular ectopics appear on the ECG?

A

Broad complex premature beat with compensatory pause

170
Q

What is the physiological difference between VT (with pulse) and Pulseless VT?

A

(Dr Clarke)

Pulseless VT is ‘loss of diastolic filling time with fast ventricular rates’

Basically the cardiac output increases with pulse up to about 160 BPM - it then falls from there (supra-ventricular tachycardia) and at about 180 BPM it becomes pulseless VT

171
Q

Three main causes of AF (Dr Clarke)?

A

IHD, Rheumatic Heart Disease, Hyperthyroidism

172
Q

Two possible explanations of an irregularly irregular pulse, how do you differentiate?

A

AF, Multiple Ventriclar Ectopics

  • Exercise (Ventricular ectopics will disappear)
173
Q

How do you assess whether the AF is well rate controlled?

A

Time the apical rate with stethoscope (<80 is good)

174
Q

Rate control management in AF?

A

Do CHA2DS2VASC2 score (AF stroke risk)
Do HASBLED (major bleeding risk, to see if you can anticoagulate)
- Consider DOAC/Warfarin

First line:
- Betablocker

Second-line:
- Diltiazem, or digoxin is pt is sedentary

Third-line:
Dual therapy with two of the above

175
Q

Rhythm control management in AF?

A

Paroxysmal AF (<48hrs) - spontaneous termination

  • Pill in pocket e.g. Flecanide
  • Rhythm control prophylaxis (below)

Indications for rhythm control

  • New onset AF, last 48hrs
  • LVH due to AF
  • Reversible cause
  • Young
  • Symptoms despite rate control
  • Acutely unwell

Rhythm control first step:
- Electrical/chemical cardioversion

Rhythm control prophylaxis

  • Betablocker
  • Amiodarone in LV dysfunction
  • Droperadone if no LV dysfunction
  • Flecanide is fo CHD or LV dysfunction
176
Q

Warfarin INR target? With and Without mechanical prosthetic valve?

A

2-3 without

3-4 with a valve

177
Q

Causes of Aortic stenosis?

A

Degenerative calcified valve
Congenitally bicuspid (will be <3y/o)
Rheumatic heart disease

178
Q

Why does the left ventricle thicken in aortic stenosis

A

PRESSURE overload

179
Q

What happens in pressure overload in the left ventricle?

A

LV thickens - inwards

180
Q

Causes of Pressure overload to the left ventricle?

A

HTN
Aortic Stenosis
Coarctation of the Aorta
Hypertrophic cardiomyopathy

181
Q

Management of Aortic Stenosis?

A

Check severity

  • Syncope
  • Angina
  • SOB

Depending on severity, valve replacement (TAVI) is definitive treatment.

182
Q

Classic changes seen in osteoarthritis on XRAY?

A
  1. Decreased joint space
  2. Osteophytes
  3. Subchondral cysts
  4. subchondral sclerosis
183
Q

Motion sickness treated with what?

A

Hyoscine
Cyclizine
Promethazine

184
Q

Way to remember the presenttaion of Argyll-robertson pupil?

A

Argyll-Robertson-Pupil (ARP)

ARP = accommodation reflex present 
PRA = Pupillary reflex (to light) absent
185
Q

What are the little red papules commonly seen on the trunk in older adults called?

A

Cherry haemangiomas

186
Q

What is the difference between spine myelopathy and radiculopathy?

A

Myelopathy - commonly seen in cervical spine myelopathy is actual reduction in function due to compression of the cord. (like cauda equina in the base)

Radiculopathy is a ‘pinched nerve’, it is when a spinal nerve is compressed resulting in parasthesia, numbness and can have weakness

187
Q

What Infusion of glucose should you administer in an unconscious patient with hypoglycaemia?

A

80ml 20% glucose or 150/160ml 10% glucose

188
Q

When would you use DPP-4 inhibitors in diabetic pts? Give an example of one?

A

Sitagliptin

Used in obese pts - no weight gain S/Es

189
Q

Becks triad suggesting cardiac tamponade?

A

Hypotensive
Muffled heart sounds
Raised JVP

190
Q

In pt’s with Myasthenia Gravis who are going to undergo General Anaesthesia what two drugs do you need to be aware will have different effects compared to the normal patient?

A

The Neuromuscular blocking drugs Suxamethonium and Rocuronium

Suxamethonium:
- Works by binding to Acetylcholine receptors in the NMJ and depolarising. In MG there are less receptors and so suxamethonium does not work as effectively, and pts need a higher dose

Rocuronium:
- Works by antagonising post-synaptic receptors at the NMJ and in MG as there are less receptors works more effectively than normal and pts will require a lower dose.

