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
which drugs can cause arrhytmias?
Taxanes and Anthracylines can cause arrhythmias
26
features of bone mets?
* pain * pathological fractures * hypercalcaemua * SCC
27
mechanism of bone mets?
* activated osteoblasts stimulate production of RANK which activates osteoclasts * osteoclasts resorb bone -> osteolysis -> release of growth factors for tumour growth
28
blastic vs lytic bone mets?
* 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.
29
aggressive mets tend to be?
lytic
30
which mets show a slower course?
sclerotic (osteoblastic) metastases generally indicate a slower course
31
3 most common sites of metastasis?
- lungs - liver - bone
32
which cancers metastasise to bone?
* Among solid cancers, breast, prostate, lung, thyroid, and kidney cancer account for 80% of all skeletal metastases.
33
bone mets commonly present at the time of diagnosis of?
multiple myeloma
34
clinical presntation of bone mets?
* 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
35
which type of bone mets cause more hypercalcaemia?
osteolytic
36
bone mets - pain?
* 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.
37
sudden severe painw ith bone mets?
* 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.
38
predominantly osteoblastic mets - cancers?
* SCLC * Hodgkin lymphoma * prostate * carcinoid
39
predom osteolytic bone mets?
* renal cell * MM * melanoma * NSCLC * NHL
40
mixed osteoblastic and osteolytic ?
* breast cancer * GI cancers
41
XR for bone mets?
* initial screen to evaluate symptomatic areas * poor sensitivity (TP rate) so generally not used to screen for bone mets
42
CT for bone mets?
* 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
43
MRI for bone mets?
* 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
44
MRI -?
* sensitive to movement * ppts with implantable devices not able to undergo * severe claustophobia
45
bone scans?
* 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.
46
bone scans are sensitive for?
* 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
47
management of bone mets - pain relief?
* analgesics - typically optiods and/ or radiotherapy * pain specialists may help relieve pain with procedures such as nerve blocks when opioid analgesics are maximized.
48
management of bone mets - pharmacological?
* Osteoclast inhibitors, such as bisphosphonates and denosumab - RANKL receptor inhibitor
49
therapeutic options for bone mets?
- Vertebroplasty and kyphoplasty - surgeries - RT - thermal ablation - cryoablation - FUS
50
Pathological fracture?
* Usually in weight bearing bones. * Associated with lytic bone metastases. * Sudden pain and loss of function.
51
Management of pathological fractures?
* Analgesia, rest & immobilisation. * Management is mainly surgical. * Many lesions will require post operative RT.
52
MSCC - common cancers?
* Breast * Prostate * Lung * Renal * Myeloma * Lymphoma * Melanoma
53
Pathophys of MSCC
54
CFs of MSCC?
* pain * weakness * bowel/ bladder * sensation loss * ataxia
55
Management of MSCC?
* Analgesia * dexamethasone * MRI * surgery, radiotherapy, chemotherapy
56
Chemotherapy?
* inhibits cell proliferation and tumour multiplication * Affects healthy cells too
57
hormone therapies - tamoxifen?
oestrogen receptor blockage in breast cancer
58
hormone therapies - aromatase inhibitors?
inhibition of androgen -> oestrogen conversion in breast cancer
59
GnRH
Decrease the ovarian production of oestrogen and testicular production of testosterone - breast and prostate cancer
60
immunotherapies - imatinib?
* targets Bcr-abl * in CML
61
hormone therapies -Erlotinib,gefitinib?
* targets EGFR * in NSCLC
62
iapatinib?
- Her1 and 2 receptor - Breast cancer
63
targeted therapies
* monoclonal antibodies * cancer growth blockers * drugs that block cancer blood vessel growth * PARP inhibitors
64
decision of cancer treatment?
The decision to use a certain anticancer drug depends on many factors, including the type and location of the cancer, its severity, whether surgery or radiation therapy can or should be used, and the side effects associated with the drug.
65
All cytotoxic drugs except ? cause bone marrow suppression
- All cytotoxic drugs except vincristine sulfate and bleomycin cause bone-marrow suppression. This commonly occurs 7 to 10 days after administration,
66
physical effects of chemo?
* pain * tiredness * insomnia * N & V * hair loss * bladder and bowel issues
67
psychological effects of chemo?
