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3a Exam > GP > Flashcards

GP Flashcards

1
Q

What is atrial fibrillation?

A

Chaotic irregular atrial arrhythmia

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2
Q

What are the different types of atrial fibrillation?

A

Permanent: Cardioversion ineffective
Persistent: >7 days
Paroxysmal: <7 days

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3
Q

What is the clinical presentation of atrial fibrillation ?

A

IRREGULARLY IRREGULAR PULSE
Dyspnoea
Chest pain
Hypotension and tachycardia: palpitations
Syncope

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4
Q

What are the investigations for atrial fibrillation?

A

ECG: F fibrillatory waves, absent P and a waves, irregularly irregular narrow QRS complexes

CHADVASc score: assesses risk of stroke in AF + when to start anticoagulation

  • 0: no anticoagulation + Aspirin alone
  • 1: consider anticoagulation + Aspirin
  • >1: offer anticoagulation (Warfarin) + Aspirin
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5
Q

What is the management for atrial fibrillation ?

A
  1. Rate control: beta-blocker (e.g. bisoprolol), CCB (not in HF) and digoxin (BCD)
  2. Rhythm control: return to normal sinus rhythm through cardioversion

Anticoagulation: asprin and Warfarin
Thrombin or Factor 10A inhibitor
Reduce Stroke risk

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6
Q

What are the 2 types of Cardioversion in AF?

A

Electrical DC

Pharmacological: Amiodarone

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7
Q

What are the risks of Cardioversion?

A

Embolism

Only attempt if symptomatic for >48 hours + long period of anticoags

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8
Q

How do you measure Stroke risk in AF?

A

CHA2DS2VASc
Score (/9):
- Congestive heart failure
- Hypertension
- Age
- 65-74 =1
- ≥75=2
- Diabetes
- Stroke/TIA
- Vascular disease
- Female

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9
Q

What is hypertension?

A

> 140/90: clinic

> 135/85: ambulatory

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10
Q

What are the causes of hypertension?

A

Primary (essential): no known cause

Secondary: a known underlying cause

ROPE

Renal disease

Obesity

Pregnancy

Endocrine (primary hyperaldosteronism, most common cause)

White coat syndrome

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11
Q

What are the causes of paediatric HTN?

A

Renal parenchymal disease (majority)
CoA

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12
Q

What type of HTN is most common?

A

Essential

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13
Q

How is HTN measured?

A

BP reading:record BP in both arms

Ambulatory blood pressure monitoring (ABPM)

Home blood pressure monitoring (HBPM)

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14
Q

How would you perform a HBPM?

A

Two consecutive measurements 1 minute apart

Patient seated

BD for 1 week

DO NOT INCLUDE 1ST DAY MEASUREMENTS (INACCURACY)

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15
Q

How would you perform a ABPM?

A

2/hr during waking hours

14 readings a day

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16
Q

What are the 3 stages of hypertension?

A

1 =
Clinical- >140/90
ABPM - >135/85

2=
Clinical- >160/100
ABPM - >150/95

3 = 180/110

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17
Q

How would you assess for end organ damage in hypertension?

A

Fundoscopy: hypertensive retinopathy
ECG: LVH or IHD

Urine dip: renal disease

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18
Q

What is the management for hypertension?

A

ABCD

Step 1
> 55 & stage 2 or above → ACEi
> 55 OR of black/African Caribbean → CCB

Step 2
ACEi / ARB + CCB (ACEi ARE CONTRAINDICATED IN BLACK/AFRICAN CARRIBEAN PEOPLE)

Step 3
ACEi/ARB + CCB + Thiazide diuretic

Step 4
Resistant HTN
Consider other drugs: sodium nitroprusside in emergencies

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19
Q

What would you do if a patient reaches stage 4 of hypertension management?

A

Resistant HTN:

Confirm elevated BP

Assess for postural Hypotension

Discuss Adherence

Potassium <4.5: low dose spironolactone

Potassium >4.5: AB or BB

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20
Q

How is hypertension monitored?

