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GP notes Flashcards

1
Q

(7)

Who is at an increased risk of AKI?

A

CKD, other organ failure/chronic disease, history of AKI, use of drugs with nephrotoxic potential within the last week, use of iodinated contrast agents within the last week, >65 years, oliguria

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2
Q

What are drugs with nephrotoxic potential?

A

NSAIDs, aminoglycoside, ACE inhibitors, angiotensin II receptor antagonists, diuretics

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3
Q

What are the ways that AKI may present?

A

Reduced urine output (oliguria), fluid overload, a rise in molecules that the kidney normally excretes/maintains a balance of

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4
Q

What is the definition of oliguria?

A

Urine output of less than 0.5ml/kg/hour

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5
Q

What symptoms are seen in AKI?

A

Reduced urine output, pulmonary and peripheral oedema, arrhythmias, features of uraemia

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6
Q

What are features of uraemia?

A

Pericarditis, encephalopathy

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7
Q

What is the diagnostic criteria for AKI?

A

50% or greater risk in serum creatinine known or presumed in last 7 days, rise in serum creatinine of 26 mmol/L or greater within 48 hours, fall in urine output to less than 0.5ml/kg/hr

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8
Q

What is the treatment in hyperkalaemia for stabilisation of the cardiac membrane?

A

IV calcium gluconate

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9
Q

What is the treatment in hyperkalaemia for short term shift in potassium from extracellular to intracellular fluid compartment?

A

Nebulised salbutamol, combined insulin/dextrose infusion

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10
Q

What is the treatment in hyperkalaemia for removal or potassium from the body?

A

Calcium resonium (orally or enema), loop diuretics, dialysis

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11
Q

What are possible complications of severe AKI?

A

Hyperkalaemia, pulmonary oedema, acidosis or uraemia (pericarditis, encephalopathy)

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12
Q

What is acute tubular necrosis?

A

Damage and death of the epithelial cells of the renal tubules. Damage occurs due to ischaemia due to hypoperfusion or due to nephrotoxins

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13
Q

What is the commonest intrinsic cause of AKI?

A

Acute tubular necrosis

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14
Q

What is seen on urinalysis in acute tubular necrosis?

A

Muddy brown casts

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15
Q

Is acute tubular necrosis reversible?

A

Yes: epithelial cells can regenerate, though this takes between 1 and 3 weeks

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16
Q

What are the investigations in AKI?

A

Urinalysis for protein, blood, leucocytes, nitrites and glucose. Ultrasound can be done to assess for obstruction when suspected post renal cause

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17
Q

What is the tx for AKI?

A
  • IV fluids
  • withhold medications that may worsen condition, and without medications that can accumulate in reduced renal function
  • relieve obstruction in post-renal AKI
  • dialysis if severe
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18
Q

What are risk factors for CKD?

A

Diabetes, HTN, certain nephrotoxic medications, glomerulonephritis, polycystic kidney disease

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19
Q

What are the symptoms of CKD? When do they present?

A

Symptoms often present very late. It is often non specific: fatigue, pallor (due to anaemia), foamy urine (proteinuria), nausea, loss of appetite, pruritus (ithching), oedema, HTN, peripheral neuropathy

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20
Q

What is the ratio that quantifies proteinuria?

A

Urine albumine:creatinine ratio

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21
Q

What is the diagnosis criteria for CKD?

A

For over 3 months:
- estimated glomerular filtration rate is sustained below 60ml/min/1.73m2
- urine albumin:creatinine ratio is sustained above 3mg/mmol

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22
Q

What is the estimated decline in eGFR annually in CKD?

A

15ml/min/1.73m^2

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23
Q

What are the potential complications of CKD?

A

anaemia, renal bone disease, cardiovascular disease, peripheral neuropathy, end stage kidney disease, dialysis related complications

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24
Q

When should someone be referred for renal specialist assessment in CKD?