* 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
68
pancytopenia?
* Lethargy * Weakness * Pallor * Bruising * Bleeding * Recurrent infections.
69
which patients need to be assessed for paralytic ileus?
* 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.
70
what are the vinca alkaloids?
vincristine, vinblastine and vinorelbine)
71
managing constipation in chemotherapy patients?
* maintaining adequate fluid intake * maintaining healthy high fibre diet * gentle exercise * movicol * docusate sodium
72
diarrhoea after chemo Tx?
* linked to 5FU and methotrexate * loperamide * coedine phosphate
73
oral thrush Tx?
* Nystatin suspension * fluconazole
74
highly emetic chemo?
* cisplatin and cyclophosphamide
75
Tx for chemo induced emesis?
* low risk: dexamethasone * moderate risk: 5-HT3 antagonist * high risk: dexamethsaone, 5-HT3 antagonost, NK1 antagonist e.g. aprepitant
76
Ix for bone marrow failure?
* FBC * peripheral blood film * haematinics: B12 and folate * reticulocyte count * bone profile * autoimmune screen * serological tests for infections * bone marrow biopsy
77
sepsis recognition?
78
neutropenic sepsis/ febrile neutropenia - emergency that is considered in those with ?
* low neutrophil count plus * Temperature ≥ 38°C or * Other signs or symptoms consistent with significant sepsis
79
when should neutropenic sepsis be considered?
* 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
80
typical non-specific sepsis symptoms?
* Fatigue * Feeling warm or cold * Rigors or shaking * Feeling sweaty or clammy * Palpitations * Dizziness * Subjective confusion or disorientation
81
General clinical findings in neutropenic sepsis may include:
* Haemodynamic instability (e.g. hypotension, tachycardia, tachypnoea, hypoxia) * Fever * Reduced urine output * Altered conscious level or confusion * Mottled/ashen appearance
82
sepsis 6 - 3 in?
* O2 * Ab - piperacillin/tazobactam * IV fluids - 500ml of crystalloid over 15 minutes
83
sepsis 6 - 3 out?
* blood cultures * urine output * lactate
84
late impacts of chemotherapy?
85
sleep stages?
* stage 3 - important for restorative sleep * REM dreaming sleep is 90 min cycle, 25% of total sleep time
86
role of NREM sleep?
*Restoration and growth - Immunity to viral infection
87
role of REM sleep?
*Memory Storage and Retention of memory *Organization and Reorganization - New Learning
88
3 types of sleep disorders?
1.Obstructive Sleep Apnoea 2.Central Sleep Apnoea 3. Mixed Sleep Apnoea
89
obst sleep apnoea pathway
90
what happens in OSA?
* narrow upper airway more likely to collapse than a wide upper airway * OSA patients have narrow upper airways, which can be due to fat deposition in the pharyngeal wall/tongue, or abnormal 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
91
Collapse of airways in OSA leads to?
* 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 to arousal from sleep and 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
92
Risk factors for obstructive sleep apnoea include:
* Obesity * Craniofacial abnormalities (such as posterior positioning of the mandible) * Increased soft tissue volume (such as adenotonsillar hypertrophy) * Male sex * Down’s syndrome
93
Sx of sleep apnoea?
* 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
94
excessive daytime sleepiness?
this can be quantified using the Epworth sleepiness scale. Patients often wake up feeling unrefreshed.
95
chronic morning headache?
this could be due to hypercapnia-induced cerebral vasodilation
96
CE in OSA
* Obesity: leads to large neck circumference * Craniofacial abnormalities (such as posterior positioning of the mandible) * Increased soft tissue volume (such as adenotonsillar hypertrophy)
97
other imp areas of OSA?
* 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
98
Ix for OSA?
- polysomnography - resp polygraphy - overnight pulse oximetru
99
Polysomnography?
* 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
Respiratory polygraphy?
* can be performed at the patients home
101
overnight pulse oximetry?
* this can also be performed at home and can demonstrate apnoeic episodes overnight.
102
Conservative management of OSA?
* weight loss regimens * oral appliances - such as mandibular advancement devices * sleeping in the lateral position
103
Ventilatory management of OSA
* CPAP holds airway open during sleep * gold standard treatment for severe OSA
104
Medical managemene of OSA?