A

Treatment targets:
* < 80 yrs: <140/90
* > 80 yrs: 150/90
* CKD, previous stroke and diabetes: >130/80

Monitor U&Es regularly when using ACEi and diuretics

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21
Q

What are the side-effects of ACEi?

A

Cough
Angioedema
Hyperkalaemia

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22
Q

What are the side-effects of CCB?

A

Ankle swelling
Headache
Flushing

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23
Q

What are the side-effects of thiazide diuretics?

A

Hyponatraemia
Hypokalaemia
Dehydration

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24
Q

What are the side-effects of ARB?

A

Hyperkalaemia

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25
Q

What is the clinical presentation of pericarditis?

A

Pleuritic chest pain: eased by leaning forwards

Worsened by lying flat

Pericardial rub
Fever

Myalgias

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26
Q

What are the investigations for pericarditis?

A

Transthoracic echocardiogram: pericardial effusion shows a ‘dancing’ heart

ECG: widespread ST saddle elevation and PR depression

Bloods: raised ESR and CRP

Troponin

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27
Q

What is the management for pericarditis?

A

Viral: NSAIDs + colchicine (anti-gout, reduces inflammation and pain)

Bacterial: antibiotics + pericardiocentesis

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28
Q

What is the clinical presentation of MSK chest pain?

A

Worse on movement

Worse on palpation

Precipitated by trauma or cough

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29
Q

What is shingles?

A

Reactivation of a measles infection (HHV-3) (normally occurring during childhood)

Causes a painful rash along a dermatome

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30
Q

What is the clinical presentation of shingles?

A

Dermatomal pain:

  • Macular vesicular rash in dermatomal distribution

Pain preceeds rash

Malaise, myalgia, headache and fever

Disseminated infection: if immunosuppressed

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31
Q

What are the investigations for shingles?

A

Clinical presentation of skin lesions

Viral PCR, culture and immunohistochemistry

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32
Q

How is shingles managed?

A

Conservatively
Oral aciclovir: if high risk
Zoster vaccine
VZV immunoglobulin
Calamine lotion and chlorphenamine (antihistamine): itching

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33
Q

What is the clinical presentation of aortic dissection?

A

Sudden severe ‘tearing’ chest pain
May radiate to the back if type B

Does not radiate to arms

Syncope

Unequal upper limb BP

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34
Q

What are the investigations for aortic dissection?

A

CT angiogram

ECG

CXR

ECHO

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35
Q

How is Aortic Dissection treated?

A

Medical emergency

Type A: open surgery

Type B: TEVAR

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36
Q

What are 4 causes of transient non-visible haematuria?

A
  • UTI
  • Menstruation
  • Vigorous exercise
  • Sexual intercourse
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37
Q

What are 6 causes of persistent non-visible haematuria?

A
  • Cancer
  • Stones
  • BPH
  • Prostatitis
  • Urethritis
  • Renal: IgA nephropathy
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38
Q

How can you investigate haematuria?

A
  • URINE DIP:
    • Persistent = 2/3 samples 2 weeks apart
  • Renal function
    • Albumin:creatinine ratio:
    • Protein:creatinine ratio PCR
      Urine microscopy
39
Q

When should you urgently refer haematuria?

A

> 45yrs+:
- Unexplained visible haematuria
- Visible haematuria persisting after UTI management
OR
60yrs+
- Unexplained non-visible haematuria
- Dysuria
- Raised WCC

40
Q

What is the Referral Guidance for chest pain?

A

Current/within 12hrs + abnormal ECG: EMERGENCY ADMISSION
12-72hrs ago: REFERRAL FOR SAME DAY ASSESSMENT
>72hrs ago: FULL ASSESSMENT, ECG + TROPONIN

41
Q

What is venous thrombus embolism (VTE)?

A

Blood clot enters circulation

42
Q

What is pulmonary embolism?

A

Obstruction of the pulmonary arteries 2° to an embolus

43
Q

How many more times common are DVTs than PEs?
What percentage of DVTs lead to PE?