A
  • eGFR <30ml/min/1.73m^2
  • urine ACR >70 mg/mmol
  • accelerated progression
  • uncontrolled hypertension despite 4 or more hypertensives
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25
Q

What are medications that can slow the disease progression of CKD?

A

ACE inhibitors (or ARBs), and SGLT-2 inhibitors (specifically dapagliflozin)

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26
Q

Why can CKD cause anaemia?

A

Healthy kidneys produce erythropoietin, which stimulates RBC production. In CKD, erythropoietin production reduces, which causes normocytic normochromic anaemia

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27
Q

Why can CKD cause renal bone disease?

A

Healthy kidneys metabolise vitamin D into its active form. Active vitamin D is essential in calcium absorption in the intestines and reabsorption in the kidneys. It is also responsible for regulating bone turnover and promoting bone reabsorption to increase the serum calcium level. Chronic kidney disease leads to less vitamin D activity and low serum calcium. There is also high serum phosphate due to reduced excretion. Parathyroid gland reacts by excreting parathydoid hormone, which stimulates osteoclast activity, increasing calcium absorption from bone.

All of this leads to osteomalacia (soft bones) and osteosclerosis (

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28
Q

What is a characteristic xray finding in CKD?

A

Rugger jersey spine: this involves sclerosis of both ends of each vertebral body (denser white) and osteomalacia in the centre of the vertebral body (less white). The name refers to the stripes found on a rugby shirt.

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29
Q

What is osteomalacia?

A

Softening of bones, occurs because of a problem with vitamin D

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30
Q

What is osteosclerosis?

A

A disorder that is characterised by abnormal hardening of bone and an elevation in bone density

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31
Q

What is the best way to differentiate between AKi and CKD?

A

Ultrasound: most patients with CKD have bilateral small kidneys.
CKD is also more likely to have hypocalcaemia

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32
Q

What UTI causative organism is most linked to renal stones?

A

Proteus sp.

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33
Q

What is the management if someone presents with queried PE but there is a delay for scan?

A

Start treatment (rivaroxaban)

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34
Q

What is the first line management of hypertension in diabetics?

A

ACE-I/ARBs

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35
Q

What is the recommended treatment for all patients in acute heart failure?

A

IV loop diuretics (furosemide or bumetanide)

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36
Q

What are the features of pericarditis?

A

Chest pain, relieved by sitting forwards, non-productive cough, dyspnoea, flu-like symptoms, pericardial rub

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37
Q

What ECG changes are seen in pericarditis?

A

Saddle shaped ST elective, PR depression (most specific)

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38
Q

What investigation should be done for all patients with pericarditis?

A

Transthoracic echocardiography

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39
Q

What is the management of pericardial effusion?

A

NSAIDs, and colchicine (reduces risk of recurrence)

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40
Q

What is the management for a patient who has a stroke whilst on warfarin?

A

Give IV vitamin K and prothrombin complex concentrate

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41
Q

What is done if there is a high INR of >8.0 and minor bleeding for a patient on warfarin?

A

Give IV vitamin K

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42
Q

What is the management for high INR of >8.0 but no bleeding for a patient on warfarin?

A

Give oral vitamin K

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43
Q

What is the target range of warfarin?

A

2.5, action needed if more than 5

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44
Q

What drug commonly interacts with statins to raise creatine kinase levels?

A

Clarithromycin

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45
Q

Who is it recommended should take statins?

A

Anyone with a 10-year cardiovascular risk >10%

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46
Q

What is first line therapy in chronic heart failure?

A

ACE inhibitor/ARBi and beta blocker

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47
Q

What is second line therapy in heart failure?

A

Aldosterone antagonist (spironolactone)

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48
Q

What is the risk factor tool for whether to anticoagulate a patient in AF?

A

CHA2DS2-VASc

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49
Q

What is first line treatment of AF?

A

Bisoprolol

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50
Q

What is a common contraindication for beta blockers?

A

Asthma

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51
Q

What is chronic heart failure?

A

Refers to the clinical features of impaired heart function, specifically the left ventricle

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52
Q

How does left ventricular failure in heart failure lead to pulmonary oedema?