* Dopamine reuptake inhibitors (such as modafinil and solriamfetol) can reduce somnolence, however, these are rarely used in OSA.
105
Surgical management of OSA?
* upper airway surgery: if CPAP and oral appliances fail * bariatic surgery
106
OSA related complications
* 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
palliative care =
* relief of a symptom or problem associated with an illness without curing the underlying disease process, and without attempting to prolong life
108
principles of palliative care?
* encompasses patients and their families with advanced ilness * should be delivered based on need not prognosiss * can be delivered alongside disease directed therapy
109
GPC?
* 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
advanced care plainning?
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
Benefits of ACP?
* patient centered * prevents over-treatment when the patient lacks capacity
112
EoL care plan:
ensures best quality of care during the patients last days
113
Indicator of deterioration?
SPICT tool - indicators of deteriation for each disease
114
advanced care planning leads to
115
pericarditis pain profile?
- 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
ticagrelor can cause?
adenosine related dysponea
117
which drugs can reduce abs of ACEi?
antacids
118
risk of rhabo with statins increases when?
* avoid high intensity exercise on statins due to increased risk of muscle breakdown secondary to rhabdomyolysis.
119
Very common adverse effects of bisoprolol ?
bradycardia, dizziness and syncope
120
Very common adverse effects of digoxin ?
arrhythmias, diarrhoea and skin reactions
121
Very common adverse effects of furosemide?
dizziness, electrolyte imbalance and muscle spasms
122
bifurcation of abd aorta?
L4
123
level at which the testicular or ovarian arteries branch off the aorta?
L2
124
branch of the inferior mesenteric artery?
l3
125
t12?
aorta passing thru diagphragm
126
monroe kelly doctrine?
* 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
aortic regurg examination findings?
* Aortic regurgitation produces an early diastolic, high-pitched, blowing murmur, which is louder on sitting forward and at the left sternal edge.
128
pulse w aortic regurg?
collapsing
129
quincke's sign?
- visible pulsing red colouration of the nails - AR
130
AS vs AR?
* Aortic stenosis does not cause a diastolic murmur or collapsing pulse. Aortic stenosis more commonly produces an ejection systolic murmur which is louder on expiration.
131
Pulse w AS?
Slow rising (collapsing in AR)
132
anatomical snuffbox contains?
radial artery - commonly injured by a scaphoid bone fracture
133
? increases risk of statin induced rhabdo?
Amiodarone
134
Bivalirudin mechanism?
reversible direct thrombin inhibitor
135
occipital lobe and cerebellum BS?
posterior cerebral artery and cerebellar arteries (which arise from the basilar and vertebral arteries) respectively.
136
Temporal lobe BS?
MCA
137
Ranolazine mechanism?
* 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
Most common ECG pattern of PE?
sinus tachy
139
how does cardiac tamponade present?
- Beck's triad': hypotension, a raised JVP and muffled heart sounds. - It may associated with dyspnoea. and tachycardia.
140
IE in an IVDU commonly affects the ? valve
tricuspid valve. All valves in the heart are derived from the endocardial cushion.
141
LVEF =
= (stroke volume / end diastolic LV volume ) * 100%
142
stroke volume =
end diastolic volume - systolic volume
143
T8 =
IVC opening in diaphragm
144
T10 ?>
Oesophagus opening in diaphragm - Oesophagus has 10 letters
145
T12?
Coeliac trunk
146
L1?
sma
147
l5?
Internal Iliac artery
148
Vitamin K acts as a cofactor in the carboxylation of clotting factors -
1972 - 10, 9, 7, 2 0 - these are affected by warfarin
149
most common cause of liver failure in the UK?
Paracetamol overdose
150
when is prev higher than indicence?
In chronic disease prevalence is greater than incidence - in acute disease the incidence is greater than the prevalence
151
marfan's syndrome?
- tall stature, pectus excavatum and joint hypermobility - RF for aortic dissection
152
CXR for aortic dissection?
widened mediastinum
153
TOE?
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
How can aortic regurg present?
dyspnoea, orthopnoea, and paroxysmal nocturnal dyspnoea.
