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Year 3 > Block 31 Week 8 > Flashcards

Block 31 Week 8 Flashcards

1
Q

Anti-metabolites?

A

5FU, gemcitabine, capecitabine

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2
Q

alkylating agents?

A

Cyclophosphamide, cisplatin, carboplatin.

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3
Q

modifying agents of the tertiary structure?

A

Etoposide, epirubicin

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4
Q

mitotic spindle poisons?

A

Vincristine

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5
Q

Taxanes?

A

Paclitaxel, docetaxel

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6
Q

Side effects of chemotherapy?

A

►Bone marrow suppression
►Alopecia
►Fatigue
►Nausea / vomiting
►Allergic reactions
► Liver / renal toxicity

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7
Q

adjuvant chemotherapy?

A

Treatment used to mop up micrometastatic disease post surgery in order to prolong surgery e.g. breast, lung and colorectal cancers.

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8
Q

neoadjuvant chemo?

A

Used to downstage tumours prior surgery e.g. oesophageal and rectal cancers.

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9
Q

curative chemo?

A

Chemotherapy is used as the sole, or main, modality to cure malignancy e.g. testicular cancers, lymphomas, leukaemias and many paediatric malignancies.

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10
Q

palliative chemo?

A

Chemotherapy is used to relieve symptoms, improve quality of life, and prolong life, but is not curative.

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11
Q

acute side effects of chemotherapy (generally reversible)

A
  • Myelosuppression
  • Nausea and Vomiting
  • Diarrhoea
  • Alopecia
  • Skin and nail changes
  • Local reactions
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12
Q

late (usually irreversible) SE of chemo?

A
  • Neuropathies
  • Sterility
  • Cardiovascular
  • Pulmonary fibrosis
  • Renal insufficiency
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13
Q

myelosuppression - red cells?

A
  • Lethargy
  • Dyspnoea
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14
Q
A
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15
Q

myelosuppression - platelets?

A
  • Purpura
  • Bleeding
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16
Q

infective complications of chemotherapy
?

A
  • Febrile Neutropaenia (Neutrophil < 1.0 x 109/L and Temperature > 38oC)
  • Septic Shock (low Blood Pressure)
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17
Q

Management of Neutropaenic sepsis?

A
  • IV fluids
  • Broad spectrum antibiotics
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18
Q

chemotherapy induced nausea and vomiting?

A
  • first 24 hrs = acute
  • delayed = 24 hrs plus
  • anticipatory - emesis before chemotherapy is given, triggered by sites or smells associated with chemotherapy administration
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19
Q

alopecia?

A
  • caused by anthracycline and taxanes
  • Always reversible
  • Can be ameliorated by scalp cooling during the period of chemotherapy administration
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20
Q

chemo induced peripheral neuropathies - drugs?

A
  • Cisplatin, Oxaliplatin
  • vinca alkaloids
  • Taxanes
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21
Q

sites affected by chemo induced peripheral neuropathies?

A
  • Hands and feet
  • Autonomic system
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22
Q

peripheral neuropathies tend to be?

A
  • Tends to be cumulative i.e. get worse with increasing cumulative dose
  • Tends to be irreversible
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23
Q

chemo induced sterility?

A
  • Tends to occur when alkylating agents are used.
  • For males sperm storage should be offered
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24
Q

which chemo agents most commonly cause cardiac problems?

A
  • anythracyclines most commonly cause cardiac problems- usually CHF
  • rare if the dose is kept below the cumulative dose level
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25
Q

which drugs can cause arrhytmias?

A

Taxanes and Anthracylines can cause arrhythmias

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26
Q

features of bone mets?

A
  • pain
  • pathological fractures
  • hypercalcaemua
  • SCC
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27
Q

mechanism of bone mets?

A
  • activated osteoblasts stimulate production of RANK which activates osteoclasts
  • osteoclasts resorb bone -> osteolysis -> release of growth factors for tumour growth
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28
Q

blastic vs lytic bone mets?

A
  • The mechanism of bone metastasis is seen radiologically; when bone-forming processes predominate the lesions appear blastic,
  • while if resorptive processes are dominant, the metastases appear lytic.
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29
Q

aggressive mets tend to be?

A

lytic

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30
Q

which mets show a slower course?

A

sclerotic (osteoblastic) metastases generally indicate a slower course

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31
Q

3 most common sites of metastasis?

A
  • lungs
  • liver
  • bone
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32
Q

which cancers metastasise to bone?