A

DVT 3x more common

16% in untreated patients

44
Q

What is the clinical presentation of VTE?

A
  • Paralysis/paresis
  • Entire leg swollen
  • Tenderness/pain
  • Erythema
  • Calf swelling >3cm compared to the other leg
  • Pitting oedema
  • Distended veins
45
Q

What is the clinical presentation of PE?

A

Dyspnoea + dyspnea
Syncope
Pleuritic chest pain
Cyanosis: hypoxia
Elevated JVP: suggests cor pulmonale
DVT signs: positive Wells score
Cough +/- haemoptysis
Haemoptysis
Tachycardia + tachypnoea
Crackles
Fever

46
Q

What is the Well’s score?

A

Calculates risk of DVT

47
Q

What comprises the Well’s score?

A

PC:
- Paralysis/paresis/recent immobilisation
- Localised tenderness along the deep venous system
- Entire leg swollen
- Calf swelling > 3cm compared to other leg measured 10cm below the tibial tuberosity)
- Pitting oedema confined to affected leg
- Collateral superficial veins present
- PMH
- Bedridden recently > 3 days or major surgery within 12 weeks
- Active cancer (treatment or palliation within 6 months)
- Previous DVT
- DH
- OCP/HRT
- SH
- Long haul flight
- Smoking

48
Q

What are the investigations for PE/DVT if the Wells score is:

≥2?
≤1?

A

Well’s Score:
≥2 = Duplex US of deep veins within 4hrs + D-Dimer
≤1 = D-Dimer within 4hrs
For both test:
FBC
U&E
LFTs
Antiphospholipid antibodies

49
Q

What are the investigations for PE?

A

Well’s Score:
- ≥2 = Duplex US of deep veins within 4hrs + D-Dimer
- ≤1 = D-dimer within 4hrs
Computed tomographic pulmonary angiography (CTPA): visualisation of clot
- ABG: Type 1 respiratory failure (O2 <8kPa)
- ECG: S1Q3T3 (inverted T in V1-V6 and RBBB)
For both test:
- CXR
- ECHO
- FBC
- U&E
- LFTs
- Antiphospholipid antibodies

50
Q

What is the gold standard in diagnosing PE?

A

CTPA

51
Q

What is the management of a VTE/DVT?

A

LMWH (e.g. enoxaparin) :
- 5 days OR INR >2.0 for 24hr
- 6 months if active cancer
Wafarin:
- 3 months
- 6 months: if unprovoked
Fondaparinux sodium: inhibits factor X
Compression stockings
IVC filters
DOAC: rivaroxaban
Unfractionated heparin: in CKD

52
Q

What should be given if the USS is delayed when diagnosing a VTE?

A

LMWH

53
Q

If the VTE is unprovoked what should be done?

A

Test for Malignancy:
- CXR
- Bloods (FBC,Ca,LFTs)
- Urinalysis
- Abdo CT or mammogram: - If >40yrs

54
Q

What is the management of PE?

A

On clinical suspicion and only stopped once ruled out:
1) LMWH (e.g. enoxaparin):
- 5 days OR INR >2.0 for 24hr
- 6 months if active cancer
2) Wafarin:
- 3 months
- 6 months: if unprovoked
3. DOAC: apixabanorrivaroxaban
4. Compression socks: prophylaxis
5. Inferior vena cava filter
6. THROMBOLYSIS (e.g. e.g. alteplase) : in haemodynamic compromise e.g. alteplase
7. Surgical embolectomy

55
Q

How do you monitor treatment in VTE/PE/DVT?

A

Anti-Xa: anti-thrombin III inhibits factor Xa and stops coagulation cascade

56
Q

What may affect a V/Q scan?

A

Previous PE
AV malformations
Vasculitis
Radiotherapy

57
Q

What are lymphomas?

A

Lymphoproliferative disorder (specifically B-cells) that predominantly involves the lymph nodes and extranodal sites

58
Q

What is Hodgkin’s lymphoma?