191
Q

Difference in voluntary and involuntary guarding?

A

Voluntary
- when the patient is tensing because they are in pain

Involuntary (True guarding - do not say guarding unless you think it is this)
- When the patient’s abdo muscle is reflexively going into spasm because of peritonitis = acute abdomen

192
Q

Features of an acoustic neuroma, (nerves?

A

Divided up into the cranial nerves it affects:

CN VIII (vestibulocochlear)

  • Hearing loss
  • Vertigo
  • Tinnitus
CN V (trigeminal)
- Loss of corneal reflex

CN VII
- Facial palsy (ipsilaterally)

193
Q

What investigation is gold standard for acoustic neuroma?

A

MRI of cerebellar pontine angle

194
Q

What malignancy are patients on long-term immunosuppressive treatment at risk of?

A

SCC

195
Q

What type of pleural effusion is an empyema? What would you find on analysis of the fluid in an empyema?

A

It is an exudate

Low Glucose, Low pH (<7.2) and High LDH

196
Q

What are the dermatological complications you get with reactive arthritis?

A
  1. keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
  2. Circinate balanitis (painless vesicles on the coronal margin of the prepuce - foreskin or clitoris)
197
Q

What type of blood cancer causes splenomegaly?

A

CML - Chronic myeloid leukaemia

198
Q

Mnemonic for remembering the live attenuated vaccines?

A

MOOBY (PT)

MMR 
Oral (Pertussis)
Oral (Typhoid)
BCG
Yellow fever
199
Q

What causes subacute combined degeneration of the cord and how does it present?

A

Often caused by B12 deficiency where folate is being replaced but B12 is not in a macrocytic anaemia.

Presents with damage to posterior columns (Proprioception, light touch and vibration) - DCML

Also has mixed UMN and LMN signs

  • UMN due to damage to lateral columns
  • LMN due to peripheral nerve damage
200
Q

What does stranding of the paranephric fat represent?

A

Spontaneously passed renal stone(s)

201
Q

What medication would you use to replace Vit D in a CKD bone disease p?

A

Alfacalcidol

202
Q

Presentation of an asymmetric, non-contiguous (non-adjacent) neuropathy affecting some motor and some sensory functions is likely…?

A

Mononeuritis multiplex

203
Q

What are the two nephrology complications that can present after an URTI, how do you differentiate?

A

IgA Nephropathy - A - FIRST - 1/2 days after URTI

Post-strep glomerulonephritis - 1-2 weeks after URTI

204
Q

What medication can you use to suppress lactation if required?

A

Cabergoline

205
Q

First and second line treatment for MRSA?

A

First: Vancomycin or teicoplanin

Second: Linezolid

206
Q

How does salicylate overdose present?

A

Initial mixed respiratory alkalosis

Then Metabolic acidosis

Other symptoms include hyperventilation, N&V, tinntus etc.

207
Q

What is Adult Respiratory Distress Syndrome (ARDS)?

A

Two stages

First stage:
- You get bilateral pulmonary infiltrates (substance in the parenchyma of the lung - in this case exudative fluid). Without any evidence of cardiac generated pulmonary oedema.

Later stage
- Fibroproliferative changes - scarring which may reduce respiratory function.

Caused by:

  • Sepsis
  • Direct lung injury
  • Trauma
  • Acute pancreatitis
  • Long bone fracture or multiple fractures (through fat embolism)
  • Head injury

Presentation:
- Acute dyspnoea and hypoxaemia hours/days after event
Multi organ failure

208
Q

Management of ARDS?

A
  1. Treat the underlying cause
  2. Antibiotics (if signs of sepsis)
  3. Negative fluid balance i.e. Diuretics
  4. Recruitment manoeuvres such as prone ventilation, use of positive end expiratory pressure
  5. Mechanical ventilation
209
Q

What are the two hyoscine drugs used in bowel colic and in respiratory secretions, what one is used for what?

A

Hyoscine Butylbromide = Bowel colic
- Think of the Bs

Hyoscine Hydrobromide
- Respiratory secretions

210
Q

Gas gangrene presents how? Normal causative organisms?

A

Black blisters, Fever, dehydration.

Normally Clostridium i.e. C diff etc.

211
Q

Types of testicular cancers?

A

Seminomas or non-seminomas

212
Q

For long term feeding what is the best option?