A
  • Among solid cancers, breast, prostate, lung, thyroid, and kidney cancer account for 80% of all skeletal metastases.
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33
Q

bone mets commonly present at the time of diagnosis of?

A

multiple myeloma

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34
Q

clinical presntation of bone mets?

A
  • Pain is the most common symptom
  • usually picked up during the staging of the cancer
  • scanned for bone mets when there’s elevated ALP or calcium
  • when ALP is elevated a fractionated alkaline phosphatase test (liver versus bone) would be indicated
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35
Q

which type of bone mets cause more hypercalcaemia?

A

osteolytic

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36
Q

bone mets - pain?

A
  • pain may be worse at night and partially alleviated by activity.
  • often insidious in onset and progresses but can also be sharp, severe and radiating
  • A complication such as invasion of adjacent structures usually results in constant, progressively worsening pain.
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37
Q

sudden severe painw ith bone mets?

A
  • Sudden severe pain may be caused by a pathologic fracture and should be urgently investigated.
  • Pathologic fractures are more likely to occur in osteolytic as compared with osteoblastic metastases.
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38
Q

predominantly osteoblastic mets - cancers?

A
  • SCLC
  • Hodgkin lymphoma
  • prostate
  • carcinoid
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39
Q

predom osteolytic bone mets?

A
  • renal cell
  • MM
  • melanoma
  • NSCLC
  • NHL
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40
Q

mixed osteoblastic and osteolytic
?

A
  • breast cancer
  • GI cancers
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41
Q

XR for bone mets?

A
  • initial screen to evaluate symptomatic areas
  • poor sensitivity (TP rate) so generally not used to screen for bone mets
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42
Q

CT for bone mets?

A
  • detect osteolytic and osteoblastic metastases within the bone marrow
  • not more sensitive than a bone scan
  • shows associated soft tissue disease and provides 3D reconstruction of images helpful for planning RT or surgery
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43
Q

MRI for bone mets?

A
  • more sensitive than CT to detect small meys
  • gold standard when MSCC or epidural disease/nerve root impingement is suspected because of the excellent soft tissue resolution.
  • It can also show the presence of spinal cord oedema.
  • can differentiate between pathological and insufficiency fractures
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44
Q

MRI -?

A
  • sensitive to movement
  • ppts with implantable devices not able to undergo
  • severe claustophobia
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45
Q

bone scans?

A
  • visualization of the entire skeleton
  • tracer accumulates in areas of inc osteoblastic activity
  • is reliable for detecting metastases in diseases like prostate and breast cancer.
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46
Q

bone scans are sensitive for?

A
  • sensitive for malignancies like breaast, lung, prostate cancer
  • less sensitive for detecting tumours with little to no osteoblastic activity (such as multiple myeloma) and for aggressive lesions with rapid bone destruction
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47
Q

management of bone mets - pain relief?

A
  • analgesics - typically optiods and/ or radiotherapy
  • pain specialists may help relieve pain with procedures such as nerve blocks when opioid analgesics are maximized.
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48
Q

management of bone mets - pharmacological?

A
  • Osteoclast inhibitors, such as bisphosphonates and denosumab - RANKL receptor inhibitor
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49
Q

therapeutic options for bone mets?

A
  • Vertebroplasty and kyphoplasty - surgeries
  • RT
  • thermal ablation
  • cryoablation
  • FUS
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50
Q

Pathological fracture?

A
  • Usually in weight bearing bones.
  • Associated with lytic bone metastases.
  • Sudden pain and loss of function.
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51
Q

Management of pathological fractures?

A
  • Analgesia, rest & immobilisation.
  • Management is mainly surgical.
  • Many lesions will require post operative RT.
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52
Q

MSCC - common cancers?

A
  • Breast
  • Prostate
  • Lung
  • Renal
  • Myeloma
  • Lymphoma
  • Melanoma
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53
Q

Pathophys of MSCC

A
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54
Q

CFs of MSCC?

A
  • pain
  • weakness
  • bowel/ bladder
  • sensation loss
  • ataxia
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55
Q

Management of MSCC?

A
  • Analgesia
  • dexamethasone
  • MRI
  • surgery, radiotherapy, chemotherapy
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56
Q

Chemotherapy?

A
  • inhibits cell proliferation and tumour multiplication
  • Affects healthy cells too
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57
Q

hormone therapies - tamoxifen?