A

A lymphoma associated with Reed-Sternberg cells (owl’s eye nuclei)

59
Q

Name the 4 different types of Hodgkins Lymphoma

A

Nodular Sclerosing: Majority + women (lacunar cells)

Mixed Cellularity (Reed-Sternberg cells)

Lymphocyte predominant

Lymphocyte depleted

60
Q

What is Non-Hodgkin’s Lymphoma?

A

Malignant proliferation of lymphocytes other then Hodgkin’s

61
Q

What are the presentations of lymphomas?

A

Painless, asymmetrical and non-tender lymphadenopathy (rubber): cervical, axillary or inguinal

B-cell symptoms: night sweats, fever & weight loss

Itching

Pain when drinking alcohol

Recurrent infections
Alcohol induced node pain
Normocytic anaemia

62
Q

What features may suggest a poor prognosis in lymphoma?

A

B-symptoms:
- Weight loss >10%
- Fever >38
- Night sweats
Poorer:
- > 45yrs
- Stage 4
- Haemoglobin < 10.5
- Lymphocytes < 600 or 8%
- Male
- Albumin
- WCC > 15000

63
Q

What s the difference between Hodgkin’s and Non-Hodgkin’s in terms of:

  • Histology
  • B-symptoms
  • Extra-nodal disease
A

Histology:
Hodgkins= Reed-Sternberg cells

B-symptoms:
Hodgkins = Early
Non-Hodgkins = Late

Extra-nodal disease:
Hodgkins = Less common
Non-Hodgkins = More common

64
Q

What are the investigations for Hodgkin’s lymphoma?

A

Blood smear: Reed-Sternberg cells

Raised serum LDH

Diagnosis: FBC, ESR, CRP, CXR and lymph node biopsy

Staging: MRI and PET scan

65
Q

What are the investigations for non-hodgkin’s lymphoma?

A

Diagnosis: FBC, ESR, CRP, CXR and excisional lymph node biopsy

Staging: MRI, CT and PET scan

66
Q

What are laboratory signs of Hodgkin’s lymphoma?

A

Lymphocyte proliferation

Reed-Sternberg cells

67
Q

What is the staging used for lymphomas?

A

Ann Arbor system:
1. 1 node

  1. ≥2 nodes on same side of the diaphragm
  2. Lymph nodes on both sides of diaphragm
  3. Extra-nodal involvement

+ A: no B symptoms
+ B: present B symptoms

68
Q

How are Hodgkin’s lymphomas managed?

A

ABVD:

Adriamycin

Bleomycin

Vinblastine sulfate

Dacarbazine

69
Q

What is the treatment for non-hodgkin’s lymphoma?

A

R-CHOP:

Rituximab

Cyclophosphamide

Hydroxydaunorubicin hydrochloride

Vincristine

Prednisone

Stem cell transplantation

70
Q

What is are the complications of lymphomas?

A

Chemotherapy: risk of leukaemia, infertility, nausea, vomiting, hair loss etc

Radiotherapy: risk of cancer and damage to tissues

71
Q

What is COPD?

A

Progressive and irreversible obstructive airway disease

72
Q

What two conditions encompass COPD?

A

Emphysema and Bronchitis

73
Q

What are the causes of COPD?

A
  • Smoking
  • Alpha-1 antitrypsin deficiency
  • Occupational exposure: dusts, chemical agents and fumes
74
Q

What is the clinical presentation of COPD?

A

Tar staining of fingers: NO CLUBBING
ESPECIALLY IF A SMOKER!
Cough + sputum production: NO haemoptysis

Blue bloater: chronic bronchitis

Pink puffer: emphysema

Dyspnea

Recurrent respiratory infections

Symptoms do not improve with salbutamol

Barrel chested

Wheezing on auscultation: from airway narrowing

Coarse crackles: sudden opening of the airways

75
Q

What are the spirometer readings for COPD?

A

All FEV1/FVC ratio of <0.7

FEV1 (% of predicted):
>80 = Stage 1 Mild
50-79 = Stage 2 Moderate
30-49 = Stage 3 Severe
<30 = Stage 4 Very Severe

76
Q

How is COPD diagnosed?

