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YEAR 4 > CCC > Flashcards

CCC Flashcards

1
Q

What are the causative factors associated with cancer?

A

1) Inherited conditions
2) Chemicals
3) Radioactivity
4) Diet
5) Drugs
6) Infective
7) Immune deficiencies

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2
Q

What are examples of inherited conditions that can cause cancer?

A
  • Neurofibromatosis
  • Adenomatous polyposis coli
  • Familial breast cancer
  • von Hippel Landau syndrome
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3
Q

What are examples of chemicals that can cause cancer?

A
  • CIGARETTE SMOKE -p53 tumour suppressor gene
  • AROMATIC AMINES- associated with bladder cancer
  • BENZENE- leukaemia
  • WOOD DUST- nasal adenocarcinoma
  • VINYL CHLORIDE- angiosarcomas
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4
Q

What are examples of radioactive causes of cancer?

A
  • high energy radiation (photons or electrons)

- high level of exposure to radioactive isotope

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5
Q

What are examples of dietary causes of cancer?

A
  • low fibre diets (colorectal cancer)
  • smoked food (gastric carcinoma)
  • nitrosamines
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6
Q

What are examples of the ways that drugs can cause cancer?

A
  • cytotoxic drugs induce DNA damage and are associated with increased risk of malignancy
  • topoisomerase inhibitors can induce characteristic translocations
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7
Q

What are examples of infective causes of cancer?

A

1) HPV (cervical and anal cancers)
2) Epstein Barr Virus (non-hodgkins lymphoma)
3) Hepatitis B virus (hepatocellular cancer)
4) Retrovirus (T-cell lymphomas)
5) Helicobacter pylori (MALT tumours)

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8
Q

What are the common presenting complaints of those with cancer?

A
  • LUMPS
  • BLEEDING
  • PAIN
  • CHANGE IN FUNCTION
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9
Q

What are some examples of lumps in a cancer patient?

A
  • breast lumps
  • changes in moles
  • nodes, nodules and MSK lumps
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10
Q

What are the types of bleeding in a cancer patient?

A
  • haemoptysis
  • rectal bleeding
  • haematuria
  • post-menstrual or intermittent bleeding
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11
Q

What are the typical types of pain in a cancer patient?

A
  • chest pain
  • abdominal pain
  • bone pain
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12
Q

What are examples of ‘change in function’ for a patient with a history of cancer?

A
  • change in bowel habit
  • new cough
  • dyspnoea
  • weight loss
  • fever
  • acute confusional state
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13
Q

How is cancer diagnosis made?

A

CONFIRMED HISTOLOGICALLY

- By biopsy of a superficial mass or lymph node or by endoscopic techniques in the lung or GI tract.

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14
Q

What is the most common way in which cancers are staged?

A

TNM

  • tumour
  • node
  • metastasis
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15
Q

What are the parameters for the T section of cancer staging?

A

T: PRIMARY TUMOUR

TX- primary tumour cannot be assessed
T0- No evidence of primary tumour
Tis- Carcinoma in situ
T1,2,3,4- Increasing size and/or local extent of the primary tumour

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16
Q

What are the parameters for the N section of cancer staging?

A

N: REGIONAL LYMPH NODE

NX- regional lymph nodes cannot be assessed
N0- No regional lymph node metastasis
N1,2,3- Increasing involvement of regional lymph nodes

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17
Q

What are the parameters for the M section of cancer staging?

A

M: DISTANT/ORGAN METASTASIS

MX: presence of distant metastasis cannot be assessed
M0: no distant metastasis
M1: distant metastasis

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18
Q

What are the definitions of cancer grading?

A

GX: grade of differentiation cannot be assessed
G1: well differentiated: similarities remain to normal tissue of the organ of origin
G2: moderately differentiated
G3: poorly differentiated: bizarre cells

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19
Q

What role does imaging play in the staging of cancers?

A
  • CT is the standard imaging tool for the evaluation of chest and abdominal malignancies.
  • MRI is used for imaging bone and soft tissue lesions, and regions where bone causes artifact in the CT appearances e.g. pelvis/posterior fossa of the brain.
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20
Q

What is the process for assessing response to cancer treatment ?

A

CT and MRI accurately measure changes in tumour dimensions.

The RECIST system is a standardized way to classify the response of disease to treatment

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21
Q

What is the RECIST classification system?

A

1) COMPLETE RESPONSE (CR)- no disease detectable radiologically
2) PARTIAL RESPONSE (PR)- all lesions have shrunk by >30% but disease still present
3) STABLE DISEASE (SD)- <20% increase in size or <30% decrease in size
4) PROGRESSIVE DISEASE (PD)- new lesions or lesions increased by >20%

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22
Q

Use of imaging in cancer screening:

A
  • Screening mammography to detect breast cancer is well established
  • Other radiological screening examination has not proven effective
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23
Q

What is the purpose of contrast in CT?

A
  • to demonstrate intra-luminal pathology or bowel obstruction
  • delineate vascular structures
  • demonstrate tumour enhancement
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24
Q

What is the main indication for MRI in cancer imaging?

A
  • neurospinal tumours
  • rectal tumours
  • prostate tumours
  • MSK tumours
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25
Q

What is contraindicated for MRI use?

A
  • Pacemakers and implantable cardiac defibrillators

- Foreign bodies in the eye or brain (vascular clips, surgical staples, metallic shards)

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26
Q

In what way is ultrasound used for the detection of cancer?

A
  • Duplex and Doppler ultrasound are used to assess tumour blood flow
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27
Q

What are alternative methods of imaging for cancer?

A
  • Nuclear medicine

- PET scanning

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28
Q

What are the various classes of tumour markers?

A
  • CELL-SURFACE GLYCOPROTEINS
  • ONCOFETAL PROTEINS
  • ENZYMES
  • INTERMEDIATE METABOLITES
  • HORMONES
  • IMMUNOGLOBULINS
  • NUCLEIC ACIDS
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29
Q

What are examples of cell surface glycoproteins?

A
  • Carcino-embryonic antigen (CEA)
  • CA125
  • CA19.9
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30
Q

What are examples of oncofetal proteins?

A
  • human chorionic gonadotrophin (hCG)

- alpha feto protein (aFP)

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31
Q

What are examples of enzymes as tumour markers?

A
  • acid phosphatase
  • alkaline phosphatase
  • lactate dehydrogenase
  • neuronespecific enolase
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32
Q

What are examples of intermediate metabolites as tumour markers?

A
  • 5-hydroxyindoeacetic acid

- vanillyl mandelic acid

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33
Q

What are examples of hormones as tumour markers?

A
  • thyroglobulin
  • antidiuretic hormone
  • adrenocorticotrophic hormone
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34
Q

What are examples of immunoglobulins as tumour markers?

A
  • Bence Jones Protein

- Light chains

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35
Q

What are examples of nucleic acids as tumour markers?

A
  • tumour specific DNA/RNA

- tissue specific DNA/RNA

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36
Q

What is the common clinical use of CEA?

A

Marker for colorectal carcinoma

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37
Q

What is the common clinical use of CA125?

A

Marker for ovarian carcinoma

also raised in pancreatic, lung, colorectal and breast cancer

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38
Q

What is the common clinical use of alpha fetoprotein (aFP)?

A

Marker for hepatocellular carcinoma and teratoma

high levels predict a poor prognosis in malignancy

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39
Q

What is the oncological clinical use of HCG?

A

Marker for gestational trophoblastic disease (hydatiform mole, choriocarcinoma)

obvs raised in pregnancy too

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40
Q

What is the clinical use of prostatic specific antigen (PSA)?

A

Marker in prostate cancer…

however elevated by BPH, rectal examination, prostatitis, UTI.

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41
Q

What is the use of immunoglobulin in tumour markers?

A

Measure of paraproteinaemias (myeloma and Waldenstroms macroglobulinaemia)

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42
Q

What are the surgical techniques for biopsy?

A
  • FINE NEEDLE ASPIRATION CYTOLOGY
  • TRU-CUT NEEDLE BIOPSY- a piece of tumour is sampled under local anaesthetic
  • INCISIONAL BIOPSY- a piece of the tumour is sampled at surgery
  • EXCISIONAL BIOPSY- the whole of a mass is removed
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43
Q

What is the purpose of surgical axillary node assessment?

A
  • to allow an accurate assessment of lymph node involvement in breast cancer
  • therefore more accurate assessment of risk of future relapse
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44
Q

How well is cancer treated by surgery?

A
  • 30% of patients are curable by surgical resection
  • this requires that the cancer is localized
  • adequate margins of clearance are required to minimize risk of local recurrence
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45
Q

What is cytoreductive surgery?

A
  • Surgery to reduce the bulk of tumour

- most likely to be of benefit if there is effective therapy for the residual tumour

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46
Q

What is chemotherapy?

A
  • Cytotoxic agents used in systemic management of cancer
  • Hormonal and biological treatments
  • Treatment to eradicate occult cancer cells must include effective systemic treatment
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47
Q

What is the mechanism of action for chemotherapy?

A
  • Target DNA directly/indirectly

- Most are preferentially toxic towards actively proliferating cells

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48
Q

What are the indications for chemotherapy?

A

1) NEOADJUVANT
2) PRIMARY
3) ADJUVANT
4) PALLIATIVE
5) CURATIVE
6) PROPHYLACTIC

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49
Q

What are the main principles of chemotherapy?

A
  • Administer drugs in combinations
  • Schedule treatment in cycles of a few weeks
  • Administer the optimal dose
  • Use the most effective route of administration
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50
Q

Why should chemotherapy drugs be administered in combinations?

A
  1. Different classes of drugs have different actions and may kill more cancer cells together with several sub-lethal cell injuries.
  2. There is less chance of drug resistant malignant cells emerging
  3. When drugs wth different sites of toxicity are combined, dose can be maintained for each drug.
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51
Q

Why should chemotherapy treatment be scheduled in cycles every few weeks?

A
  • The cells affected are the HAEMATOPOIETIC STEM CELLS and the lining of the GI tract, producing low blood counts and mucositis
  • Treatment every 3-4 weeks allow these cells to recover
  • Each cycle on kills a proportion of tumour cells, so repeated cycles are required to get tumour clearance
  • Most treatments are maximally effective after a 6 month course
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52
Q

When is chemotherapy toxicity justified?

A

Only when long term survival or cure are possible

e.g. HODGKINS DISEASE AND EWINGS SARCOMA

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53
Q

What is an example of prolonged chemotherapy treatment?

A
  • CHILDHOOD LEUKAEMIA

- 18 months maintenance chemotherapy following induction of a complete remission

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54
Q

What are the features of oral administration of chemotherapy?

A
  • advantage of freeing the patient from lengthy hospital visits and invasive procedures
  • doesn’t reduce toxicity
  • regular review still required
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55
Q

Which chemotherapy drugs are available orally?

A
  • CYCLOPHOSPHAMIDE
  • ETOPOSIDE
  • CAPECITABINE
  • TAMOXIFEN
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56
Q

What are the features of systemic chemotherapy treatment?

A
  • most given intravenously as bolus injection or short infusion
  • some given as a continuous infusion via a central venous line, either peripherally placed or tunneled under the skin to reduce the chances of infection
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57
Q

What are the three forms of regional administration for chemotherapy?

A

1) INTRAVESICAL - superficial bladder cancer
2) INTRAPERITONEAL- directly into the peritoneal cavity for tumours that spread trans-coelomically (e.g. ovarian cancer)
3) INTRA-ARTERIAL- tumours that have well-defined blood supply is potentially suitable for intra-arterial chemotherapy

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58
Q

How are chemotherapy doses calculated?

A

PATIENT’S BODY SURFACE AREA

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59
Q

What is the formula used for Body Surface Area calculation?