A

Leads to a chronic backflow of blood waiting to flow through left side of heart. LA + pulmonary veins + lungs experience increased volume and pressure blood. Fluid leaks -> pulmonary oedema

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53
Q

What is a normal ejection fraction?

A

> 50%

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54
Q

What is heart failure with reduced ejection fraction?

A

When the ejection fraction is less than 50%

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55
Q

What causes heart failure?

A

Ischaemic heart disease, valvular heart disease (mostly aortic stenosis), hypertension, arrythmias, cardiomyopathy

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56
Q

What is the presentation of chronic HF?

A
  • breathlessness, worsened by exertion
  • cough (frothy)
  • orthopnoea (breathless when lying flat)
  • PND
  • peripheral oedema
  • fatigue
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57
Q

What signs are seen on examination in heart failure?

A

Tachycardia, tachypnoea, HTN, murmurs, 3rd heart sound, bilateral basal crackles (pulmonary oedema), raised JVP (due to backlog to right heart), peripheral oedema

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58
Q

What is done to establish a diagnosis of heart failure?

A
  • N-terminal pro-B-type natriuretic peptide
  • ECG
  • ECHO
  • CXR + lung function tests
  • bloods
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59
Q

What is the New York Heart Association Classification?

A

Class I: no limitation on activity
Class II: comfortable at rest but symptomatic with ordinary activity
Class III: symptomatic with any activity
Class IV: symptomatic at rest

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60
Q

How does NT-proBP result guide ECHO?

A

If 400-2000 ng/litre: ECHO within 6 weeks, >2000 ng/litre within 2 weeks

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61
Q

What are the four pillars of heart failure treatment?

A

ACEI, beta blocker, aldosterone antagonist, SGLT2i

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62
Q

How do SLGT-2i work in heart failure?

A

Reduce glucose reabsorption and increase urinary glucose excretion (increased risk of UTI)

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63
Q

What vaccines should be given in heart failure patients?

A

Influenza annually and one off pneumococcal vaccine

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64
Q

What should be monitored if ACEI and aldosterone antagonists taken together?

A

Renal function: both can cause hyperkalaemia (tall tented t waves)

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65
Q

What is diagnostic of hypertension?

A

Blood pressure above 140/90 in a clinical settings, confirmed with ambulatory or home readings above 135/85

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66
Q

What are potential secondary causes of hypertension?

A

Renal disease, obesity, pregnancy induce (pre-eclampsia), endocrine, drugs (alcohol, steroids, NSAIDs, oestrogen)

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67
Q

What investigation should be done for very high blood pressure that is not responding to treatment?

A

Duplex ultrasound or MRI/CT angiogram, for renal artery stenosis

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68
Q

How often does NICE recommend measuring blood pressure for HTN?

A

Every 5 years, or every year in T2DM

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69
Q

What is stage 1 vs 2 vs 3 hypertension?

A

1: >140/90, 2: >160/100, 3: 180/120

70
Q

What investigations should be done for end organ damage on diagnosis of HTN?

A

Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria, bloods for HbA1c/renal function, fundus examination, ECG (especially left ventricular hypertrophy)

71
Q

What is starting dose of statin?

A

20mg

72
Q

What is step 1 anti HTN?

A

If <55 years of T2D<: ACEI or ARB

If >55 + no T2DM, or Afro caribbean + no T2DM: CCB

73
Q

Why should renal function be checked 2-3 weeks after starting ACE-I?

A

May worsen kidney function intially

74
Q

What are the common s/e of ACE-I?

A

COUGH, angioedema, hyperkalaemia

75
Q

What is second line drug treatment of HTN?

A

ACE-I + CCB or ACE-I + diuretic

76
Q

What is an alternative to CCB?

A

thiazide diuretic if not tolerated

77
Q

What is the common complaint for CCB?

A

Ankle oedema

78
Q

What is the preferential drug in black patients out of ACE-I or ARB?

A

ARB

79
Q

What is step 4 hypertension management?