155
risk of aortic dissection inc w
rheumatic fever
156
signs of aortic regug?
wide pulse pressure (114mg) and nail-bed pulsation (Quincke's sign).
157
aortic regurg is a ? murmur
early diastolic
158
Continuous machine-like murmur ?
heard with patent ductus arteriosus.
159
EJM?
heard with aortic stenosis, pulmonary stenosis, atrial septal defects, tetralogy of Fallot, and hypertrophic obstructive cardiomyopathy.
160
late systolic murmur?
heard with mitral valve prolapse and coarctation of the aorta.
161
pansystolic murmur?
mitral regurgitation, tricuspid regurgitation, or ventricular septal defect.
162
Diastolic murmur + AF → ?
mitral stenosis
163
ECG features of hypokalaemia?
* small or absent T waves (occasionally inversion) * prolong PR interval * ST depression * long QT * U waves
164
mneumonic for systolic murmurs?
MR ASS mitral regurg, aortic stenosis (systolic murmurs)
165
mneumonic for aortic regurg?
aortic regurg, mitral stenosis (diastolic murmurs)
166
feature that indicates DC cardioversion is needed?
In the context of a tachyarrhythmia, a systolic BP < 90 mmHg → DC cardioversion
167
Complete heart block following a MI -> ? lesion
right coronary artery lesion
168
ACS: ? are contraindicated in hypotension
Nitrates are contraindicated in patients with hypotension (< 90 mmHg)
169
Ehlers danlos syndrome?
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
what is assoc a marfan's?
Mitral valve prolapse and mitral regurgitation are associated with Marfan's and Ehlers-Danlos syndromes. Mitral regurgitation would produce a pansystolic murmur
171
Electrolyte abnormalities which can cause long QT syndrome ?
hypokalaemia, hypomagnesemia and hypocalcaemia
172
Pulmonary embolism and renal impairment →
- 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
lateral MIs are causd by a lesion in the?
LC artery
174
anterolateral MI?
lAD lesion
175
Inferior MI?
RCA lesion
176
What should be done for bradcyardia and shock?
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
features of aortic dissection?
- 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
what can be seen with the cardiac symptoms that would make you need to rule out aortic dissection?
- neurological changes
179
neuro signs of AD can be?
- 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
most specific ECG finding in acute pericarditis ?
PR depression
181
what should never be taken concurrently?
Verapamil and beta-blockers should never be taken concurrently - possibility of heart block and fatal arrest
182
Rupture of the papillary muscle due to a myocardial infarction →
acute mitral regurgitation → widespread systolic murmur, hypotension, pulmonary oedema
183
HTN in diabetes?
- HTN with Diabetes without renal vascular disease: rampiril - diabetes w renal vascular disease: amlodepine - ACE/ARB CI
184
loop diuretics are assoc w ?
- electrolyte disturbances such as hypokalemia, hyponatremia, and hypomagnesemia - Also hypocalcaemia -> osteoporosis - e.g bumetanide
185
causes of torsades?
Hypocalcaemia, hypokalemia, hypomagnesaemia, hypothermia
186
motor + cardiac symptoms ->
dissection
187
If new BP >= 180/120 mmHg + no worrying signs then the first step is ?
urgent investigations for end-organ damage
188
rare but serious side effect of ACEi?
- angioedema - characterised by marked tongue and facial swelling - can occur at any time during treatment, even weeks or months after initiation.
189
most common association for aortic dissection?
HTN
190
Asthmatic features/features suggesting steroid responsiveness in COPD:
* 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
30-40 year old with basal emphysema and abnormal LFTs → ?
alpha-1 antitrypsin
192
What most commonly causes a cavitating pneumonia in the upper lobes?
Klebsiella most commonly causes a cavitating pneumonia in the upper lobes, mainly in diabetics and alcoholics
193
hypertrophic obstructive cardiomyopathy is the leading cause of?
sudden cardiac death in young atheles, common cause of sudden death - ventricular arrythmias
194
HOCM genetics?
Usually due to a mutation in the gene encoding β-myosin heavy chain protein
195
Arrhythmogenic right ventricular dysplasia?
- epsilon wave - terminal notch in QRS - ECG abnormalities in V1-3, typically T wave inversion
196
what happens in arrhythmogenic right ventricular dysplasia?