A

-DuBois and DuBois

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60
Q

What are some specific forms of dose calculation for specific drugs?

A

CARBOPLATIN- dose calculated using renal function

MONOCLONAL ANTIBODY TRASTUZUMAB- calculated on body weight alone

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61
Q

What are the main aims for the use of combination chemotherapy regimes?

A

1) MAXIMIZE CELL KILL
2) MINIMIZE TOXICITY
3) MINIMIZE DRUG RESISTANCE

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62
Q

What are the immediate complications/SEs of chemotherapy?

A
  • Nausea and vomiting
  • Myelosuppression
  • GI
  • Alopecia
  • Neurological
  • GU
  • Cardiac
  • Hepatic
  • Skin and soft tissue toxicity
  • Others
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63
Q

Features of N+V SE in chemotherapy:

A
  • most drugs cause N+V
  • Nausea because there is direct stimulation of the vomiting centre
  • treatment for this is 5-HT serotonin antagonist drugs (ONDANSETRON)
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64
Q

Features of myelosuppression SE in chemotherapy

A
  • This occurs due to the killing of haematopoeitic progenitor cells.
  • Leads to leucopenia and thrombocytopenia 10-14 days after the beginning of each cycle
  • NADIR= lowest point of this drop
  • Haematopoietic recovery usually occurs after 3-4 weeks, enabling further cycles of chemotherapy to be given
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65
Q

Features of GI SE in chemotherapy

A
  • oral mucositis
  • diarrhoea due to colitis or small bowel mucosal inflammation
  • constipation fue to dehydration
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66
Q

Features of alopecia SE in chemotherapy

A
  • rapidly dividing cell population at the hair follicle

- alopecia can be controlled by the use of a cold cap which reduces blood flow to the scalp

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67
Q

Features of neurological SE in chemotherapy

A
  • peripheral neuropathies
  • autonomic neuropathy
  • central neurological toxicity
  • ototoxicity
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68
Q

Features of genitourinary SE in chemotherapy

A
  • nephrotoxicity

- bladder toxicity

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69
Q

Features of cardiac SE in chemotherapy

A
  • Doxorubicin and paclaitaxel cause ACUTE ARRHYTHMIAS

- 5-FU causes CORONARY ARTERY SPASM

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70
Q

Features of hepatic SE in chemotherapy

A

transient rise of liver enzymes

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71
Q

Features of skin and soft tissue SE in chemotherapy

A
  • extravasion
  • palmar plantar erythema
  • photosensitivity
  • pigmentation
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72
Q

What are the long term side effects of chemotherapy?

A
  • SECOND MALIGNANCIES
  • INFERTILITY
  • PULMONARY FIBROSIS
  • ACUTE CONDUCTION DEFECTS
  • CARDIAC FIBROSIS
  • PSYCHOLOGICAL DAMAGE
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73
Q

What is neutropenia?

A

TOTAL WHITE CELL COUNTS <1x10^9/L
FEVER >38
SIGNS OF SEPSIS

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74
Q

How is neutropenia managed?

A

It is an EMERGENCY

  • A, B, C
  • Gain IV access for bloods and rehydration
  • Urgent broad spectrum intravenous antibiotics (tazocin within 1 hour)
  • Monitor urine output, BP, O2 sats, pulse
  • O2 if required
  • septic screen to find source BUT no rectal/vaginal examinations
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75
Q

What are the septic signs associated with neutropenia?

A
  • systolic blood pressure <90mmHg (or >40mmHg fall from baseline)
  • heart rate >130 bpm
  • oxygen saturations <91%
  • RR >25 breaths per minute
  • responds only to voice or pain/unresponsive
  • lactate >2.0mmol
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76
Q

What is involved in the septic screen for a neutropenic patient?

A
  • FBC, U+E, CRP, LFT
  • Blood culture (x2 anaerobes and aerobes. 2x from line (all ports) and 2x peripheral
  • swabs
  • sputum culture
  • urine analysis and culture
  • stool analysis and culture
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77
Q

What should be elicited in the history of a neutropenic patient?

A
  • chemo drugs and timing (7-14 days), line and access, stents
  • previous episodes
  • localize the symptoms to look for source
  • allergies
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78
Q

What should be done in examination of a neutropenic patient?

A
  • ABC
  • MEWS
  • Full systematic examination of each system
  • focus on potential site
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79
Q

What should be done if there is failure to respond to antibiotics in a neutropenic patient?

A
  • failure to respond within first 48 hours, change to second line broad spectrum antibiotics
  • if persistently fever, consider anti fungal/antiviral agents
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80
Q

What are example of targeted agents in cancer treatment?

A
  • MONOCLONAL ANTIBODIES (drug name ends in -mab)- IV
  • TYROSINE KINASE INHIBITORS (drug name ends in -ib)- ORAL
  • mTOR INHIBITORS (drug name ends in -us)
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81
Q

Why are targeted agents dosed chronically?

A
  • better tolerated

- ongoing target blockade may be necessary for benefit

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82
Q

What does chronic dosing lead to?

A

1) Chronic toxicity: low grade symptoms
2) Emergent toxicity: thyroid disturbance
3) Risk of drug interaction
4) Mounting costs

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83
Q

How is hormone therapy used in cancer treatment?

A
  • Used to shrink primary tumours before/ instead of surgery
  • Used to prevent or delay the growth of micro metastases following surgery
  • Used to shrink established metastases and improve quality and duration of life
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84
Q

What are the three main forms of hormone therapy in cancer treatment?

A
  • REMOVING THE SOURCE OF A GROWTH PROMOTING HORMONE
  • HORMONE INHIBITORS
  • INCREASING HORMONES
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85
Q

How do hormone inhibitors work?

A
  • drugs that block the binding of hormones to their receptors in tumour cells
    e. g. TAMOXIFEN= anti-oestrogen in breast cancer
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86
Q

What are the two main type of anti-androgen?

A

1) STEROIDAL (cyproterone acetate)

2) NON-STEROIDAL (bicalutamide)

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87
Q

How does increasing hormones help with cancer treatment?

A

GLUCOCORTICOIDS in high concentration induce apoptosis in malignant lymphoid cells and help treat lymphoid leukemias, lymphomas, myeloma and Hodgkin’s disease

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88
Q

What is radiotherapy?

A

Ionizing radiation in the management of cancer

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89
Q

What are the ways in which radiotherapy can be used?

A

1) RADICAL/CURATIVE/DEFINITVE e.g. prostate
2) NEO-ADJUVANT SETTING
3) ADJUVANTLY
4) PALLIATION

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90
Q

What is the science behind radiotherapy?

A
  • X-Rays = high energy and short wavelength
  • X-rays penetrate body tissue whilst sparing the over-lying skin, producing secondary electrons and free radicals
  • these cause DNA damage
  • cancer cells commonly have defective DNA repair pathways and die
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91
Q

What is the unit of a dose of radiation?

A

gray (Gy)

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92
Q

What is the typical schedule for a head a neck cancer?

A

70Gy in 35 fractions over 7 weeks

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93
Q

What are the factors associated with tumour kill and radiotherapy toxicity?

A

1) total dose, the total volume treated, dose per fraction and overall treatment time
2) co-morbidities
3) intrinsic radio-sensitivity of the cancer cells

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94
Q

What are the main 2 side effects of radiotherapy?

A

1) ACUTE- after first 5-10 fractions

2) LATE- >3months after radiotherapy

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95
Q

What is the management for radiotherapy with head and neck cancer?

A
  • Mouth care- mudguard, saline mouthwash, aspirin gargles
  • skin care
  • opiate analgesia
  • nutritional support PEG/NG
  • admission
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96
Q

What is brachytherapy?

A

Radiation treatment where radiation sources are placed within or close to the tumour.

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97
Q

What are the benefits of brachytherapy?

A

This minimizes damage to local tissue whilst delivering high dose to a small area.

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98
Q

When is brachytherapy used?

A
  • used in prostate cancer
  • gynaecological cancers
  • esophageal cancer
  • head and neck cancer
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99
Q

What are the two main types of brachytherapy?

A

1) INTRACAVITY

2) INTERSITIAL

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100
Q

What is intracavity brachytherapy?

A

the radioactive material is placed inside a body cavity such as the uterus and cervix

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101
Q

What is interstitial brachytherapy?

A

where the material is put into the target such as the prostate

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102
Q

What is the most common radioisotope?

A

radioactive iodine I-131

used in the management of thyroid cancer

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103
Q

What are the main objectives of phase 1 clinical trials?

A

1) to determine toxicity and establish maximum tolerated dose
2) to trial new anti-cancer treatment on patients wth any tumour in whom no conventional therapy is appropriate
3) patients must be fit have near normal renal and hepatic function

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104
Q

What are the main features of phase 2 clinical trials?

A

1) to assess the particular anti-tumor activity of a new treatment in a range of different cancers
2) radiological tumour shrinkage
3) not necessary to have a control arm and random allocation of treatment

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105
Q

What are the main features of phase 3 clinical trials?

A

1) randomised trials comparing new with stablished treatments
2) primary endpoints assessed are usually length of life whatever the cause of death or length of life until the cancer grows
3) radiological shrinkage and quality of life are secondary

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106
Q

What is the definition of overall survival in clinical trials?

A

time between entry into trial and death from whatever cause

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107
Q

What is the definition of disease free survival in clinical trials?

A

time between entry into trial and recurrence of the tumour, or death from other causes

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108
Q

What is the definition of time to progression in clinical trials?

A

time between entry into the trial and disease progression or recurrence

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109
Q

How are WHO toxicity criteria classified?

A

grade 1= least toxic

grade 4= most toxic

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110
Q

What is the benefit of randomisation in clinical trials?

A

Reduces bias by assigning individuals to each arm of the trial by chance alone.

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111
Q

What determines the number of patients in a trial?

A

The size of the effect under study and the statistical significance required

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112
Q

What are ‘survival curves’?

A

(Kaplan Meier curves) with the probability of survival plotted against time.

The data represented can be:

1) ACTUAL SURVIVAL - follow-up data is complete for patients
2) ACTUARIAL SURVIVAL- patients lost to follow up

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113
Q

What is the definition for quality of life?

A
  • the subjective evaluation of life as a whole
  • patient’s appraisal of and satisfaction with their current level of functioning compared with what they perceive to be possible or ideal
  • physical, mental and social well-being, not merely the absence of disease or infirmity
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114
Q

How is quality of life measured?

A

1) PHYSICAL FUNCTIONING- self care activities, functional status, mobility, physical activities, role activities
2) DISEASE AND TREATMENT RELATED SYMPTOMS- pain, SoB, or SE of therapy
3) PSYCHOLOGICAL FUNCTIONING- emotional distress, anxiety, depression
4) SOCIAL FUNCTIONING- family interactions, time with friends, recreation activities
5) OTHERS- spiritual/existential concerns, cognitive function, sexual functioning and body image, satisfaction with health care

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115
Q

What are examples of generic quality of life instruments?

A
  • Medical Outcome Study (MOS)
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116
Q

What are examples of cancer specific quality of life instruments?

A
  • EORTC QL Questionnaire

- FACT (Functional Assessment of Cancer Therapy)

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117
Q

What are examples of cancer site specific quality of life instruments?

A
  • Breast Cancer Chemotherapy Questionnaire

- EORTC Lung Cancer Module

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118
Q

What are examples of QL domain specific instruments?

A
  • Hospital Anxiety and Depression (HAD)
  • Karnofsky Performance Status
  • Memorial Symptom Assessment Scale (MSAS)
  • Morrow Assessment of Nausea and Emesis (MANE)
  • McGill Pain Questionnaire (MPQ)
  • Memorial Pain Assessment Card (MPAC)
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119
Q

What are the three main clinical applications for assessing quality of life?