A

oestrogen receptor blockage in breast cancer

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58
Q

hormone therapies - aromatase inhibitors?

A

inhibition of androgen -> oestrogen conversion in breast cancer

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59
Q

GnRH

A

Decrease the ovarian production of oestrogen and testicular production of testosterone - breast and prostate cancer

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60
Q

immunotherapies - imatinib?

A
  • targets Bcr-abl
  • in CML
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61
Q

hormone therapies -Erlotinib,gefitinib?

A
  • targets EGFR
  • in NSCLC
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62
Q

iapatinib?

A
  • Her1 and 2 receptor
  • Breast cancer
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63
Q

targeted therapies

A
  • monoclonal antibodies
  • cancer growth blockers
  • drugs that block cancer blood vessel growth
  • PARP inhibitors
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64
Q

decision of cancer treatment?

A

The decision to use a certain anticancer drug depends on many factors, including the type and location of the cancer, its severity, whethersurgeryorradiation therapycan or should be used, and the side effects associated with the drug.

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65
Q

All cytotoxic drugs except ? cause bone marrow suppression

A
  • All cytotoxic drugs except vincristine sulfate and bleomycincause bone-marrow suppression. This commonly occurs 7 to 10 days after administration,
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66
Q

physical effects of chemo?

A
  • pain
  • tiredness
  • insomnia
  • N & V
  • hair loss
  • bladder and bowel issues
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67
Q

psychological effects of chemo?

A
  • mood shifts, depression, anxiety
  • stress and trouble adjusting to the change in routine
  • chemo brain - thinking and memory problems that can happen during and after cancer treatment
  • frustration and anger
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68
Q

pancytopenia?

A
  • Lethargy
  • Weakness
  • Pallor
  • Bruising
  • Bleeding
  • Recurrent infections.
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69
Q

which patients need to be assessed for paralytic ileus?

A
  • patients receiving vinca alkaloids need to be assessed for paralytic ileus which would present with constipation and absence of bowels sounds, ultra sound may be indicated.
  • This is a medical emergency due to the risk of perforation.
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70
Q

what are the vinca alkaloids?

A

vincristine, vinblastine and vinorelbine)

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71
Q

managing constipation in chemotherapy patients?

A
  • maintaining adequate fluid intake
  • maintaining healthy high fibre diet
  • gentle exercise
  • movicol
  • docusate sodium
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72
Q

diarrhoea after chemo Tx?

A
  • linked to 5FU and methotrexate
  • loperamide
  • coedine phosphate
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73
Q

oral thrush Tx?

A
  • Nystatin suspension
  • fluconazole
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74
Q

highly emetic chemo?

A
  • cisplatin and cyclophosphamide
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75
Q

Tx for chemo induced emesis?

A
  • low risk: dexamethasone
  • moderate risk: 5-HT3 antagonist
  • high risk: dexamethsaone, 5-HT3 antagonost, NK1 antagonist e.g. aprepitant
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76
Q

Ix for bone marrow failure?

A
  • FBC
  • peripheral blood film
  • haematinics: B12 and folate
  • reticulocyte count
  • bone profile
  • autoimmune screen
  • serological tests for infections
  • bone marrow biopsy
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77
Q

sepsis recognition?

A
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78
Q

neutropenic sepsis/ febrile neutropenia - emergency that is considered in those with ?

A
  • low neutrophil count plus
  • Temperature ≥ 38°C or
  • Other signs or symptoms consistent with significant sepsis
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79
Q

when should neutropenic sepsis be considered?

A
  • recent chemotherapy - commonly within 7-10 days causes neutropenia through BM suppression
  • considered in any patient at risk of neutropenia who presents unwell, regardless of temperature bc it can present without fever in some patients including older patients and those taking immunosuppressive medications such as steroids
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80
Q

typical non-specific sepsis symptoms?

A
  • Fatigue
  • Feeling warm or cold
  • Rigors or shaking
  • Feeling sweaty or clammy
  • Palpitations
  • Dizziness
  • Subjective confusion or disorientation
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81
Q

General clinical findingsin neutropenic sepsis may include:

A
  • Haemodynamic instability (e.g. hypotension, tachycardia, tachypnoea, hypoxia)
  • Fever
  • Reduced urine output
  • Altered conscious level or confusion
  • Mottled/ashen appearance
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82
Q

sepsis 6 - 3 in?