A

Spironolactone or alpha blocker or beta blocker

80
Q

When is spironolactone used in step 4 HTN management?

A

If serum potassium less than 4.5 mmol, then spironolactone. If >4.5, then alpha or beta blocker

81
Q

Is nitrites or leucocytes a better indicator of UTI?

A

Nitrites

82
Q

What patients is a urine dipstick not a valid investigation for UTI?

A

Women >65, men, and anyone catheterised

83
Q

What are the most common causes of UTI?

A

E.coli. Also: Klebsiella pneumoniae, enterococcus, pseudomonas

84
Q

What is the first line management of UTI?

A

Trimethoprime or nitrofurantoin for 3 days

85
Q

What is the management for UTI in men?

A

7 days abx (tri or nitro)

86
Q

What eGFR should nitrofurantoin be avoided in?

A

<45

87
Q

What is the management of symptomatic UTI in pregnant women?

A

Nitrofurantoin, amoxicillin 2nd line

88
Q

What is the management of acute pyelonephritis?

A
  • consider hospital admission
  • local guidelines abx
  • broad spectrum cephalosporin or quinolone for 7-10 days
89
Q

What is the cells in oesophagus vs stomach?

A

Oesophagus: squamous epithelial, stomach: columnar epithelial

90
Q

What is the symptoms of dyspepsia?

A

Heartburn, acid regurg, retrosternal or epigastric pain, bloating, nocturnal cough

91
Q

What is red flag symptoms in GORD?

A

Dysphagia, >55 years, weight loss, upper abdo pain, reflux, treatment resistance, N+V, upper abdo mass, low haemoglobin

92
Q

What is management for GORD proven with endoscopy?

A

Full dose PPI for 1-2 months. If no response double

93
Q

What is the management for endoscopically negative reflux disease?

A

Full dose PPI for one month. If no response then H2RA or prokinetic

94
Q

What does H.pylori cause?

A

Can damage epithelial lining of the stomach, leading to gastritis, ulcers and increase stomach cancer

95
Q

Who should be tested for H.pylori?

A

Anyone with dyspepsia

96
Q

What should be done before H.pylori testing?

A

Stop PPI for 2 weeks

97
Q

What is the investigation for H.pylori?

A

Stool antigen test, urea breath test, rapid urease test

98
Q

What is eradication for H.pylori?

A

PPI + amoxicillin + clarithromycin/metronidazole (7 days)

99
Q

What is the management for H.pylori if pencillin allergic?

A

PPI + metronidazole + clarithromycin

100
Q

What is the RF for peptic ulcer disease?

A

H.pylori, NSAIDs/SSRIs/steroids/bisphosphonates

101
Q

What makes up CURB-65?

A

Confusion, urea >7mmol, resp rate >30, blood pressure <90/60, age over 65

102
Q

What does CURB-65 predict?

A

Mortality with pneumonia

103
Q

What does 0/1 CURB-65 score suggest?

A

Treatment at home

104
Q

What does CURB-65 2 or more suggest?

A

Consider hospital admission

105
Q

What does CURB-65 3 or more suggest?

A

Consider intensive care

106
Q

What are the most common causes of pneumonia?

A

S.pneumoniae, h.influenzae

107
Q

What is a possible cause of pneumonia in COPD patients?

A

Moraxella catarrhalis and H.influenzae

108
Q

What are potential causes of pneumonia in cystic fibrosis?

A

Pseudomonas aeruginosa and S.aureus

109
Q

What complication can legionella pneumophilia cause?

A

SIADH and hyponatraemia

110
Q

How is legionella pneumophilia diagnosed?

A

Urine antigen test

111
Q

What pneumonia may occur in HIV/immunocompromised patients, and what is the prophylaxis?

A

Pneumocystis jirovecii. Co-trimoxazole is treatment/prophylaxis

112
Q

What is the treatment for COVID-19 pneumonia?

A

Respiratory support, dexamethasone, monoclonal antibodies

113
Q

What is the treatment for CAP?