A

1) CLINICAL TRIALS
2) HEALTH ECONOMICS
3) PSYCHOSOCIAL ONCOLOGY

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120
Q

What are the characteristics that make tumours more suitable to be screened?

A
  • Curable when detected early in the majority of patients
  • Be relatively common
  • Have a long pre-invasive or non-metastatic stage
  • be able to be detected by relatively simple tests
  • be distinct from benign lesions
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121
Q

What are the ADVANTAGES of cancer screening?

A
  • reduction of mortality by detecting early disease that is curable
  • less radical treatment hence reducing morbidity
  • saving on health service resources by increased cure rates
  • reassurance given by a negative test
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122
Q

What are the DISADVANTAGES of cancer screening?

A
  • increased length of anxiety and morbidity if no effective intervention is possible
  • the over-investigation of false positive cases with associated morbidity
  • false reassurance from a false negative result
  • possible harmful effects if the screening test
  • cost of screening a large population
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123
Q

What are the key ways to achieve useful screening programs?

A

1) Limit screening to at-risk populations, improving compliance, sensitivity and specificity
2) Develop an effective infra-structure to increase awareness and uptake of at-risk populations

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124
Q

What are the features of cervical cancer screening?

A
  • Most effective screening programme to date
  • All women between 25-64
  • 25-49= every 3 years
  • 50-64= every 5 years
  • In Scotland and Wales, starts at 20
  • Long pre-invasive period during which early detection can occur and an effective treatment for early disease
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125
Q

What are the features of breast cancer screening?

A
  • Regular mammography all women between 50 and 70 every 3 years
  • Ability to reduce mortality is controversial
  • Younger patients who are at increased risk should be considered for a package of care including screening if appropriate by referral to a breast cancer service
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126
Q

What are the features of colorectal cancer screening?

A
  • Men and women are offered bowel screening using faecal occult blood
  • Every 2 years from 60-74
  • Scotland 50-74
  • At risk patients (UC, strong family history, or previous primary tumour)
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127
Q

What is the WHO definition of palliative medicine?

A

Improves the quality of life of patients and their families facing the problems associated with life-threatening illness, through the prevention and relief of suffering by means of early identification and impeccable assessment and treatment of pain and other problems (physical, psychosocial and spiritual)

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128
Q

What are the features of palliative care?

A
  • relief from pain and other distressing symptoms
  • physical, psychological, social and spiritual care
  • affirms life and regards dying as a normal process
  • neither hastens or postpones death
  • helps patients to live as actively as possible until death
  • offers support to help the family/carers during the patients illness and into bereavment
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129
Q

Which patients are eligible for palliative care?

A
  • Oncology patients
  • Any other advanced progressive disease
  • e.g. motor neurone disease
  • heart failure
  • COPD
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130
Q

Who is on the MDT for palliative medicine?

A
  • Doctors
  • Nurses
  • Social Workers
  • Chaplains
  • Physiotherapists
  • Occupational therapists
  • psychologists
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131
Q

What is cancer pain?

A
  • Has physical psychological, social and spiritual dimensions
  • Occurs in 80% of patients
  • May be caused by disease, or treatment of disease
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132
Q

How is cancer pain assessed?

A
  • SOCRATES
  • Effects on sleep, work, mood
  • Current treatment
  • treatments tried and results
  • understanding of illness
  • expectations
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133
Q

What are the features of bone pain in cancer?

A
  • Dull ache over a large area or well localized tenderness over the bone
  • Worse on weight bearing or with movement
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134
Q

What is the treatment for bone pain in cancer?

A
  • NSAIDs (diclofenac 50mg tds)
  • Radiotherapy
  • Bisphosphonates (e.g. pamidronate infusion)
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135
Q

What are the features of headache in cancer?

A
  • Dull oppressive pain
  • worse on waking
  • worse on coughing, sneezing, N+V
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136
Q

What is the treatment for headache in cancer?

A
  • Corticosteroids to reduce oedema (DEXAMETHASONE 16mg PO daily in the morning with PPI)
  • NSAIDs
  • paracetamol
  • review response after 7 days
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137
Q

What are the features of neuropathic pain in cancer?

A
  • Pain in an area of abnormal sensation
  • Localised to specific dermatomes or over a wider, less defined area
  • Altered sensation e.g. numbness or hyperesthesia
  • Autonomic changes such as pallor or sweating
  • Pins and needles of burning
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138
Q

What is the treatment of neuropathic pain in cancer?

A
  • Antidepressants [TCA] (AMITRIPTYLINE 10-75mg NOCTE)
  • Anticonvulsants (GABAPENTIN 100-1200mg TDS/ PREGABALIN 25-300mg BD)
  • Compression of a nerve may be helped by corticosteroids
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139
Q

What are the features of visceral pain in cancer?

A
  • Dull, deep seated, poorly localized pain
  • Tenderness over a particular organ (e.g. liver)
  • Visceral pain is spasmodic such as bladder spasm or bowel colic
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140
Q

What is the treatment for visceral pain in cancer?

A
  • Analgesic ladder
  • NSAIDs or corticosteroids to reduce inflammation
  • ANTICHOLINERGIC DRUGS e.g. SC hyoscine butylbromide for bowel colic
  • Oral oxybutynin for bladder spasm
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141
Q

What are the features of infection pain in cancer?

A
  • Pleuritic pain of pneumonia

- Pain of cellulitis

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142
Q

What is the treatment for infection pain in cancer?

A

TREAT INFECTION

abx

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143
Q

What is on the analgesic ladder for the management of cancer pain?

A
  • NON OPIOID
  • WEAK OPIOID
  • STRONG OPIOID
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144
Q

How should pain medication be given?

A

Drugs should be used at optimal dose regularly

Drugs should be given orally if patient can swallow

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145
Q

When should alternative routes of administration be considered in cancer patients?

A
  • dysphagia
  • gastric stasis
  • intractable vomiting
  • impaired consciousness (syringe driver)
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146
Q

What are the doses and strengths of co-codamol?

A

WEAK: 8mg CODEINE/500mg PARACETAMOL (2 tablets QDS)
15MG CODEINE/500MG PARACETAMOL (2 tablets QDS)
STRONG: 30mg CODEINE/500mg PARACETAMOL (2 tablets QDS)

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147
Q

What are the main SEs associated with the use of strong opioids?

A
  • CONSTIPATION is universal- ALWAYS prescribe a laxative e.g. co-danthramer
  • NAUSEA AND VOMITING- prescribe prn anti-emetic
  • DROWSINESS
  • CONFUSION AND VISUAL HALLUCINATION (rare)
  • RESPIRATORY DEPRESSION (rare)
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148
Q

What are the signs and symptoms indicative of opioid toxicity?

A
  • persistent nausea and vomiting
  • persistent drowsiness
  • confusion
  • visual hallucinations
  • myoclonic jerks
  • respiratory depression
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149
Q

What is parenteral diamorphine?

A

An SC preparation of morphine that is 3 TIMES more potent than oral morphine

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150
Q

How should parenteral diamorphine be administered?

A

TOTAL 24h SC CONTINUOUS INUSION DIAMORPHINE DOSE SHOULD BE 1/3 OF THE TOTAL 24h ORAL MORPHINE DOSE

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151
Q

What are examples of transdermal analgesics?

A
  • FENTANYL TRANSDERMAL PATCHES
  • Duration: 72 hours
  • Suitable for patients with severe chronic pain already stabilized on other opioids.
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152
Q

What are alternative examples of stone opioids?

A

OXYCODONE to be given second line for those who cannot tolerate morphine

  • alfentanil
  • methadone
  • fentanyl (sublingual, buccal, nasal)
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153
Q

What are non-pharmacological treatments for pain in cancer?

A
  • palliative radiotherapy (for bone pain)
  • palliative chemotherapy (for masses compressing viscera/nerves)
  • surgery
  • anesthetic and neurosurgical interventions (e.g. paravertebral nerve block)
  • psychological interventions (CBT)
  • Transcutaneous Electrical Nerve Stimulations (TENS)
  • Complementary therapies (e.g. aromatherapy)
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154
Q

What are the main gastrointestinal problems associated with palliation?

A
  • MOUTH PROBLEMS
  • ANOREXIA
  • NAUSEA AND VOMITING
  • CONSTIPATION
  • INTESTINAL OBSTRUCTION
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155
Q

What are some of the causes of mouth problems in palliation?

A
  • dry moth (xerostomia) from reduced intake of oral fluid
  • SE from drugs
  • radiotherapy to head and neck
  • loss in taste, halitosis, dysphagia, infection
  • oral candidiasis (treat with systemic antifungals)
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156
Q

What are some of the causes of anorexia in palliation?

A
  • Elicit any reversible cause (e.g. thrush, nausea, pain, constipation, depression)
  • Megetrol acetate 160mg is effective for long term but may cause fluid retention
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157
Q

What are the main causes for nausea and vomiting in palliation?

A

1) GASTRIC STASIS AND IRRITATION
2) TOXIC
3) CEREBRAL CAUSES
4) ANXIETY/ANTICIPATORY N+V
5) INDETERMINATE
6) HYPERCALCAEMIA
7) VESTIBULAR DISTURBANCE
8) DISTENSION, COMPRESSION/ DISTURBANCE OF ABDOMINAL/PELVIC ORGANS

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158
Q

What are the simple measures to manage nausea and vomiting in palliation?

A
  • Access to a large bowl, tissues and water
  • Calm environment away from where food is usually prepared/consumed
  • Small and palatable meals
  • Cool fizzy drinks
  • Parenteral hydration (may help reduce persistent nausea)
  • CBT for anticipatory nausea/vomiting
  • AVOID nasogastric suction
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159
Q

What is the management for gastric stasis/irritation in palliation?

A

SC METOCLOPRAMIDE 10-20mg every 8hrs

OR

SC (continuous infusion) METOCLOPRAMIDE 30-100mg/24hrs

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160
Q

What is the management for toxic causes of nausea and vomiting in palliation?

A

PO/SC HALOPERIDOL 1.5-5mg NOCTE

up to 10mg daily (5mg BDS)

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161
Q

What is the management for cerebral causes of nausea and vomiting in palliation?

A

PO DEXAMETHASONE 8-16mg up to 7days
AND
PO* CYCLIZINE 25-50mg every 8 hours (max dose 150mg/24hr)

*SC 150mg/24hr

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162
Q

What is the management for anticipatory nausea and vomiting in palliation?

A

BENZODIAZEPINES

  • SUBLINGUAL LORAZEPAM 0.5mg-1mg
  • PO LEVOMEPROMAZINE 3-6mg
  • SC LEVOMEPROMAZINE 2.5-6.25mg

CBT
COMPLEMENTARY THERAPIES

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163
Q

What is the management for the indeterminate causes of nausea and vomiting in palliation?

A

HALOPERIDOL

  • PO 1.5mg NOCTE or BDS (max of 10mg/24h)
  • PRN 1.5mg, SC 1.25-2.5mg
  • Syringe Driver: 2.5-10mg/24h

if not effective, ADD CYCLIZINE

  • PO 25-50mg every 8hrs (max of 150mg/24h)
  • PRN: PO/SC 1.5mg
  • Syringe Driver: 50-150mg/24h

If end of life:
- SC LEVOPROMAZINE 6.25mg

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164
Q

What is the management for hypercalcemia causing nausea and vomiting in palliation?

A
  • HOSPITAL ADMISSION
  • intravenous rehydration and BISPHOSPHONATES
  • PO/SC HALOPERIDOL 1.5-5mg NOCTE (max 10mg/24h)
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165
Q

What is the management for vestibular disturbance causes of nausea and vomiting in palliation?