A
  • O2
  • Ab - piperacillin/tazobactam
  • IV fluids - 500ml of crystalloid over 15 minutes
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83
Q

sepsis 6 - 3 out?

A
  • blood cultures
  • urine output
  • lactate
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84
Q

late impacts of chemotherapy?

A
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85
Q

sleep stages?

A
  • stage 3 - important for restorative sleep
  • REM dreaming sleep is 90 min cycle, 25% of total sleep time
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86
Q

role of NREM sleep?

A

*Restoration and growth
- Immunity to viral infection

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87
Q

role of REM sleep?

A

*Memory Storage and Retention of memory
*Organization and Reorganization
- New Learning

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88
Q

3 types of sleep disorders?

A

1.Obstructive Sleep Apnoea
2.Central Sleep Apnoea
3. Mixed Sleep Apnoea

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89
Q

obst sleep apnoea pathway

A
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90
Q

what happens in OSA?

A
  • narrow upper airway more likely to collapse than a wide upper airway
  • OSA patients have narrow upper airways, which can be due tofat depositionin the pharyngeal wall/tongue, orabnormal skeletal features(such as posterior positioning of the mandible).
  • During sleep,all muscles relax, including the pharyngeal dilator muscles. This increases the risk of upper airway collapse
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91
Q

Collapse of airways in OSA leads to?

A
  • collapse of the upper airway can cause hypoxaemia and hypercapnia
  • This is detected by peripheral chemoreceptors, which stimulate the respiratory control centre in the brainstem and the sympathetic nervous system.
  • This leads toarousal from sleepand activation of the pharyngeal dilator muscles, resulting in airway patency.
  • if sleep resumes after this the upper airway can collapse again - this cycle can repeat
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92
Q

Risk factorsfor obstructive sleep apnoea include:

A
  • Obesity
  • Craniofacial abnormalities (such as posterior positioning of the mandible)
  • Increased soft tissue volume (such as adenotonsillar hypertrophy)
  • Male sex
  • Down’s syndrome
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93
Q

Sx of sleep apnoea?

A
  • Excessive daytime somnolence:
  • Chronic morning headache:
  • Arousal during sleep with choking/gasping: this may be observed by the patient’s bed partner
  • Habitual snoring
  • Restless sleep
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94
Q

excessive daytime sleepiness?

A

this can be quantified using theEpworth sleepiness scale. Patients often wake up feeling unrefreshed.

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95
Q

chronic morning headache?

A

this could be due to hypercapnia-induced cerebral vasodilation

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96
Q

CE in OSA

A
  • Obesity: leads to large neck circumference
  • Craniofacial abnormalities (such as posterior positioning of the mandible)
  • Increased soft tissue volume (such as adenotonsillar hypertrophy)
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97
Q

other imp areas of OSA?

A
  • surgical history - tooth extractions and difficult intubations can lead to craniofacial abns
  • FHx of OSA
  • occupational history: patients with excessive sleepiness for >3 months must inform the DVLA
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98
Q

Ix for OSA?

A
  • polysomnography
  • resp polygraphy
  • overnight pulse oximetru
99
Q

Polysomnography?

A
  • gold standard diagnostic test for OSA
  • involves ppt being monitored in sleep lab overnight
  • monitors brain activity, muscle and respiratiry activity
  • OSA is diagnosed if the apnoea-hypopnoea index (number of apnoeic/hypnoeic events per hour) is ≥15 per hour, or ≥5 per hour if there are OSA symptoms/cardiovascular comorbidities.
100
Q

Respiratory polygraphy?

A
  • can be performed at the patients home
101
Q

overnight pulse oximetry?

A
  • this can also be performed at home and can demonstrate apnoeic episodes overnight.
102
Q

Conservative management of OSA?

A
  • weight loss regimens
  • oral appliances - such as mandibular advancement devices
  • sleeping in the lateral position
103
Q

Ventilatory management of OSA

A
  • CPAP holds airway open during sleep
  • gold standard treatment for severe OSA
104
Q

Medical managemene of OSA?

A
  • Dopamine reuptake inhibitors(such as modafinil and solriamfetol) can reduce somnolence, however, these are rarely used in OSA.
105
Q

Surgical management of OSA?