A

PEG feed

213
Q

Acute management of AFib in three steps?

A
  1. If unstable then DCCV
  2. Treat sepsis (if has)
  3. Rate control with beta-blocker and NOAC
214
Q

Most common types of leukaemia in adults and kids?

A

Kids (acute)

  • ALL (by far)
  • AML

Adults

  • CLL
  • AML
215
Q

How do you remember xray changes in RA and in OA?

A

RA: ‘LESS’- Loss of joint space, Erosions, Soft bones (osteomalacia), Soft tissue swelling.

OA: ‘LOSS’- Loss of joint space, Osteophytes, Subchondral sclerosis, Subchondral cysts.

216
Q

What are the blood abnormalities associated with SLE?

A

Anti-dsDNA and anti-smith are specific

ANA is positive, but not specific

You get low C3 and C4

217
Q

Features of CREST syndrome?

A

CREST syndrome:

Calcinosis
Raynaud's phenomenon
oEsophageal dysmotility
Sclerodactyly
Telangiectasia
218
Q

What drugs may cause polymorphic VT (torsades des pointes)?

A 
Clarithromycin
tricyclic antidepressants
antipsychotics
chloroquine
terfenadine
erythromycin
219
Q

What is polymorphic VT (torsades des pointes)?

A

A rare arrythmia associated with a long QT

220
Q

Dermatitis herpetiformis is associated with what condition?

A

Coeliac disease

221
Q

Common causes of Mitral Regurg?

A
  1. Congenital
  2. Endocarditis
  3. Degeneration
222
Q

Mitral Regurgitation signs found on examination?

A

Apex beat displacement
Quiet first heart sound
Pansystolic murmur radiates LOUDLY to the axilla

223
Q

What are the main systolic and diastolic murmurs?

A

Systolic

  • Aortic Stenosis
  • Mitral regurgitation

Diastolic

  • Mitral stenosis
  • Aortic regurgitation
224
Q

Signs of mitral stenosis?

A

Loud first heart sound (high atrial pressure keeps valve open until systole pushes it shut).

Malar flush (pulmonary HTN)
JVP not raised until late

No displaced apex beat

225
Q

Signs of aortic regurgitation?

A

Collapsing pulse
JVP not raised
Displaced apex beat
‘lub taar’

226
Q

Sound of mitral stenosis and aortic regurgitation?

A

Mitral Regurgitation
- Lub de de or lub de durr

Aortic regurgitation
- Lub taaar

227
Q

ECG changes in ACS?

A

T wave inversion
Q waves
New LBBB

ST elevation and reciprocal depression

228
Q

Three cardinal signs of ACS

A

Cardiac chest pain
Troponin change
ECG changes

229
Q

What ACS is troponin negative in?

A

Unstable Angina

230
Q

What investigations do you do in ACS and why?

A

FBC - Anaemia associated with Cardiac ischaemia
U&Es - Hypo/hyperkalaemia & Renal function (baseline for ACEI)
LFTs - Baseline for statins, ticagrelor
Lipids
Troponin
Serial ECG
Glucose

231
Q

A-E for management post MI?

A 
Ace-inhibitor 
Beta blocker
Cholesterol lowering statin
Dual antiplatelet (Clopidogrel or ticagrelor &amp; Aspirin)
Echo - left ventricle dysfunction
232
Q

What is the dual antiplatelet therapy given post-MI?

A

Clopidogrel/Ticagrelor - atl a year

Aspirin - lifelong

233
Q

Mnemonic for complications post-MI?

A

sudden death on PRAED street

Sudden death 
Pump failure
Rupture of papillary muscles of septum
Aneurysm or arrhythmias
Emobolism
Dresslers syndrome (late pericarditis) and Acute pericarditis (more common)
234
Q

Qualities of pericardial pain?

A

Sharp and worse on inspiration (like pleurisy)
Retrosternal and radiates to left (like angina)
Worse lying flat and better sitting forward (it’s own)

235
Q

What is PTH’s effect on phosphate?

A

Increases renal excretion of phosphate

236
Q

Tumours in Men 1 and Men 2a?

A

Men 1

  • 3 Ps, named after organs
  • Pancreatic, pituitary, parathyroid hyperplasia

Men 2a

  • Not all Ps
  • Medullary thyroid, Phaeochromocytoma, parathyroid hyperplasia
237
Q

What is the rate of insulin infusion in DKA?

A

0.1ml/kg/hr

238
Q

What is used to treat gastroparesis?