A
  • CYCLIZINE

- HYOSCINE

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166
Q

What is the management for nausea and vomiting in palliation caused by distension, compression or disturbance of abdo/pelvic organs?

A

CYCLIZINE

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167
Q

Which drugs for nausea and vomiting should NOT be combined?

A

PROKINETICS (metoclopramide/domperidone) with ANTIMUSCARINICS (hyoscine/cyclizine/levopromazine)

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168
Q

What investigations should be done in those with nausea and vomiting in palliation?

A
  • IF ANY (dependent on patient wishes)
  • Blood tests to exclude hypercalcaemia or uraemia
  • Radiography to exclude constipation/ ultrasonography to detect ascites
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169
Q

How which classes of laxatives can be used in constipation for palliative patients?

A
  • STOOL SOFTENERS
  • STIMULANTS

NOT BULK FORMING

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170
Q

What are examples of stool softeners that can be used in constipation for palliative patients?

A
  • LACTULOSE (may cause significant bloating and flatulence)

- MOVICOL/MACROGEL (softener but may also stimulate bowel motions)

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171
Q

What are examples of stimulants that can be used in constipation for palliative patients?

A
  • SENNA
  • DANTRON
  • BISACODYL
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172
Q

How does subacute intestinal obstruction in advanced cancer present?

A
  • incomplete, intermittent and in multiple sites.

- high incidence in patients with ovarian/bowel cancer

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173
Q

What are the symptoms of subacute intestinal obstruction?

A
  • nausea and vomiting
  • colicky pain
  • abdominal distension
  • dull aching pain
  • diarrhoea and/or constipation
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174
Q

What should be considered in palliative patients if there is a sudden onset of dyspnoea?

A
  • asthma
  • pulmonary oedema
  • pulmonary embolism
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175
Q

How should sudden onset of dyspnoea in palliative patients be managed?

A
  • asthma- BRONCHODILATORS
  • pulmonary oedema- DIURETICS, DIAMORPHINE
  • pulmonary embolism- ANTICOAGULANTS
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176
Q

What should be considered in palliative patients if there is dyspnoea arisen over several days?

A
  • exacerbation of COPD
  • Pneumonia
  • Bronchial obstruction by tumour
  • SVC obstruction
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177
Q

How should dyspnoea that has arisen over several days in palliative patients, be managed?

A
  • exacerbation of COPD- ANTIBIOTICS/BRONCHODILATORS
  • Pneumonia- ANTIBIOTICS/PHYSIOTHERAPY
  • Bronchial obstruction by tumour- DEXAMETHASONE/ STENTS/LASER
  • SVC obstruction- DEXAMETHASONE- URGENT STENTING
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178
Q

What should be considered in palliative patients if there is a gradual onset of dyspnoea?

A
  • congestive cardiac failure
  • anaemia
  • pleural effusion
  • ascites
  • lymphangitis carcinomatosis
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179
Q

How should gradual onset of dyspnoea in palliative patients be managed?

A
  • congestive cardiac failure- DIURETICS, DIGOXIN, ACEi
  • anaemia- TRANSFUSION
  • pleural effusion- PLEURAL ASPIRATION+PLEURODESIS
  • ascites- PARACENTESIS
  • lymphangitis carcinomatosis- DEXAMETHASONE
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180
Q

What is the non-pharmacological treatment for palliative patients with dyspnoea?

A
  • breathing retraining (pursed lip breathing, breathing exercise, coordinated breathing training)
  • relaxation
  • fan directed onto the face
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181
Q

What iii the pharmacological treatment for palliative patients with dyspnoea?

A

OPIOIDS (low doses)
e.g. ORAL MORPHINE 2.5mg/4h

BENZODIAZEPINES
e.g. LORAZEPAM 0.5mg-1mg sublingual

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182
Q

What are examples of palliative care emergencies?

A
  • METASTATIC SPINAL CORD COMPRESSION
  • SUPERIOR VENA CAVA OBSTRUCTION
  • HYPERCALCAEMIA
  • MAJOR HAEMORRHAGE
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183
Q

What are the common cancers in which MSCC occurs?

A
  • breast
  • bronchus
  • prostate

but CAN occur with any tumour

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184
Q

What is MSCC?

A

tumour or metastases in the vertebral body or paraspinal region pressing on the spinal cord

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185
Q

What are the symptoms of MSCC?

A
  • Back pain/ nerve root pain may be aggravated my movement, coughing or laying flat
  • Leg motor weakness
  • subjective sensory disturbance “feels like i’m walking on cotton wool”
  • urinary retention/faecal incontinence
  • pyrexia
  • contant pain at night and at rest
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186
Q

What are the signs associated with MSCC?

A
  • weakness/paraparesis/paraplegia
  • changes in sensation occur below the level of compression
  • reflexes increased below the level of the lesion
  • clonus and painless bladder distension may be present
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187
Q

What is the investigation for MSCC?

A

WHOLE SPINE MRI

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188
Q

What is the management for MSCC?

A
  • Adequate analgesia
  • Corticosteroids (DEXAMETHASONE 16mg) with PPI if a clinical suspicion of cord compression pending definitive investigations
  • Surgery (advanced metastatic disease, comorbidities, poor prognosis)
  • radiotherapy (single fraction to that particular site)
  • chemotherapy
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189
Q

What is the prognosis for MSCC?

A

if treated <24h, 57% will walk again

if all motor function lost for >48h, unlikely to walk again

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190
Q

What is superior vena cava obstruction?

A

Caused by extrinsic compression, thrombosis or invasion of the wall of the SVC
- common in lung cancer and lymphoma

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191
Q

What are the malignant causes of SVC obstruction?

A
  • lung cancer
  • lymphoma
  • mediastinal lymphadenopathy
  • germ cell tumours
  • thymoma
  • oesophageal
  • tumour associated thrombus
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192
Q

What are the benign causes of SVC obstruction?

A
  • non-malignant tumours (goiter)
  • mediastinal fibrosis
  • infection (e.g. TB)
  • aortic aneurysm
  • thrombus associated with indwelling catheters
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193
Q

What are the symptoms associated with SVC obstruction?

A
  • Headache/ feeling of fullness in the head
  • facial/arm/neck swelling
  • dyspnoea
  • cough
  • hoarse voice
  • visual disturbance
  • collateral vessels across the chest
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194
Q

What are the signs of SVC obstruction?

A
  • facial oedema
  • prominent (swollen) blood vessels on the neck, trunk and arms
  • cyanosis
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195
Q

What is the management of SVC obstruction?

A
  • High dose corticosteroids (DEXAMETHASONE 16mg daily with PPI)
  • Arrange imaging
  • speak to interventional radiology
  • vascular stent followed by radiotherapy or chemotherapy depending on the primary tumour
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196
Q

Dependent on the cause… what are other management options for SVC obstruction?

A
  • Vascular stent (radiological guidance)
  • Radiotherapy
  • Chemotherapy
  • LMWH
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197
Q

In which cancers does hypercalcaemia typically present?

A
  • breast cancer
  • lung cancer
  • squamous cell carcinomas
  • myeloma
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198
Q

Why does hypercalcaemia occur in cancer?

A

Due to INAPPROPRIATE PTH SECRETION from cancer cells

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199
Q

What is the mechanism for increased plasma calcium in cancer?

A
  • a tumour associated protein that mimics PTH, stimulates bone reabsorption and increases plasma calcium
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200
Q

What are the early symptoms associated with hypercalcaemia in cancer?

A
  • lethargy
  • malaise
  • anorexa
  • polyuria
  • THIRST
  • NAUSEA AND VOMITING
  • CONSTIPATION
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201
Q

What are the late symptoms associated with hypercalcaemia in cancer?

A
  • confusion
  • drowsiness
  • fits
  • coma
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202
Q

What are the investigations associated with hypercalcaemia?

A

SERUM CALCIUM corrected for SERUM ALBUMIN

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203
Q

What is the management for hypercalcaemia in cancer?

A

REHYDRATION SALINE
IV BISPHOSPHONATE* (pamdronate or zoledronic acid)

*bisphosphonates inhibit osteoclastic bone resorption

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204
Q

What is the management for hypercalcaemia if there have been arrhythmias or seizures?

A

CALCITONIN and CORTICOSTEROIDS
can be used in combination and are effective at lowering the serum calcium

(usually SC/IM calcitonin is given with PO prednisolone)

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205
Q

What is the best way to manage major haemorrhage in palliative patients?

A
  • Symptom control

- Green towels to absorb AND reduce the visual impact of blood loss.

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206
Q

What key factors are important in terminal care?

A
  • Recognise when death is imminent
  • Withdraw unnecessary treatments
  • Prepare patient and family/carers for death
  • Must have irreversible life threatening illness or advanced/progressive disease
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207
Q

What are the signs and symptoms to indicate that prognosis is short?

A
  • Step wise change in physical functioning
  • Profound weakness
  • Bed bound for most of the day
  • Drowsy and disorientated for extended periods
  • Severely limited attention span
  • losing interest in food and drink
  • too weak to swallow medication
  • managing sips only
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208
Q

What should be done in the last days of life?

A
  • DIAGNOSE DYING
  • Communication
  • Preferred place of death and goals of care
  • Psycho-spiritual needs
  • Family needs
  • Nursing needs
  • Physical symptoms
  • Medication review
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209
Q

Which drugs are ESSENTIAL in terminal care?

A

1) ANALGESIC
2) ANTIEMETIC
3) ANXIOLYTIC
4) ANTISECRETORY

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210
Q

Which drugs should you consider stopping in terminal care?

A
  • Corticosteroids (in ICP headache)
  • Hypoglycaemics (keep in DM1)
  • Anticonvulsants (can stop if commenced on midazolam)
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211
Q

Which drugs are non essential in terminal care?

A
  • Antihypertensives
  • Antidepressants
  • Laxatives
  • Anti-ulcerr drugs
  • Anticoagulants
  • Long term antibiotics
  • Iron
  • Vitamins
  • Diuretics
  • Arrhythmics
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212
Q

What are the FOUR KEY drugs in terminal care?

A

1) DIAMORPHINE (analgesic)
2) LEVOMEPROMAZINE (antiemetic)
3) MIDAZOLAM (anxiolytic)
4) HYOSCINE BUTYLBOMIDE (anti-secretory)

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213
Q

What is the management for terminal restlessness?

A
  • look for reversible causes e.g. pain, urinary retention etc.
  • if there is no reversible cause, consider sedation
  • SC MIDAZOLAM either by stat doses (2.5-5mg) or INFUSION starting at 10mg/24h
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214
Q

What is death rattle?

A
  • Movement of secretions in the upper airways generally in patients who are woo weak to expectorate effectively
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215
Q

How can death rattle be managed?

A
  • Repositioning

- Antisecretory drugs (HYOSCINE BUTYLBROMIDE)

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216
Q

What are the indications for using syringe drivers?

A
  • Inability to swallow drugs due to reduced conscious level, often in the last few days of life
  • persistent nausea and vomiting
  • intestinal obstruction
  • malabsorption of drugs
  • dysphagia
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217
Q

Which drugs are unsuitable for subcutaneous administration as too irritant?

A

1) DIAZEPAM
2) CHLORPROMAZINE
3) PROCHLORPERAZINE

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218
Q

What are the risk factors for breast cancer?

A
  • increasing age
  • oestrogen exposure (late childbearing, nulliparity, early menarche, late menopause)
  • obesity
  • use of HRT
  • prolonged use of OCP
  • alcohol
  • smoking
  • diet
  • ionizing radiation
  • family history (BRCA1, BRCA2, P53)
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219
Q

What is the histology of breast cancer?