A
  • upper airway surgery: if CPAP and oral appliances fail
  • bariatic surgery
106
Q

OSA related complications

A
  • CV - hypertension and MI from increases SNS activation and oxidatiev stress
  • diabetes: increased sympathetic nervous system activation inhibits the release of hormones that are involved in glucose metabolism
  • Motor vehicle accidents
107
Q

palliative care =

A
  • relief of a symptom or problem associated with an illness without curing the underlying disease process, and without attempting to prolong life
108
Q

principles of palliative care?

A
  • encompasses patients and their families with advanced ilness
  • should be delivered based on need not prognosiss
  • can be delivered alongside disease directed therapy
109
Q

GPC?

A
  • core aspect of care for all patients and their families with advanced diseases
  • includes:
  • holistic needs assessment and provision of basic symptom control
  • referral to specialist palliative care
110
Q

advanced care plainning?

A

process of discussion between and indiv and their care providers
- facilitates and enables individuals to think abt the care that they would like to receive
- allows them to choose where they want to die

111
Q

Benefits of ACP?

A
  • patient centered
  • prevents over-treatment when the patient lacks capacity
112
Q

EoL care plan:

A

ensures best quality of care during the patients last days

113
Q

Indicator of deterioration?

A

SPICT tool - indicators of deteriation for each disease

114
Q

advanced care planning leads to

115
Q

pericarditis pain profile?

A
  • This is usually a retrosternal chest pain, that is typically relieved by sitting forward.
  • There may be a history of recent viral illness, or myocardial infarction (Dressler’s syndrome).
116
Q

ticagrelor can cause?

A

adenosine related dysponea

117
Q

which drugs can reduce abs of ACEi?

118
Q

risk of rhabo with statins increases when?

A
  • avoid high intensity exercise on statins due to increased risk of muscle breakdown secondary to rhabdomyolysis.
119
Q

Very common adverse effects of bisoprolol ?

A

bradycardia, dizziness and syncope

120
Q

Very common adverse effects of digoxin ?

A

arrhythmias, diarrhoea and skin reactions

121
Q

Very common adverse effects of furosemide?

A

dizziness, electrolyte imbalance and muscle spasms

122
Q

bifurcation of abd aorta?

123
Q

level at which the testicular or ovarian arteries branch off the aorta?

124
Q

branch of the inferior mesenteric artery?

125
Q

t12?

A

aorta passing thru diagphragm

126
Q

monroe kelly doctrine?

A
  • Intra cerebral pressure is governed by Monroe-Kelly Doctrine which considers brain as closed box, changes in pressure are offset by loss of CSF. When this is no longer possible ICP rises
127
Q

aortic regurg examination findings?

A
  • Aortic regurgitation produces an early diastolic, high-pitched, blowing murmur, which is louder on sitting forward and at the left sternal edge.
128
Q

pulse w aortic regurg?

A

collapsing

129
Q

quincke’s sign?

A
  • visible pulsing red colouration of the nails
  • AR
130
Q

AS vs AR?

A
  • Aortic stenosisdoes not cause a diastolic murmur or collapsing pulse. Aortic stenosis more commonly produces an ejection systolic murmur which is louder on expiration.
131
Q

Pulse w AS?

A

Slow rising (collapsing in AR)

132
Q

anatomical snuffbox contains?

A

radial artery - commonly injured by a scaphoid bone fracture

133
Q

? increases risk of statin induced rhabdo?

A

Amiodarone

134
Q

Bivalirudin mechanism?

A

reversible direct thrombin inhibitor

135
Q

occipital lobe and cerebellum BS?

A

posterior cerebral artery and cerebellar arteries (which arise from the basilar and vertebral arteries) respectively.

136
Q

Temporal lobe BS?

137
Q

Ranolazine mechanism?

A
  • Ranolazine inhibits persistent or late sodium current in heart muscle in various voltage-gated sodium channels.
  • This leads to reduced intracellular calcium levels, which subsequently reduces the tension in the heart muscle, lowering its oxygen demand.
138
Q

Most common ECG pattern of PE?

A

sinus tachy

139
Q

how does cardiac tamponade present?

A
  • Beck’s triad’: hypotension, a raised JVP and muffled heart sounds.
  • It may associated with dyspnoea. and tachycardia.
140
Q

IE in an IVDU commonly affects the ? valve

A

tricuspid valve. All valves in the heart are derived from the endocardial cushion.

141
Q

LVEF =

A

= (stroke volume / end diastolic LV volume ) * 100%

142
Q

stroke volume =

A

end diastolic volume - systolic volume

143
Q

T8 =

A

IVC opening in diaphragm

144
Q

T10 ?>

A

Oesophagus opening in diaphragm - Oesophagus has 10 letters

145
Q

T12?