A

5 days of oral abx, such as amoxicillin, clarithromycin

114
Q

What is the treatment for moderate/severe pneumonia?

A

IV tazocin, or doxycycline

115
Q

What are two causes of atypical pneumonia?

A

Mycoplasma pneumoniae, legionella pneumophilia

116
Q

What are risk factors for pneumonia?

A

Under 5 or over 65, smoking, recent viral URTI, chronic respiratory diseases, immunosuppression, IVDU

117
Q

What pneumonia is classically seen in alcoholics?

A

Klebsiella pneumoniae

118
Q

What type of pneumonia does influenza infection precede?

A

S.aureus

119
Q

What is the scoring system for severity of LUTS symptoms in men?

A

International prostate symptom score

120
Q

What categories can LUTS be separated into?

A

Voiding symptoms, storage symptoms, post micturition, complications

121
Q

What investigations are done for men with LUTS?

A
  • DRE
  • abdo exam
  • urinary frequency volume chart for 3 days
  • urine dipstick
  • PSA
122
Q

What are possible causes of raised PSA?

A

Prostate cancer, BPH, prostatitis, UTIs, vigorous exercise, recent ejaculation or prostate stimulation

123
Q

What are the two medical options for BPH?

A
  • alpha blockers (tamsulosin) to relax smooth muscles. Rapid improvement in symptoms
  • 5-alpha reductase inhibitors (finasteride) to gradually reduce size
124
Q

What is first line BPH tx?

A

Alpha blockers: tamsulosin

125
Q

What are potential s/e of tamsulosin?

A

Dizziness, postural hypotension, dry mouth, depression

126
Q

When is 5-alpha reductase inhibitors indicated?

A

Significantly enlarged prostate at high risk of progression

127
Q

What are potential s/e of 5-alpha reductase inhibitors?

A

Erectile dysfunction, reduced libido, ejaculation issues, gynaecomastia

128
Q

What type of tumours are the majority of prostate cancers?

A

adenocarcinomas

129
Q

What are the risk factors for prostate cancer?

A

Increasing age, FHx, black african, tall stature, anabolic steroids

130
Q

What is the initial drug therapy for ACS?

A

Aspirin (300mg), oxygen (if <94%), morphine if severe pain, nitrates. (MONA)

131
Q

What should be offered in smoking cessation?

A

Nicotine replacement therapy, varenicline, or bupropion

132
Q

What is the advice for smoking cessation and pregnant women?

A
  • test with carbon monoxide detectors
  • CBT first line. Can use nicotine replacement therapy
  • varenicline and buprorion contraindicated
133
Q

What unfavourable side effect can spironolactone cause?

A

gynaecomastia

134
Q

What is the typical presentation of COPD, and what symptoms should not be attributed to COPD and lead to further investigations?

A

COPD: dyspnoea, cough, sputum production, wheeze, recurrent resp infections

Further Ix: clubbing, haemoptysis, chest pain

135
Q

What is the MRC dyspnoea scale?

A

Grade 1: breathless on strenuous exercise
Grade 2: breathless on walking uphill
Grade 3: breathless that stops them walking on the flat
Grade 4: breathlessness stopping them walking more than 100m on the flat
Grade 5: unable to leave the house

136
Q

How is COPD dx? Results?

A

Spirometry: obstructive picture, FEV1:FVC ratio <70%. No response to reversibility testing

137
Q

What vaccines should be given in COPD?

A

Pneumococcal and annual flu vaccine

138
Q

What is initial medical tx for COPD?

A

SABA (salbutamol) and SAMA (ipratropium bromide)

139
Q

What are the two types of COPD treatment?

A

Determined by whether asthmatic/steroid responsive features, or not

140
Q

What is the management of steroid responsive COPD, 2nd stage?

A

LABA (tiotropium) + ICS

141
Q

What is the management of COPD not steroid responsive, 2nd stage?

A

LABA + LAMA

142
Q

What is the final stage management of COPD?