A

Considered in any patient >35yrs who are current/ex-smokers with ≥1 symptoms of COPD

Spirometry:

  • FEV1/FVC ratio <0.7
  • Bronchodilator does not reverse

Chest X-ray: flattened diaphragm, hyperinflation and bullae

Pulse oximetry

ABG: detects cyanosis

77
Q

What is the management of COPD?

A
  1. SABA(salbutamol)/ SAMA (ipratropium)
  2. LABA + LAMA ((salmetrol or tiotrium) Anoro Ellipta) or LABA+ICS (Fostair ****if asthmatic)
  3. LABA + LAMA + ICS (Trimbo)

Stop smoking

78
Q

When should long term oxygen therapy be offered in COPD?

A

O2 for ≥ 15 hours per day if:
- pO2 < 7.3
OR pO2 7.3 – 8 AND:
- Secondary polycythaemia
- Peripheral oedema
- Pulmonary hypertension
- Non-smoker

79
Q

What is a major complication of COPD?

A

Cor Pulmonale

80
Q

What is Cor Pulmonale?

A

Pulmonary hypertension from chronic lung disease that can cause right sided HF

81
Q

What is the clinical presentation of cor pulmonale?

A
  • Peripheral oedema
  • Increased JVP
  • Parasternal heave
  • Loud P2
82
Q

What is the management of Cor pulmonale in COPD?

A

Loop Diuretic Furosemide
Long term O2

83
Q

What are features of an acute COPD exacerbation?

A

Worsening of:
- Dyspnoea
- Cough
- Wheeze
- Sputum
- Hypoxia
- Confusion

84
Q

Name 2 exacerbation organisms of COPD

A

Haemophilus Influenzae

Strep Pneumoniae

Moraxella Catarrhalis

85
Q

What is the management of acute exacerbation in COPD?

A

Prednisolone for 7-14 days
Increased nebulised salbutamol dose
Oral Abx if purulent sputum or signs of pneumonia:
- Amoxicillin

86
Q

What is Gout?

A

Hyperuricaemia and deposition of monosodium urate crystals causing attacks of acute inflammatory arthritis- crystal arthropathy

Usually affects small joints and kidneys

87
Q

What causes hyperuricaemia and thus gout?

A

Idiopathic: Majority
Increased production: psoriasis, genetics, diet (shellfish, red meat and alcohol)

Decreased excretion from the kidneys: CKD, NTN, thiazides and alcohol

88
Q

What is the clinical presentation of gout?

A

Rapid-onset severe pain

Flares

Joint stiffness and tenderness

1st metatarsophalangeal and carpo-metacarpal joint

Monoarticular

Swelling and joint effusion

Tophi: subcutaneous deposits near the ears island fingers

Erythema and warmth

89
Q

What can precipitate Gout?

A

Diuretics
Cold
Alcohol

90
Q

What are the investigations for Gout?

A

Arthrocentesis (aspiration) synovial fluid analysis:
-High WBC
-Presence of needle shaped monosodium urate crystals with negative birefringence
X-ray shows:
1) Soft tissue swelling
2) Peri-articular erosions
3) Norma joint space

Serum urate

91
Q

What is the management of Gout?

A

NSAID: for acute episodes

Corticosteroids

Allopurinol: lowers uric acid levels (long term)

Colchicine: anti-gout and reduces inflammation and pain (aCute)
Lose weight

Stop drinking

Avoid meats with high purines (red meat, shellfish)

92
Q

What is pseudogout?

A

Calcium pyrophosphate deposition causing synovitis (arthritis)

93
Q

What investigations are ordered for the diagnosis of pseudogout?

A

Arthrocentesis with synovial fluid analysis:

Presence of rhomboidal, weakly positively birefringent crystals under polarized light microscopy

Joint X-ray: crystals

94
Q

What is the management of pseudogout?

A

Intra-articular corticosteroids

NSAIDs

DMARD: methotrexate

3a Exam (9 decks)

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