A

Coeliac trunk

146
Q

L1?

147
Q

l5?

A

Internal Iliac artery

148
Q

Vitamin K acts as a cofactor in the carboxylation of clotting factors -

A

1972 - 10, 9, 7, 2 0 - these are affected by warfarin

149
Q

most common cause of liver failure in the UK?

A

Paracetamol overdose

150
Q

when is prev higher than indicence?

A

In chronic disease prevalence is greater than incidence - in acute disease the incidence is greater than the prevalence

151
Q

marfan’s syndrome?

A
  • tall stature, pectus excavatum and joint hypermobility
  • RF for aortic dissection
152
Q

CXR for aortic dissection?

A

widened mediastinum

153
Q

TOE?

A

Transoesophageal echocardiography (TOE) is more suitable for patients with suspected aortic dissection who are unstable and therefore too risky to take to the CT scanner.

154
Q

How can aortic regurg present?

A

dyspnoea, orthopnoea, and paroxysmal nocturnal dyspnoea.

155
Q

risk of aortic dissection inc w

A

rheumatic fever

156
Q

signs of aortic regug?

A

wide pulse pressure (114mg) and nail-bed pulsation (Quincke’s sign).

157
Q

aortic regurg is a ? murmur

A

early diastolic

158
Q

Continuous machine-like murmur?

A

heard with patent ductus arteriosus.

159
Q

EJM?

A

heard with aortic stenosis, pulmonary stenosis, atrial septal defects, tetralogy of Fallot, and hypertrophic obstructive cardiomyopathy.

160
Q

late systolic murmur?

A

heard with mitral valve prolapse and coarctation of the aorta.

161
Q

pansystolic murmur?

A

mitral regurgitation, tricuspid regurgitation, or ventricular septal defect.

162
Q

Diastolic murmur + AF → ?

A

mitral stenosis

163
Q

ECG features of hypokalaemia?

A
  • small or absent T waves (occasionally inversion)
  • prolong PR interval
  • ST depression
  • long QT
  • U waves
164
Q

mneumonic for systolic murmurs?

A

MR ASS mitral regurg, aortic stenosis (systolic murmurs)

165
Q

mneumonic for aortic regurg?

A

aortic regurg, mitral stenosis (diastolic murmurs)

166
Q

feature that indicates DC cardioversion is needed?

A

In the context of a tachyarrhythmia, a systolic BP < 90 mmHg → DC cardioversion

167
Q

Complete heart block following a MI -> ? lesion

A

right coronary artery lesion

168
Q

ACS: ? are contraindicated in hypotension

A

Nitrates are contraindicated in patients with hypotension (< 90 mmHg)

169
Q

Ehlers danlos syndrome?

A

Widespread joint hypermobility along with skin changes indicated by striae should make you think of a collagen disorder - these findings are commonly present in Ehlers-Danlos syndrome.

170
Q

what is assoc a marfan’s?

A

Mitral valve prolapse and mitral regurgitation are associated with Marfan’s and Ehlers-Danlos syndromes. Mitral regurgitation would produce a pansystolic murmur

171
Q

Electrolyte abnormalities which can cause long QT syndrome ?

A

hypokalaemia, hypomagnesemia and hypocalcaemia

172
Q

Pulmonary embolism and renal impairment →

A
  • Pulmonary embolism and renal impairment → V/Q scan is the investigation of choice -
  • CTPA when no renal impairment bc CTPA can cause renal damage
173
Q

lateral MIs are causd by a lesion in the?

174
Q

anterolateral MI?

A

lAD lesion

175
Q

Inferior MI?

A

RCA lesion

176
Q

What should be done for bradcyardia and shock?

A

Patients with bradycardia and signs of shock require 500micrograms of atropine (repeated up to max 3mg) - cardioversion is not used for bradycardias but pacing can be used

177
Q

features of aortic dissection?

A
  • It usually presents with abrupt, severe pain; and is often described as sharp, as opposed to tight/crushing pain experienced in myocardial infarction.
  • Hypertension and aortic valve pathologies are also risk factors for aortic dissection.
  • Patients often present with acute hypotension, due to aortic regurgitation or cardiac tamponade.
178
Q

what can be seen with the cardiac symptoms that would make you need to rule out aortic dissection?