A

1) INFILTRATING OR INVASIVE DUCTAL CARCINOMA
2) LOBULAR CARCINOMA
3) MEDULLARY, COLLOID, COMEDO AND PAPILLARY

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220
Q

What is the presentation of breast cancer?

A
  • breast lump
  • nipple change
  • nipple discharge
  • bloodstained discharge from the nipple
  • skin contour changes
  • axillary lumps
  • breast pain/mastalgia
  • symptoms of metastatic disease
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221
Q

What are the investigations for suspected breast cancer?

A

TRIPLE ASSESSMENT

  • CLINICAL EXAMINATION (full history and examination)
  • MAMMOGRAPHY
  • ULTRASOUND + BIOPSY of symptomatic breast and axillae
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222
Q

How is diagnosis of breast cancer confirmed?

A
  • fine needle aspiration cytology (FNAC)
  • needle biopsy
  • incisional or excisions biopsy
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223
Q

What should be done if there is a high risk of disseminating disease?

A
  • isotopic bone scan
  • liver imaging
  • ultrasound/ CT scan
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224
Q

When should an MRI be performed in breast cancer investigation?

A
  • if there is a discrepancy between clinic examination, mammogram and ultrasound findings.
  • if breast density preludes accurate mammogram assessment
  • if histology is lobular
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225
Q

What is the T classification within TNM staging for breast cancer?

A 
T0- No primary tumour
Tis- in situ disease, non-invasive
T1- Invasive tumour <2cm
T2- Tumour between 2-5cm
T3- Primary tumour >5cm
T4- Skin involvement
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226
Q

What is the N classification within TNM staging for breast cancer?

A

N0- No lymph nodes
N1 - Mobile axillary nodes
N2- Fixed axillary nodes
N3- Internal mammary nodes

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227
Q

What is the M classification within TNM staging for breast cancer?

A

M0- No metastases

M1- Distant metastases

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228
Q

What is the staging for breast cancer?

A 
STAGE 0: Tis, N0, M0
STAGE 1: T1, N0, M0
STAGE 2: T2/3, N0, M0 OR T0/1/2, N1, M0
STAGE 3: T or N > stage II, M0
STAGE 4: Any T, Any N, M1
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229
Q

What is the surgical management for breast cancer?

A
  • mastectomy
  • wide local excision
  • with post operative radiotherapy
  • axillary clearance
  • sentinel node biopsy
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230
Q

What is the radiological management for breast cancer?

A
  • ALL have radiotherapy to the residual breast tissue
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231
Q

What is the systemic therapy for breast cancer?

A
  • ENDOCRINE OR CHEMOTHERAPY to treat both micro metastatic disease in an adjuvant setting and recurrent/metastatic disease.
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232
Q

What are examples of adjuvant endocrine therapies for breast cancer?

A

TAMOXIFEN
AROMATASE INHIBITORS (anastrozole)
TRASTUZAMAB (herceptin)

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233
Q

How does tamoxifen work?

A

Blocks the effects of estrogen on ER receptors. This helps to stop breast cancer cells to grow.
Use for 5 years

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234
Q

What are the side effects associated with tamoxifen?

A
  • hot flushes
  • mood changes
  • vaginal discharge
  • loss of libido
  • endometrial changes
  • DVT/PE/Stroke
  • Fluid retention
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235
Q

When should aromatase inhibitors be used in breast cancer management?

A

ONLY IN POST-MENOPAUSAL women with breast cancer

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236
Q

How does trastuzamab work?

A

It is effective in over-expression of the target epithelial growth factor receptor (HER-2)

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237
Q

What are the risk factors for colorectal cancer?

A

1) DIET (animal fats and meat)
2) INFLAMMATORY DISEASE (uc)
3) FAMILIAL ASSOCIATION

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238
Q

What are the familial risk factors of colorectal cancer?

A
  • HNPCC (Hereditary Non-Polyposis Colon Cancer)
  • FAP (Familial Adenomatous Polyposis)
  • Gardner’s syndrome
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239
Q

What is the histology for colorectal cancers?

A

ADENOCARCINOMAS (95%)

  • epithelial (mucinous/signet ring)
  • carcinoid
  • gastrointestinal stromal tumour
  • primary malignant lymphoma
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240
Q

What is the clinical presentation for colorectal cancer?

A
  • altered bowl habits
  • weight loss
  • rectal bleeding
  • vague abdominal pain
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241
Q

What are the red flag symptoms associated with colorectal cancer?

A
  • weight loss
  • altered blood rectally
  • change in bowel habit
  • abdominal pain
  • rectal mucous
  • anorexia
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242
Q

What can be seen on examination of those with colorectal cancer?

A
  • loss of weight
  • signs of anaemia
  • abdominal mass
  • mass on rectal examination
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243
Q

What investigations should be done for patients with suspected colorectal cancer?

A
  • digital examination
  • rigid sigmoidoscopy
  • flexible sigmoidoscopy
  • colonoscopy
  • CT (provides staging)
  • Tumour marker CEA (not diagnostic but can be useful to monitor disease?
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244
Q

What is the T classification within TNM staging for colorectal cancer?

A

TX: Primary tumour cannot be assessed
T0: No evidence of primary tumour
T1: Tumour invades submucosa
T2: Tumour invades muscular propria
T3: Tumour extends through muscular propria into peri-colic tissues
T4: Tumour invades visceral peritoneum or invades/adheres to adjacent organ or structure

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245
Q

What is the N classification within TNM staging for colorectal cancer?

A

N0: No regional lymph node involvement
N1: Involvement of 1-3 lymph nodes
N2: Involvement of 4 or more lymph nodes

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246
Q

What is the M classification within TNM staging for colorectal cancer?

A

MX: Distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis
M1a: Confined to one organ or site, but not peritoneum
M1b: 2 or more sites (but not peritoneum)
M1c: Peritoneal spread

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247
Q

What is the Duke Staging for colorectal cancer?

A

A- Invasion into but not through the bowel wall
B- Invasion through the bowel wall but not into the nodes
C- Lymph node involvement
D- Distant metastasis

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248
Q

What are the management options for rectal cancer?

A

1) NEOADJUVANT THERAPY
2) RADIOTHERAPY
3) SURGERY

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249
Q

What are the surgical options for rectal cancer?

A
  • Anterior resection (higher tumours, join ends, no stoma)
  • APER (lower tumours, proximal tumours)
  • Hartmans (higher tumour, no anastomosis, stoma)
  • Total mesorectum excision
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250
Q

What are the management options for colon cancer?

A

1) NEOADJUVANT THERAPY

2) SURGERY

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251
Q

What are the features of surgical management for colorectal cancer?

A
  • Early stage colorectal carcinoma can be cured by surgical resection alone
  • Resection of liver metastases in addition to the primary may be beneficial
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252
Q

What are examples of adjuvant chemotherapy in colorectal cancer?

A
  • 5-FU (Fluorouracil) is the most active agent in colorectal carcinoma.
  • e.g. OXALIPLATIN and IRINOTECAN
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253
Q

What is assessed in follow up for colorectal cancer patients?

A
  • bowel changes
  • bladder changes
  • sexual impotence
  • infertility
  • psychological (stoma)
  • financial
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254
Q

What are the risk factors for lung cancer?

A
  • Age- risk increases >40 years old
  • Smoking
  • Occupation
  • Asbestos exposure
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255
Q

How are lung tumours classified?

A

1) SMALL CELL LUNG CANCER (15%)

2) NON-SMALL CELL LUNG CANCER (85%)

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256
Q

What are the features of small cell leg cancers?

A
  • highly aggressive tumours which grow rapidly
  • usually metastasized and become inoperable prior to diagnosis
  • poor prognosis
  • associated with paraneoplastic syndromes (SIADH, Cushing’s, LEMS)
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257
Q

What are the main types of non-small cell lung cancers?

A
  • SQUAMOUS CELL CARCINOMAS
  • ADENOCARCINOMAS
  • LARGE CELL CARCINOMAS
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258
Q

What are the features of squamous cell lung carcinomas?

A
  • central
  • close to the bronchi
  • can present with bronchial obstruction
  • closely linked to cigarette smoking
  • secrete PTH related peptide (PTHrp) which can lead to hypercalcaemia
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259
Q

What are the features of adenocarcinoma?

A
  • peripheral
  • more frequent in women
  • non-smokers
  • patients with previous asbestos exposure
  • associated with activation mutations in EGFR and ALK
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260
Q

Wha are the features of large cell carcinomas?

A
  • less differentiated the other NSCLCs

- tend to metastasis early

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261
Q

What are the other types of NSCLCs?

A
  • carcinoid
  • mesothelioma
  • sarcoma
  • lymphoma
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262
Q

What is the clinical presentation* for lung cancer?

A
  • Most present at stage 4 (metastasis)
  • cough
  • dyspnoea
  • haemoptysis
  • chest pain
  • recurrent chest infection
  • bone pain
  • RUQ pain
  • headaches/nausea/neurological
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263
Q

What clinical features will be present in apical tumours?

A
  • HORNER’S SYNDROME (miosis, anhidrosis, ptosis)

- PANCOAST’S SYNDROME (pain in the distribution of the brachial plexus nerve routes)

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264
Q

What clinical features will present in mediastinal disease?

A
  • Recurrent laryngeal nerve palsy (hoarsness, difficulty speaking)
  • SVC obstruction
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265
Q

What clinical presentations are associated with specific histologies in lung cancer?

A

1) CLUBBING- squamous cell carcinoma
2) EXCESSIVE SPUTUM PRODUCTION- broncho-alveolar carcinoma
3) NEURO-ENDOCRINE FACTORS- small cell lung cancers

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266
Q

What investigations are done in lung carcinoma?

A
  • CXR
  • Sputum cytology
  • Bronchoscopy
  • Other biopsy techniques (trans thoracic biopsy, mediastinoscopy and biopsy)
  • CT chest and upper abdomen (for staging)
  • PET scan
  • Other diagnostic tests
  • Tumour markers

CARDIOPULMONARY EXERCISE TESTING (to assess fitness for surgical resection

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267
Q

What is the T classification within TNM staging for lung cancer?

A

T1- <3cm surrounded by lung or visceral pleura not invading a main bronchus
T2- >3cm but <7cm OR invading main bronchus OR invading visceral pleura
T3- >7cm or local invasion
T4- Organ invasion: mediastinum, heart, great vessels, recurrent laryngeal nerve, oesophagus, vertebral body, carina or separate tumour nodules in a different ipsilateral lobe

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268
Q

What is the N classification within TNM staging for lung cancer?

A

N1- Ipsilateral bronchopulmonary and hilarious nodes
N2- Ipsilateral mediastinal node or subcarinal
N3- Contralateral mediastinal or contralateral hilar nodes, or supraclavicular nodes

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269
Q

What is the M classification within TNM staging for lung cancer?

A

M0- No metastases
M1a- Separate tumour nodes in contralateral lung, malignant pleural of pericardial effusion
M1b- Distant metastases

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270
Q

What are the management options for SCLC?

A
  • radiotherapy

- chemotherapy

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271
Q

What are the features of chemotherapy use in the management of SCLC?

A

-90% of SCLC will respond to combination chemotherapy

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272
Q

What are the 3 indications for radiotherapy in the management of SCLC

A

1) Treatment of primary tumour
2) Prophylactic cranial irradiation (reduce brain mets)
3) Palliative

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273
Q

What are the prognostic factors for SCLC?

A

WITHOUT TREATMENT- median survival 2-4months

TREATED WITH SYSTEMIC CHEMO- median survival 11 months

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274
Q

What are the management options for NSCLC?