A

Metoclopramide

239
Q

What does sarcoidosis do to the PR interval?

A

Prolongs the PR interval

240
Q

What effect on heart sounds would a short PR interval have?

A

Loud S1

241
Q

What is brugada syndrome?

A

Autosomal dominant condition, more common in asians, Ion channel dysfunction.

Presents with:

  • Sudden death
  • ST elevation V1-3, followed by neg, T wave
  • Partial RBBB
242
Q

What is a penis?

A

dunno but Matt Olney’s massive

243
Q

ECG changes in Hypokalaemia?

A

U waves
Prolonged PR
ST depression
Small T waves

244
Q

ECG changes in hyperkalaemia

A 
tall tented T waves
Flat p wave 
Broad bizarre QRS
Slurring into ST segment
eventually VF
245
Q

Causes of a LBBB?

A

IHD
HTN
Aortic Stenosis
Cardiomyopathy

246
Q

Effect of hypercalcaemia on the ECG?

A

Shortened QT interval

247
Q

What factor is deficient in Haemophilia A?

A

Factor VIII

248
Q

ECG changes in SAH?

A

ST elevation and depressed T waves

249
Q

ECG changes in digoxin toxicity?

A

a short QT interval
ST depression
a prolonged PR interval
inverted T waves

250
Q

ECG changes in cor pulmonale?

A

Increased P wave amplitude
Right bundle branch block
Right axis deviation

251
Q

Which are the dihydropyridine calcium channel blockers and the non ones?

A

NON

  • Verapamil
  • Diltiazem

Dihydropyridine

  • Amlodipine
  • Nifedipine
  • All others
252
Q

How to remember the ECG changes in Cor pulmonale and in PE?

A

cor Pulmonale

P = Peaked P waves

PE

T wave inversion

Both have RBBB and Right axis deviation

253
Q

What anticoagulant strategy is used in AF?

A

DOAC or Warfarin - Pt choice

254
Q

Posterior MI ECG changes?

A

Tall R waves in V1 - 2

255
Q

In carotid sinus hypersensitivity, when doing carotid sinus massage (and ECG monitoring) what would you expect to see?

A

Ventricular pause >4 seconds.

256
Q

What are the changes in ECG that warrant immediate PCI?

A

ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR

ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR

New Left bundle branch block

257
Q

When do you thrombolyse in PE?

A

Circulatory failure - Hypotension

258
Q

What cardiac drug cis associated with angioedema

A

ACEI

259
Q

How does an ASD present in adults?

A

Ejection systolic murmur radiates to the back (and split S2)

Can cause paradoxical stroke

260
Q

Anticoagulant treatment following stroke with AF?

A

Aspirin 300mg for 2 weeks, then anticoagulation lifelong (warfarin recommended)

261
Q

How can you differentiate Cardiac tamponade and Constrictive pericarditis?

A

Kussmauls sign in constrictive pericarditis

262
Q

BP target for diabetics? What factor do you need to consider?

A

End organ damage, if no damage then
- 140/80

IF damage then
- 130/80

263
Q

What timing of murmurs are Aortic Regurg and Mitral stenosis associated with?

A

Aortic regurg = EARLY

Mitral Stenosis = MID-LATE

264
Q

Q RISK score for recommendation of statins?

A

> 10%

265
Q

Main signs of VSD?

A

Ejection systolic murmur
Jerky pulse - Can be bisferiens
Others

266
Q

Cardiac abnormality associated with polycystic kidney disease?

A

Mitral Valve prolapse

267
Q

In what situations do you treat stage 1 hypertension?

A

< 80 yers old AND:

  • Qrisk > 20%
  • Diabetes
  • End organ damage
  • Renal disease
  • Established cardiovascular disease
268
Q

Definitive treatment of Wolff Parkinson White?

A

Ablation

269
Q

How do you differentiate NSTEMI and Unstable angina?

A

Troponin rise in NSTEMI, not in Unstable angina

270
Q

Management of Aortic dissection?

A

Type A (proximal) - surgical aortic root replacement

Type B (More distal) - Medically - BP reduction and analgesia

271
Q

In anaphylaxis how often can you give adrenaline and salbutamol nebs?

A

Adrenaline every 5 mins

Back to Back salbutamol nebs if signs of respiratory distress still present

272
Q

What is otosclerosis?

A

Autosomal dominant condition associated with hearing loss that is conductive at a young age, can be precipitated by pregnancy.

5th (Final year) (34 decks)

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