A
  • neurological changes
179
Q

neuro signs of AD can be?

A
  • Focal neurological deficits occur due to propagation of the intimal tear to branch arteries, or due to mass effects as the expanding aorta compresses surrounding structures.
  • can be with symptoms of Horner’s syndrome (classically ptosis, miosis and anhidrosis) due to compression of the sympathetic trunk by the expanding aortic dissection.
180
Q

most specific ECG finding in acute pericarditis ?

A

PR depression

181
Q

what should never be taken concurrently?

A

Verapamil and beta-blockers should never be taken concurrently - possibility of heart block and fatal arrest

182
Q

Rupture of the papillary muscle due to a myocardial infarction →

A

acute mitral regurgitation → widespread systolic murmur, hypotension, pulmonary oedema

183
Q

HTN in diabetes?

A
  • HTN with Diabetes without renal vascular disease: rampiril
  • diabetes w renal vascular disease: amlodepine - ACE/ARB CI
184
Q

loop diuretics are assoc w ?

A
  • electrolyte disturbances such as hypokalemia, hyponatremia, and hypomagnesemia
  • Also hypocalcaemia -> osteoporosis
  • e.g bumetanide
185
Q

causes of torsades?

A

Hypocalcaemia, hypokalemia, hypomagnesaemia, hypothermia

186
Q

motor + cardiac symptoms ->

A

dissection

187
Q

If new BP >= 180/120 mmHg + no worrying signs then the first step is ?

A

urgent investigations for end-organ damage

188
Q

rare but serious side effect of ACEi?

A
  • angioedema
  • characterised by marked tongue and facial swelling
  • can occur at any time during treatment, even weeks or months after initiation.
189
Q

most common association for aortic dissection?

190
Q

Asthmatic features/features suggesting steroid responsiveness in COPD:

A
  • previous diagnosis of asthma or atopy
  • a higher blood eosinophil count
  • substantial variation in FEV1 over time (at least 400 ml)
  • substantial diurnal variation in peak expiratory flow (at least 20%)
191
Q

30-40 year old with basal emphysema and abnormal LFTs → ?

A

alpha-1 antitrypsin

192
Q

What most commonly causes a cavitating pneumonia in the upper lobes?

A

Klebsiella most commonly causes a cavitating pneumonia in the upper lobes, mainly in diabetics and alcoholics

193
Q

hypertrophic obstructive cardiomyopathy is the leading cause of?

A

sudden cardiac death in young atheles, common cause of sudden death - ventricular arrythmias

194
Q

HOCM genetics?

A

Usually due to a mutation in the gene encoding β-myosin heavy chain protein

195
Q

Arrhythmogenic right ventricular dysplasia?

A
  • epsilon wave - terminal notch in QRS
  • ECG abnormalities in V1-3, typically T wave inversion
196
Q

what happens in arrhythmogenic right ventricular dysplasia?

A
  • right V myocardium replaced by fatty tossie
197
Q

causes of dilated cardiomyopathy?

A
  • alc
  • coxsackie B
  • doxorubicin
198
Q

Classical causes of restrictive cardiomyopathy?

A
  • amyloidosis
  • post radiotherapy
199
Q

Takotsubo cardiomyopathy?

A
  • stress induced
  • transient apical ballooning of myocardium
200
Q

infective cardiomyopathy?

A

chagas disease, coxsackie B virus

201
Q

Toxicity cardiomyopathy??

A

doxorubicin, alcoholic cardiomyopathy

202
Q

HOCM CF?

A
  • externtional dyspnoea - most cpmmon
  • angina
  • syncope
  • palpitations
  • HF
203
Q

Murmur in HCOM?

A
  • Harsh ejection systolic
  • heard best at left lower sternal border
  • typically increases with Valsalva manoeuvre and decreases with squatting or handgrip.
204
Q

pulse in HCOM?

A

Bifid carotid pulse: A rapid upstroke followed by a mid-systolic dip may be observed, known as the ‘spike and dome’ pulse

205
Q

dilated cardiomyopathy?

A
  • most common cardiomyopathy
  • mostly idopathic
206
Q

pathophys of DCM?

A
  • dilated heart leading to predominately systolic dysfunction
  • all 4 chambers are dilated, but the left ventricle more so than right ventricle
  • eccentric hypertrophy (sarcomeres added in series) is seen
207
Q

Features of dilated CM?