A

CURATIVE treatment- Stage 1,2,3
SYMPTOM management- Stage 4

  • SURGERY
  • RADIOTHERAPY
  • CHEMOTHERAPY
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275
Q

What are the features for surgical management of NSCLC?

A
  • Stage 1+2- surgical resection has a good prognosis and possibility of cure
  • Mediastinal involvement is considered a contraindication to surgery by most surgeons
  • Following surgery adjuvant chemotherapy is given to fit patients
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276
Q

What are the features of radiotherapy in NSCLC?

A
  • If patients aren’t suitable for surgery, radical radiotherapy
  • Use of CHART
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277
Q

What is CHART?

A

Continuous Hyperfractionated Accelerated RadioTherapy:

  • given 3 times a day for 12 consecutive days
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278
Q

What are the features of chemotherapy in NSCLC?

A
  • response rate of 30%
  • CARBOPLATIN and PACLITAXEL
  • In large bulky tumours, chemotherapy can be given to shrink the tumour so that radical radiotherapy may follow
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279
Q

What is targeted therapy in NSCLC?

A 
TYROKINASE INHIBITORS (erlotinib or gefitinib).
- can be used first like as alternative to chemotherapy
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280
Q

What are the risk factors for prostate cancer?

A
  • radiation exposure
  • diet
  • anabolic steroids
  • age
  • Afro-Caribbean
  • family history
  • maternal breast cancer
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281
Q

What is the histology of prostate cancer?

A

> 95% are ADENOCARCINOMAS in glandular tissue in the posterior or peripheral part of the prostate gland

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282
Q

What histological grading system is used in prostate cancer?

A

GLEASON GRADE

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283
Q

What are the clinical features of prostate cancer?

A
  • Diagnosed by routine rectal examination
  • Enlarged, hard, craggy gland
  • Obliteration of the median sulcus
  • Prostatism: poor stream, nocturne, dribbling, increased frequency, impotence
  • Metastatic symptoms- anaemia, pathological fracture/bone pain, spinal cord compression
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284
Q

What investigation is done in prostate cancer?

A
  • Transrectal biopsy under ultrasound guidance
  • PSA
  • isotope bone scan
  • MRI
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285
Q

What is the T classification within TNM staging for prostate cancer?

A

TX: Primary tumour cannot be assessed
T0: No evidence of primary tumour
T1: Clinically unapparent tumour not palpable or visible with imaging
T2: Tumour confined within the prostate
T3: Tumour extends through the prostate capsule
T3a: Extracapsular extension (uni/bilateral)
T3b: Tumour invades seminal vesicle
T4: Tumour is fixed or invades adjacent structures: bladder neck, external sphincter, rectum, levator muscles, pelvic wall

286
Q

What is the N classification within TNM staging for prostate cancer?

A

N0: No regional lymph node involvement
NI: Regional lymph node involvement

287
Q

What is the M classification within TNM staging for prostate cancer?

A

MX: Distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis
M1a: Nonregional lymph nodes
M1b: Bone
M1c: other/multiple sites, with or without bone disease

288
Q

What are the management options for prostate cancer?

A
  • OBSERVATION
  • SURGERY
  • RADIOTHERAPY
  • HORMONAL THERAPY
  • CHEMOTHERAPY
289
Q

What are the features of surgical management for prostate cancer?

A
  • Localised disease= radical prostatectomy

- TURP can be used to relieve prostatic symptoms/obstruction

290
Q

When is radiotherapy appropriate management for prostate cancer?

A
  • Alternative to surgery in T1/T2 cancers where PSA is low

- more appropriate for the control of advanced local disease

291
Q

What are the side effects of radiology treatment of prostate cancer?

A
  • dysuria
  • rectal bleeding
  • diarrhoea
  • impotence
  • incontinence
292
Q

What are the indications of hormonal therapy and how does it work in management of prostate cancer?

A
  • ADVANCED DISEASE

- Inhibits endogenous androgens

293
Q

What are examples of hormonal therapies for prostate cancer management?

A
  • LHRH agonists (GOSERELIN + BUSERELIN)
  • Oestrogen therapy
  • Anti-androgens (BICALUTAMIDE, MEGESTROL ACETATE)
  • Bilteral orchidectomy
  • GnRH antagonist
294
Q

What is an example of a chemotherapy drug used to treat prostate cancer?

A
  • docataxel

- cabazitaxel

295
Q

What are the risk factors of testicular cancer?

A
  • Maldescent of testes
  • testicular atrophy
  • family history
296
Q

What is the histology of testicular cancer?

A
  • SEMINOMAS
  • NON-SEMINOMATOUS GERM CELL TUMOURS
  • (malignant teratoma)
  • (combined seminoma/non-seminoma)
  • (yolk sac tumour)
297
Q

Does testicular cancer often spread?

A
  • spread is common via lymphatics to para-aortic nodes

- reflecting the embryological origin from primitive para-renal tissue

298
Q

What is the clinical presentation for testicular cancer?

A
  • painless testicular swelling
  • cough/dyspnoea due to lung mets
  • lower back pain due to para-aortic involvement
299
Q

What are the investigations associated with testicular cancer?

A
  • TUMOUR MARKERS (bHCG and AFP)
  • Orchidectomy
  • CT scanning of chest, abdomen, pelvis
300
Q

What is the Royal Marsden Staging?

A

STAGE 1- Confined to the testicle
STAGE 2- involving para-aortic lymph nodes below the diaphragm
STAGE 3- involving para-aortic lymph nodes above the diaphragm
STAGE 4- involving visceral metastases

301
Q

What is the IGCCC?

A

International prognostic grouping to assess severity of testicular cancer

302
Q

What is the management for testicular cancer?

A
  • SURGERY
  • CHEMOTHERAPY
  • RADIOTHERAPY
303
Q

What are the surgical options for management of testicular cancer?

A
  • orchidectomy (via the inguinal canal)

- resection of residual mass following chemotherapy in metastatic teratoma

304
Q

What are the chemotherapy options for testicular cancer?

A

BEP

  • Bleomycin
  • Etoposide
  • Cisplatin
305
Q

What markers are associated with a poor prognosis?

A
  • Markedly raised AFP
  • bHCG
  • LDH
306
Q

What are the possible sites of primary cancer in cancer of unknown primary?

A

LIVER METS- Colon, lung, breast primaries
LUNG METS- breast, lung, kidney primaries
BRAIN METS- lung, breast, melanoma primaries
BONE METS- breast, bronchus, kidney, prostate, thyroid primaries
PERITONEAL METS- ovary, GI tract, pancreas primaries

HIGH CERVICAL NODE METS- head, neck, thyroid, lung primaries
LOWER CERVICAL NODE METS- head, neck, lung, breast, GI tract primaries
AXILLARY NODE METS- breast, lung, melanoma primaries
INGUINAL NODE METS- ovary, prostate, anorectal, vulval primaries

307
Q

What are the investigations for cancer of unknown primary?

A
  • Full clinical assessment and examination
  • FBC, U+Es, LFTs, calcium, urinalysis
  • CXR
  • Myeloma screen
  • Symptom directed endoscopy
  • CT chest, abdo, pelvis
  • PSA
  • CA125, AFP, bHCG
  • Testicular US
  • Biopsy
308
Q

What is COPD?

A

Airflow limitation/obstruction that is not fully reversible by bronchodilator.

  • It is an ABNORMAL INFLAMMATORY response of the lungs to noxious particles or gases
  • Combines CHRONIC BRONCHITIS, CHRONIC ASTHMA, EMPHYSEMA
309
Q

What is the ratio definition of COPD?

A

FEV1/FVC < 0.7

310
Q

What are the red flag symptoms associated with COPD?

A
  • weight loss
  • effort intolerance
  • waking at night
  • ankle swelling
  • fatigue
  • occupational hazards
  • chest pain
  • haemoptysis
311
Q

What are the three main mechanisms that lead to limitation of airflow in the small airways?

A

1) LOSS OF ELASTICITY and alveolar attachments due to EMPHYSEMA. This reduces the elastic recoil, and airways collapse during expiration
2) INFLAMMATION AND SCARRING which causes the small airways to narrow
3) MUCUS SECRETION that blocks the airways

312
Q

How does cigarette smoking contribute to COPD?

A
  • increased number of neutrophil granulocytes that release elastase and proteases.
  • Inhibits alpha-antitrypsin (anti-protease)
313
Q

What is the MRC Dyspnoea Scale?

A

1- Not troubled by breathlessness except on strenuous exercise

2- Short of breath when hurrying to walking up a slight hill

3- Walks slower than contemporaries on level group because of breathlessness, or has to stop for breath when walking at own pace

4- Stops for breath after walking about 100m or after a few minutes on level ground

5- Too breathless to leave the house, or breathless when dressing or undressing

314
Q

What are the clinical features of COPD?

A

Must be >35 with chronic symptoms of:

  • SOB
  • Wheeze
  • Smoker’s cough
  • White/clear sputum normally but purulent when infective exacerbation
  • Recurrent chest infections
  • History of smoking or occupational exposure
315
Q

What are the clinical signs of COPD?

A
  • cyanosis
  • raised JVP
  • cachexia
  • hyper inflated chest
  • use of accessory muscles
  • pursed lip breathing
  • wheeze or quiet breath sounds
  • peripheral oedema
316
Q

What is cor pulmonale?

A
  • Right heart failure secondary to lung disease

- caused by pulmonary hypertension due to hypoxia

317
Q

What are the features of cor pulmonale?

A
  • peripheral oedema
  • raised JVP
  • systolic parasternal heave
  • a loud pulmonary second heart sound (over 2nd left intercostal space)
  • widening of the descending pulmonary artery on chest X-ray
  • right ventricular hypertrophy on ECG
318
Q

What are subsequent systemic effects of COPD?

A
  • hypertension
  • osteoporosis
  • depression
  • metabolic problems causing weight loss and loss of muscle mass
319
Q

What can be seen in late disease of COPD patients?

A

RESPIRATORY FAILURE
- PaO2<8kPa
OR
- PaCO2> 7kPa

320
Q

What are the differential diagnoses associated with COPD?

A
  • asthma
  • bronchiectasis
  • heart failure
  • lung cancer
  • interstitial lung disease
  • anaemia
  • tuberculosis
321
Q

How is diagnosis of COPD made?

A
  • SPIROMETRY which measures the volume of air that the patient is able to expel after full inspiration
  • spirometry is done post bronchodilator
322
Q

What is FEV1?

A

The volume of air that the patient can exhale in the FIRST SECOND of forced expiration

323
Q

What is FVC?

A

The total volume of air that the patient can forcible exhale in one breath.

324
Q

What is PEF?

A

The greatest flow that can be sustained for 10ms on forced expiation starting from maximal inspiration (monitors conditions of upper/large airways)

325
Q

What other investigations are relevant in COPD?

A

CXR

  • can show over inflation of lungs
  • flattened diaphragms
  • large bullae
  • blood vessels

FBC
- Hb level may be raised due to prolonged hypoxemia

ECG
- in advance cor pulmonale- p waves TALLER and RBBB

326
Q

What are the management options for COPD?

A
  • SMOKING CESSATION
  • Various inhaled therapies
  • Add theophylline to treatment if symptomatic
  • Mucolytics (e.g. CARBOSYSTEINE) for productive cough with excess sputum
  • Oral corticosteroids (prednisolone) for acute exacerbations
  • if >65 prophylactic treatment for osteoporosis
  • Bullectomy or transplant in late stages
  • Nutritional support
  • physiotherapy
  • palliative care
  • annual review
327
Q

What is the pathway for inhaled therapy in COPD?