A

Combination of LABA/LAMA/ICS

143
Q

When is long term oxygen therapy used in COPD?

A

If chronic hypoxia (sats <92%), though C/I from smking

144
Q

What is cor pulmonale?

A

Right sided heart failure. Due to increased pressure in pulmonary arteries, causes back pressure into right atrium, vena cava

145
Q

What is the most common cause of cor pulmonale?

A

COPD

146
Q

What is seen in an arterial blood gas in COPD exacerbation?

A

Acidosis: low PH, low PO2, raised CO2 (retention), raised bicarb

147
Q

What is the first line management of acute exacerbation of COPD?

A

Steroids (pred for 5 days), regular meds

148
Q

what prophylaxis is given in COPD?

A

azithromycin

149
Q

What is the most common infective cause of exacerbation of COPD?

A

H.influenzae

150
Q

What is prophylaxis of DVT in hospital? What are the C/I?

A

LMWH (such as enoxaparin). C/I: active bleeding, existing anticoagulation

151
Q

What can cause a raised d-dimer?

A

PE, pneumonia, malignancy, heart failure, surgery, pregnany

152
Q

What Wells score indicates a DVT is likely?

A

2 points or more

153
Q

What should be done if Well score =2 or more?

A

Doppler ultrasound within 4 hours. If positive, start treatment

154
Q

What should be done if Wells score =1 or less?

A

D dimer within 4 hours

155
Q

What is first line management of DVT?

A

Apixaban or rivaroxaban (DOACs), for at least 3 months if provoked, 6 months if unprovoked

156
Q

What is an example of LMWH?

A

enoxaparin, dalteparin

157
Q

What are examples of DOACs?

A

Apixaban/rivaroxaban

158
Q

What can be investigated for in a completely unprovoked DVT?

A

Antiphospholipid syndrome, hereditary thrombophilias

159
Q

What is first line imaging for PE?

A

CTPA (first line)

160
Q

What ABG is often seen in PE?

A

Respiratory alkalosis: hypoxia leads to tachypnoea, and blowing off extra CO2, meaning blood becomes alkalotic

161
Q

What Wells Score indicates PE is likely? What step should be taken?

A

4 or more. Do a CTPA

162
Q

What are the baseline investigations for angina?

A

Physical exam, ECG, FBC, U+Es, LFTs, lipid profile, TFTs, HbA1c

163
Q

What is the management for immediate symptomatic relief of angina?

A

GTN spray. Take GTN when symptoms start, second dose 5 mins later if symptoms remain, 3rd dose 5 mins later if remain, call ambulance after 5 mins is symptoms remain

164
Q

What are key s/e of GTN?

A

Dizziness and headaches

165
Q

What are the long term medications for angina?

A

Aspirin, statin, beta blocker or CCB

166
Q

When is a statin offered to patients?

A
  • QRISK >10%
  • CKD <60 eGFR
  • T1DM for more than 10 years or are over 40years
167
Q

How do statins work?

A

Reduce cholesterol production in the liver by inhibiting HMG CoA reductase

168
Q

What is secondary prevention of CVD?

A

Antiplatelet (aspirin/clopidogrel), atorvastatin (80mg), atenolol, ACE-I

169
Q

What ABGs indicate someone with COPD should receive O2 therapy?

A

2 measurements of <7.3 kPA

170
Q

What are investigations for target organ damage in HTN?

A
  • albumin:creatinine ratio
  • urinalysis (haematuria+proteinuria)
  • HbA1c
  • electrolytes
  • eGFR
  • cholesterol
  • fundoscopy
  • 12 lead ECG
171
Q

What pathogen are you worried about in a child presenting in GP with tonsilitis?

A

Group A Strep (S.pyogenes)

172
Q

What are methods of ensuring people with communication difficulties are understanding during a consultation? (5)

A
  • chunking (breaking information down into smaller sections)
  • visual support
  • large text/pictures
  • stop and check the person has understood at regular intervals
  • slow + don’t rush

Phase 3a (19 decks)

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