A
  • Classical features of HF
  • systolic murmurs - mitral and tricuspid regurg
  • S3
  • balloon app of heart on CXR
208
Q

Which scale is used to characterise murmurs?

A
  • Grade 1: very quiet, heard by experts
  • Grade 2: slight murmur, should be heard by most examiners
  • Grade 3: moderate, easily heard, no palpable thrill
  • Grade 4: loud, palpable thrill
  • Grade 5: very loud, palpable thrill
  • Grade 6: can be heard without a stethoscope
  • It is very rare for a diastolic murmur to be grade 5 or above and as such, they are typically graded 1-4

Levine Scale.

209
Q

HCOM mumur?

A
  • ejection systolic
  • best heard at the lower left sternal edge
  • best heard at the apex and may radiate to the axilla
210
Q

Aetiology of MR?

A
  • IE
  • degenerative
  • Rheumatic heart disease
211
Q

Symptoms of acute MR?

A
  • Rapid development of HF, flash pulm oedema
212
Q

Symptoms of chronic MR?

A
  • Dyspnoea, orthopnea
213
Q

Additional signs of MR?

A
  • Soft S1
  • S3
  • mid-systolic click
214
Q

Causes of primary TR?

A
  • Rheumatic hd
  • Carcinoid syndrome
    = IE
215
Q

Causes of secondary TR?

A
  • Pulm HTN
  • dilation of RV
216
Q

Additional signs of TR?

A
  • Prominent, pulsatile JVP
  • Large cv wave in JVP
  • S3/S4
  • Liver may be enlarged and pulsatile
217
Q

where is AS heard

A

aortic area and left sternal edge

218
Q

where is PS heard?

219
Q

Where is HOCM heard?

A
  • lower left sternal edge
  • apex
220
Q

Where is MR heard?

221
Q

Where is tricuspid regurg heard?

A

lower left sternal edge

222
Q

Where is VSD heard?

A

left sternal edge

223
Q

What are the ejection systolic murmurs ?

A

AS, PS, HCOM

224
Q

which is a mid-late systolic murmur?

225
Q

what are the pansystolic/ holosytolic murmurs?

A
  • trisucpid regurg
  • mitral regurg
  • VSD
226
Q

mitral vs triscuspid regurg?

A
  • Mitral: accenuated on exp: ME
  • Trucspid: inspiration

TIME

227
Q

aetiology of acute AR?

A
  • IE
  • arotic dissection
  • acute rheumatic fever
228
Q

Aetiology of chronic AR?

A
  • Rheumatic HD
  • biscispid aortic valve
229
Q

which murmur is best heard on on expiration with the patient leaning forward, at the left sternal edge, fourth intercostal space.

A

aortic regurg

230
Q

low-pitched mid-diastolic rumble?

231
Q

Best heard: at the apex with breath held in expiration, with the patient lying on their left side. It is best heard with the bell of the stethoscope.

A

Mitral stenosis

232
Q

Signs of MS?

A
  • Mitral facies
  • Pulm HTN
  • RHF
233
Q

RHF signs?

A
  • Raised JVP
  • Peripheral oedema
  • Hepatomegaly
234
Q

early diastolic murmurs>?

A
  • aortic regurg
  • pulm regurg
  • these are decresndo murmurs
235
Q

what are the mid diastolic murmurs?

A
  • MS
  • tricisid stenosis
236
Q

Aortic regurg accenuation?

A
  • heard in the left sternal edge, 4th ics
  • Exp, leaning forward
237
Q

Pulm regurg is heard?

A
  • pulm area
  • inspiration
238
Q

Mitral stenosis heard?

A
  • expiration, lying on left side
  • apex
239
Q

Tricuspid stenosis is heard?

A
  • insp
  • keft sternal edge
240
Q

myocarditis pres?

A

Myocarditis presents with ST elevation and acute pulmonary oedema in a young patient with a recent flu-like illness

241
Q

Ix for angina

A
  • 1st line: CT coronary angiography
  • 2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)
  • 3rd line: invasive coronary angiography
242
Q

Angina - Examples of non-invasive functional imaging:

A
  • myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
    stress echocardiography or
  • first-pass contrast-enhanced magnetic resonance (MR) perfusion or MR imaging for stress-induced wall motion abnormalities
243
Q

macrolides can cause…

244
Q

broad complex tachy after an MI

A
  • Broad complex tachycardia following a myocardial infarction is almost always due to ventricular tachycardia.

Year 3 (45 decks)

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