A

1) SABA (e.g. salbutamol inhaler) or SAMA (e.g. ipratropium)
2) LABA (e.g. salmeterol inhaler)
3) LABA + ICS (e.g. salmeterol plus fluticasone propionate [SERETIDE 500/ Symbicort]
4) LAMA (e.g. tiotropium inhalation powder)

328
Q

What are the indications for LTOT (long term oxygen therapy)?

A
  • PaO2 <7.3kPa when stable
  • 8kPa >PaO2 >7.3kPa when stable AND ONE OF:
    • secondary polycythemia
    • nocturnal hypoxaemia
    • peripheral oedema
    • pulmonary hypertension
329
Q

What is an acute exacerbation of COPD?

A

Sustained worsening with worsening SOB, cough, increased sputum production and change in sputum colour, FEVER

330
Q

What are the investigations for acute exacerbation of COPD?

A
  • Sputum culture in hospital
  • SpO2
  • CXR
  • ABG
  • ECG
  • FBC
  • blood cultures
331
Q

What is the management for acute exacerbation of COPD?

A

1) Nebulised bronchodilators
2) Systemic corticosteroids (PREDNISOLONE 30mg OD 7-14days)
3) Antibiotics (AMOXICILLIN 500mg TDS OR CLARITHROMYCIN 500mg BD)
4) IV THEOPHYLLINE
5) O2 therapy
6) NIV in hypercapnia respiratory failure

332
Q

What are the side effects of beta2-agonists?

A
  • Fine tremor
  • Palpitations
  • Headache
  • Seizure
  • Anxiety
333
Q

What is asthma?

A

A chronic inflammatory condition of the airways. Asthma is characterized by recurrent episodes of dyspnoea, cough and wheeze caused by reversible airway obstruction.

334
Q

What are the three factors that contribute to airway obstruction in asthma?

A

1) Bronchial muscle contraction: triggered by a variety of stimuli
2) Mucosal swelling/inflammation: caused by mast cell and basophil degranulation resulting in the release of inflammatory mediators
3) Increased mucus production

335
Q

What are the different types of asthma?

A

1) EXTRINSIC: definite external cause for asthma

2) INTRINSIC: no causative agent found. Usually starts at middle age

336
Q

What are the triggers for asthma?

A
  • Allergens: house dust mites, animal dander, pollen, fur
  • Pollution
  • Cold air
  • Exercise
  • Emotion
  • Smoking (including passive)
  • URTI
  • Drugs: NSAIDs, beta blockers
337
Q

What are the risk factors for asthma?

A
  • family history of asthma or atopy
  • inner city environment
  • viral infection in early childhood
  • Prematurity and low birth weight
  • maternal smoking
  • smoking
  • work triggers e.g. paint sprays, welders
338
Q

What are the clinical features for asthma?

A
  • Dyspnoea
  • Wheeze (bilateral, expiratory)
  • Cough (often nocturnal)
  • Sputum production
  • disturbed sleep
  • chest tightness
  • Diurnal variation (worse at night)
  • Tachypnoea
  • Hyperinflated chest
  • Hyper-resonant percussion note
  • Diminished air entry
  • Prolonged expiration
  • Increased RR
339
Q

How is asthma diagnosed in children?

A

MAINLY CLINICAL DIAGNOSIS
If symptomatic and there is a high probability of asthma:
- start a trial of bronchodilators and assess response

340
Q

How is asthma diagnosed in adults?

A

MAINLY CLINICAL DIAGNOSIS

  • trial of bronchodilators
  • Spirometry: low FEV1 (FEV1:FVC<0.7) showing obstruction and reversibility
  • PEFR
  • CXR (hyper inflated chest)
341
Q

What is the management for asthma in <5

A

STEP 1: Inhaled SABA
STEP 2: Add ICS or leukotriene antagonist
STEP 3: Add ICS or LRA if not taking it
STEP 4: Refer to Paeds

342
Q

What is the management for asthma in 5-12?

A 
STEP 1: Inhaled SABA
STEP 2: Add ICS (200mcg)
STEP 3: Add LABA. Increase ICS to 400mcg
STEP 4: Increase to 800mcg
STEP 5: Daily OCS. Refer to paeds
343
Q

What is the management for asthma in >12?

A

STEP 1: Inhaled SABA
STEP 2: Add ICS (400mcg)
STEP 3: Add LABA. Increase ICS to 800mcg
STEP 4: Increase to 2000mcg, add LRA, theophylline
STEP 5: Daily OCS. Refer to secondary care

344
Q

What is the primary prevention for asthma?

A
  • avoid triggers, NSAIDs, BB
  • healthy diet, exercising
  • breast feeding during pregnancy
345
Q

What is the secondary prevention for asthma?

A
  • clean to remove dust mites
  • stop smoking
  • weight loss
  • physiology and breathing exercises
346
Q

What are the clinical features of hypertension?

A
  • often asymptomatic
  • sweating
  • palpitations
  • headaches
347
Q

What are the clinical features of severe hypertension?

A
  • headaches
  • epistaxis
  • nocturia
  • SOB due to LVH or HF
  • angina
  • PVD
348
Q

What are the primary causes of hypertension?

A

1) GENETICS
2) LOW FETAL BIRTH WEIGHT
3) LIFESTYLE- (obesity/smoking/alcohol/ stress/anxiety/ salt)
4) METABOLIC SYNDROME
5) HYPERINSULINAEMIA
6) AGE

349
Q

What are the secondary causes of hypertension?

A

1) CONGENITAL (e.g. adrenal hyperplasia, aortic coarctation.)
2) ACQUIRED: renal disease, diabetic neuropathy, chronic glomerulonephritis
3) ENDOCRINE: Conn’s syndrome, adrenal hyperplasia, phaechromocytoma, Cushing’s syndrome, acromegaly
4) Drugs: OCP, NSAIDs, cyclosporin, steroids
5) Pregnancy
6) White coat syndrome

350
Q

How is hypertension diagnosed?

A

ABPM or HBPM (2x daily readings for 7 days)

351
Q

How is hypertension classified?

A

STAGE 1: >140/90mmHg
STAGE 2: >160/100mmHg

SEVERE: >180 systolic OR >110 diastolic

ACCELERATED HTN: 180/110 with signs of papilloedema and/or retinal haemorrhage

POSTURAL HYPOTENSION: Systolic BP decreases by 20mmHg on standing for 1min

352
Q

What are the classifications for hypertension on fundoscopy?

A

KEITH WAGENER

Grade 1: Tortuosity of retinal arteries with increased reflectiveness (silver wiring)

Grade 2: grade 1 + A-V nipping producing when thickened retinal arteries pass over retinal veins

Grade 3: grade 2 + flame haemorrhages and soft exudates due to small infarcts

Grade 4: grade 3 + papilloedema (blurring margins of optic disc)

353
Q

Which of these fundoscopy findings are indicative of malignant hypertension?

A

GRADES 3 + 4

354
Q

What other investigations should be done in hypertension?

A
  • ECG: LVH, haematuria
  • Urine: protein, blood, albumin: creatinine ratio
  • bloods: fasting blood for lipids and glucose, serum total cholesterol and HDL, cholesterol, U+Es, HbA1c
  • CXR: coarctation of aorta
  • Examine funds for HTN retinopathy
355
Q

What are the conservative treatments for hypertension?

A
  • diet (salt, caffeine), exercise, relaxation therapy, alcohol + smoking, local initiatives for healthy living
356
Q

What are the criteria for pharmacological treatments in hypertension?

A

STAGE ONE: Offer treatment if-

  • <80
  • end organ damage
  • CV or renal disease
  • Diabetes
  • 10 year CV risk of >20%

STAGE ONE: <40- specialist evaluation

STAGE TWO: everyone gets treatment

357
Q

What is step 1 in hypertension pharmacological management?

A

AGE <55- ACE INHIBITOR

OR

AGE >55/ AFRO-CARIBBEAN- CALCIUM BLOCKER

358
Q

What is step 2 in hypertension pharmacological management?

A

ACEi + CALCIUM BLOCKER

359
Q

What is step 3 in hypertension pharmacological management?

A

ACEi + CALCIUM BLOCKER + THIAZIDE DIURETIC

360
Q

What is step 4 in hypertension pharmacological management?

A

RESISTANT HYPERTENSION

ACEi + CALCIUM BLOCKER + THIAZIDE DIURETIC + additional DIURETIC OR alpha/beta blocker

361
Q

What should be used if ACEi is not tolerated?

A

ARB

but NEVER combine the two.

362
Q

What should be considered when prescribing an ACEi?

A
  • START LOW DOSE (2.5mg)
  • advise first dose in the evening
  • check renal function (creatinine and eGFR) before upward titration
  • maximum dose 10mg
363
Q

What are the side effects associated with ACEi?

A
  • hypotension
  • persistent dry cough
  • hyperkalaemia
  • cause/ worsen renal failure
364
Q

Where are ACEi contraindicated?

A
  • recurrent angioedema
  • pregnancy
  • breastfeeding
365
Q

What should be considered when prescribing a CCB?

A
  • START LOW (5mg)

- titrate up for 4 weeks until target BP achieved

366
Q

What are the side effects associated with CCB?

A
  • ankle swelling
  • headache
  • flushing
  • nausea
  • dizziness
367
Q

Where are CCBs contraindicated?

A
  • hepatic impairment
  • renal impairment
  • heart failure
  • cardiac outflow obstruction
  • 2nd degree heart block
368
Q

How do CCBs work?

A
  • decreases calcium entry into vascular + cardiac cells, thus reducing intracellular calcium concentration
  • cause relaxation and vasodilation in arterial smooth muscle
  • reduce myocardial contractility
  • suppresses cardiac conduction
369
Q

What should be considered when prescribing thiazide-like diuretic?

A
  • check creatinine, eGFR, U+Es before starting treatment

- recheck in 4-6 weeks after upward titration

370
Q

What are the side effects associated with thiazide-diuretics?

A
  • excessive diuresis
  • hypokalaemia
  • postural hypotension
  • gout
  • DM
  • impotence
  • dizziness
371
Q

When are thiazide-diuretics contraindicated?

A
  • gout
  • refractory hypokalaemia
  • hyponatraemia
  • hypercalcaemia
  • severe hepatic impairment
  • Addison’s
  • pregnancy
  • eGFR
372
Q

What is type 1 diabetes?

A

An absolute insulin deficiency causing persistent hyperglycemia caused by autoimmune destruction of insulin producing beta cells in the pancreatic islets of Langerhans.

373
Q

What are the clinical features of type 1 diabetes?

A

RAPID ONSET (over days/ weeks)

  • polyuria
  • polydipsia
  • weight loss
  • hyperglycemia
  • lack of energy and fatigue
  • ketonuria and breath smelling of ketones
  • infections: UTIs, candida
  • cramps and abdominal pain
374
Q

What is diabetic keto acidosis characterized by?

A
  • nausea and vomiting
  • acidotic breathing
  • ketones on the breath
375
Q

What are the investigations for type 1 diabetes?

A
  • OGTT (oral glucose tolerance test)
  • fasting blood glucose
  • random blood glucose
  • urinalysis (positive for glucose and ketones)
  • bloods: FBC, U+Es, LFTs, TFTs, random lipids and HbA1c
  • Autoantibody test: confirming autoimmune disease
376
Q

OGTT:

A

> 11.1 mmol/l , 2hrs after 75g anhydrous glucose

377
Q

Fasting blood glucose

A

> 7 mmol/l

378
Q

Random blood glucose:

A

> 11 mmol/l

379
Q

HbA1c:

A

> 48mmol/l

380
Q

How is the diagnosis for type 1 diabetes made?

A
  • CLASSICAL SYMPTOMS + 1 raised glucose measurement

- NO CLASSICAL SYMPTOMS + 2 raised glucose measurements

381
Q

What is the conservative management for type 1 diabetes?