- right V myocardium replaced by fatty tossie
197
causes of dilated cardiomyopathy?
- alc - coxsackie B - doxorubicin
198
Classical causes of restrictive cardiomyopathy?
- amyloidosis - post radiotherapy
199
Takotsubo cardiomyopathy?
- stress induced - transient apical ballooning of myocardium
200
infective cardiomyopathy?
chagas disease, coxsackie B virus
201
Toxicity cardiomyopathy??
doxorubicin, alcoholic cardiomyopathy
202
HOCM CF?
- externtional dyspnoea - most cpmmon - angina - syncope - palpitations - HF
203
Murmur in HCOM?
- Harsh ejection systolic - heard best at left lower sternal border - typically increases with Valsalva manoeuvre and decreases with squatting or handgrip.
204
pulse in HCOM?
Bifid carotid pulse: A rapid upstroke followed by a mid-systolic dip may be observed, known as the 'spike and dome' pulse
205
dilated cardiomyopathy?
- most common cardiomyopathy - mostly idopathic
206
pathophys of DCM?
- 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
Features of dilated CM?
- Classical features of HF - systolic murmurs - mitral and tricuspid regurg - S3 - balloon app of heart on CXR
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Which scale is used to characterise murmurs?
- 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***.
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HCOM mumur?
- ejection systolic - best heard at the lower left sternal edge - best heard at the apex and may radiate to the axilla
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Aetiology of MR?
- IE - degenerative - Rheumatic heart disease
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Symptoms of acute MR?
- Rapid development of HF, flash pulm oedema
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Symptoms of chronic MR?
- Dyspnoea, orthopnea
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Additional signs of MR?
- Soft S1 - S3 - mid-systolic click
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Causes of primary TR?
- Rheumatic hd - Carcinoid syndrome = IE
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Causes of secondary TR?
- Pulm HTN - dilation of RV
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Additional signs of TR?
- Prominent, pulsatile JVP - Large cv wave in JVP - S3/S4 - Liver may be enlarged and pulsatile
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where is AS heard
aortic area and left sternal edge
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where is PS heard?
pulm area
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Where is HOCM heard?
- lower left sternal edge - apex
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Where is MR heard?
Apex
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Where is tricuspid regurg heard?
lower left sternal edge
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Where is VSD heard?
left sternal edge
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What are the ejection systolic murmurs ?
AS, PS, HCOM
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which is a mid-late systolic murmur?
HCOM
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what are the pansystolic/ holosytolic murmurs?
- trisucpid regurg - mitral regurg - VSD
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mitral vs triscuspid regurg?
- Mitral: accenuated on exp: ME - Trucspid: inspiration TIME
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aetiology of acute AR?
- IE - arotic dissection - acute rheumatic fever
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Aetiology of chronic AR?
- Rheumatic HD - biscispid aortic valve
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which murmur is best heard on on expiration with the patient leaning forward, at the left sternal edge, fourth intercostal space.
aortic regurg
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low-pitched mid-diastolic rumble?
MS
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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.
Mitral stenosis
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Signs of MS?
- Mitral facies - Pulm HTN - RHF
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RHF signs?
- Raised JVP - Peripheral oedema - Hepatomegaly
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early diastolic murmurs>?
- aortic regurg - pulm regurg - these are decresndo murmurs
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what are the mid diastolic murmurs?
- MS - tricisid stenosis
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Aortic regurg accenuation?
- heard in the left sternal edge, 4th ics - Exp, leaning forward
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Pulm regurg is heard?
- pulm area - inspiration
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Mitral stenosis heard?
- expiration, lying on left side - apex
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Tricuspid stenosis is heard?
- insp - keft sternal edge
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myocarditis pres?
Myocarditis presents with ST elevation and acute pulmonary oedema in a young patient with a recent flu-like illness
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Ix for angina
* 1st line: CT coronary angiography * 2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia) * 3rd line: invasive coronary angiography
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Angina - Examples of non-invasive functional imaging:
- 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
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macrolides can cause...
torsades
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broad complex tachy after an MI
- Broad complex tachycardia following a myocardial infarction is almost always due to ventricular tachycardia.