A
  • Give dietary advice and offer referral to dietician
  • smoking cessation and reduced alcohol consumption
  • medical emergency ID bracelet
  • advise DVLA of diagnosis (drivers stop every 2 hrs to check glucose)
382
Q

What are the blood sugar targets for type 1 diabetes?

A
  • blood sugar before meals: between 4-7mmol/l

- blood sugar after meals: between 5-9 mmol/l

383
Q

What is available in insulin therapy?

A

1) SHORT ACTING INSULINS: give 15-30mins before meals and in emergencies
2) INTERMEDIATE and LONG ACTING: used to mimic the effect of basal insulin that is secreted continuously.
3) BIPHASIC INSULIN PREPARATIONS: contain a premixed combination of a short acting and an intermediate acting insulin

384
Q

What are the insulin regimes?

A
  • ONCE DAILY: long acting given at bedtime (T2)
  • TWICE DAILY: Biphasic given pre-breakfast and pre-dinner
  • BASAL-BOLUS: Long acting given at bedtime. Short acting before meal times
  • CONTINOUS SUBCUT INSULIN INFUSION: Useful in pts with recurrent hypos, unpredictable lives and delayed meals.
385
Q

What should be checked in the annual review for type 1 diabetes?

A
  • HbA1c levels monitored every 3-6 months
  • Blood pressure (intervene if >140/80)
  • Cholesterol and triglyceride levels
  • Weight monitoring
  • Microalbumin screen- urine albumin:creatinine ratio and blood serum creatinine
  • Kidney damage
  • abdominal adiposity
  • annual retinopathy screening
  • diabetic foot check
  • monitor sexual dysfunction
  • diet advice
  • psychological check
386
Q

What are the metabolic complications associated with T1DM?

A
  • hyperglycaemic ketoacidosis
  • hypoglycaemia
  • dyslipidaemia
387
Q

What are the macrovascular complications associated with T1DM?

A
  • Cardiovascular disease (MI)
  • Cerebrovascular disease (stroke)
  • peripheral vascular disease
388
Q

What are the microvascular complications associated with T1DM?

A
  • retinopathy
  • nephropathy
  • sensory, motor, and autonomic neuropathy
389
Q

What are the psychological complications associated with T1DM?

A
  • depression

- anxiety

390
Q

What are the complications in children and your adults associated with T1DM?

A
  • family conflict

- risky behaviour (non-adherence to recommended management)

391
Q

What are the infective complications associated with T1DM?

A
  • fungal infections

- skin conditions, for example granuloma annulare or necrobiosis diabeticorum

392
Q

What is Type 2 Diabetes Mellitus?

A

Insulin resistance and a relative insulin deficiency result in persistent hyperglycemia

393
Q

What are the risk factors associated with T2DM?

A
  • obesity
  • lack of physical activity
  • calorie and alcohol excess
  • genetic influence (polygenic)
  • history of gestational diabetes
  • impaired glucose tolerance/ impaired fasting glucose
  • drugs
  • smoking
  • PCOS
394
Q

What are the clinical features associated with T2DM?

A
  • polyuria
  • polydipsia
  • weight loss
  • lethargy
  • fatigue
  • blurred vision
395
Q

How is the diagnosis for type 2 diabetes made?

A
  • CLASSICAL SYMPTOMS + 1 raised glucose measurement

- NO CLASSICAL SYMPTOMS + 2 raised glucose measurements

396
Q

What are the investigations for T2DM?

A
  • OGTT >11mmol/l
  • fasting blood glucose >7mmol/l
  • random blood glucose >11mmol/l
  • HbA1c >48mmol/l
397
Q

What is the overall management for T2DM?

A
  • Stepwise approach
  • Diet and lifestyle changes
  • Oral antidiabetic drug
  • Insulin
  • Monitored by measuring the level of HbA1c in the blood, every 3-6 months
  • Every 6 months once blood glucose levels and treatment is stable
398
Q

What is the lifestyle advice associated with T2DM?

A
  • Diabetes education
  • Dietary advice
  • Weight loss if over weight
  • Encourage regular exercise
  • Smoking cessation
399
Q

What is the general process for the administration of oral anti-diabetics?

A

1) Metformin
2) Metformin + gliclazide /sitagliptin/ pioglitazone/emaglifozain
3) Metformin + gliclazine + sitagliptin
4) Insulin therapy

400
Q

What is metformin?

A

A BIGUANIDE that improves responsive to insulin

401
Q

What should be considered when initiating metformin?

A
  • assess renal function
  • starting dose of 500mg OD (with breakfast) for 1 week
  • 500mg BD (with breakfast and dinner) 1 week
  • 500mg TDS (breakfast, lunch, dinner) 1 week
  • maximum daily dose 2g
  • can drink alcohol BUT no more than 1 pint or glass of wine/day
402
Q

What are the contraindications associated with metformin?

A
  • impaired renal function
403
Q

What are the side effects associated with metformin?

A
  • GI side effects
  • abdo pain
  • diarrhoea
  • nausea
  • altered taste
  • lactic acidosis
  • impaired renal function
  • allergic reaction
404
Q

What is gliclazide?

A

A SULFONYLUREA that increases insulin secretion and only effective when some residual pancreatic B-cell function is present

405
Q

What should be considered when starting a sulfonylurea?

A
  • Discuss the possibility of hypoglycaemia and how to minimize the risk (carry sweets)
  • Start with a low dose and titrate up to 1-2 weeks
  • Take in the MORNING with BREAKFAST
  • inform DVLA of medication
  • MAX DOSE: 320mg (2x80mg at breakfast and at dinner)
  • During pregnancy switch to insulin
406
Q

What are the side effects associated with gliclazide?

A
  • hypoglycaemia
  • weight gain
  • stomach ache or indigestion
  • nausea
  • vomiting/diarrhoea
  • constipation
  • allergy= rash swelling
  • GI and liver
407
Q

What are the early warning signs of hypoglycaemia?

A
  • feeling hungry
  • trembling or shaking
  • sweating
  • confusion
  • difficulty concentrating
408
Q

What is sitagliptin?

A

it is a DDP-4 INHIBITOR that causes an increase in insulin secretion.

409
Q

What should be considered when prescribing sitagliptin?

A
  • ONE tablet per day
  • same time every day
  • swallow with glass of water
  • 100mg once daily
410
Q

What are the side effects associated with sitagliptin?

A

VERY FEW

  • headache
  • constipation
  • renal or liver disease
  • allergic reaction
411
Q

What is pioglitazone?

A

a THIAZILODNINEDIONE that increases insulin action.

412
Q

What are the adverse effects associated wth pioglitazone?

A
  • Heart failure
  • oedema
  • fluid retention
  • anaemia
  • fractures
413
Q

What are the contraindications associated with pioglitazone?

A
  • cardiac disease

- severe liver/renal disease

414
Q

What can be used in secondary prevention for diabetes?

A
  • MANAGING THE BLOOD PRESSURE (monitor yearly if no diagnosis of HTN, 4-6months if diagnosis present)
  • STATIN (aim for cholesterol level of <4mmol)
  • ASPIRIN 75mg-
  • diabetic foot exam
  • yearly retinopathy screening
  • assess for renal damage
415
Q

What is epilepsy?

A

Epilepsy is a disorder of the brain characterized by a predisposition to epileptic seizures with at least 2 seizure more than 24 hours apart

416
Q

What is an epileptic seizure?

A

Epileptic seizure is a transient disturbance of consciousness, behaviour, emotion, motor function, or sensation, due to abnormal electrical activity in the brain.

417
Q

What are the risk factors for epilepsy?

A
  • FHx of epilepsy
  • Childhood epilepsy or neurocutaneous syndromes
  • Febrile seizures in childhood
  • Previous intracranial infections, brain trauma or surgery
  • CVA or tumours
418
Q

What are precipitating factors for seizures in epileptics?

A
  • Inadequate sleep
  • alcohol abuse
  • medications: tricyclic antidepressants
419
Q

How are seizures classified?

A
  • SIMPLE: NO loss of consciousness

- COMPLEX: loss of consciousness

420
Q

What are the features of a partial seizure?

A
  • focal onset, with features referable to a part of one hemisphere of the brain
  • focal motor: jerking movements start in the face or hand and spread to the limbs
  • focal sensory: abnormal sensations
  • temporal complex: auras
421
Q

What are the features of generalized seizure?

A
  • simultaneous onset of electrical discharge throughout the cortex
422
Q

What can be seen in a tonic seizure?

A
  • impairment of consciousness and increased muscle tone
423
Q

What can be seen in clonic seizure?

A
  • jerking rhythmically with impairment of consciousness
424
Q

What can be seen in tonic- clonic seizures?

A
  • post-ictal confusion and drowsiness
425
Q

What can be seen in absence seizures?

A
  • pauses and stares for 10 secs
426
Q

What can be seen in myoclonic seizures?

A
  • brief shock like contraction of the limbs, face or trunk
427
Q

What can be seen atonic (akinetic) seizures?

A
  • brief, sudden loss of tone associated with falls, without loss of consciousness.
428
Q

What are the clinical features of epilepsy?

A
  • PRODROME
  • AURAS
  • POST-ICTALLY
  • RESIDUAL SYMPTOMS
429
Q

What is prodrome?

A

Change in mood or behaviour

lasting hours to days, may rarely precede the seizure; not part of the seizure itself.

430
Q

What are auras?

A

Stereotyped perception caused by initial focal electrical events before a partial seizure

  • unexpected tastes
  • smells
  • paraesthesia
  • flashing lights
  • deja vu
431
Q

What can be experienced post-ictally?

A
  • headache
  • confusion
  • myalgia
  • sore tongue
  • temporary weakness after a partial motor
432
Q

How is diagnosis of epilepsy made?

A
  • clinical with collateral history
  • if the diagnosis cannot be established, consider further investigations/referral to an epilepsy specialist
  • Classify epileptic seizures and epilepsy syndrome using a multi-axial diagnostic scheme
  • Consider: description of seizure, seizure type: syndrome and aetiology
433
Q

What investigations are done in epilepsy?

A

TO SUPPORT CLINICAL DIAGNOSIS

  • EEG
  • ECG

TO DETERMINE CAUSE OF EPILEPSY / SEIZURE

  • MRI/CT
  • Bloods
  • urine biochemistry
  • genetic testing
434
Q

What is the management for those with epilepsy?

A
  • REFERRAL (confirm diagnosis within 2 weeks)

- ANTI-EPILEPTIC DRUGS

435
Q

Match the seizure type to the anticonvulsant:

FOCAL SEIZURES

A

CARBAMAZEPINE OR LAMOTRIGINE

436
Q

Match the seizure type to the anticonvulsant:

ABSENCE SEIZURES

A

ETHOSUXIMIDE OR SODIUM VALPROATE

437
Q

Match the seizure type to the anticonvulsant:

TONIC-CLONIC SEIZURES

A

SODIUM VALPROATE (LAMOTRIGINE IF WOCBA)

438
Q

Match the seizure type to the anticonvulsant:

MYOCLONIC SEIZURES

A

SODIUM VALPROATE

439
Q

Match the seizure type to the anticonvulsant:

TONIC/ATONIC SEIZURES

A

SODIUM VALPROATE

440
Q

What should be considered when prescribing sodium valproate?

A
  • 600mg daily in 1-2 divided doses
  • Increase insteps of 150-500mg every 3 days
  • maintenance dose of 1-2g daily
  • monitor liver function
  • avoid abrupt withdrawal
441
Q

When is sodium valproate contraindicated?

A
  • pregnancy
  • hepatic impairment
  • family history of severe hepatic dysfunction
  • acute porphyria
442
Q

What are the side effects associated with sodium valproate?

A
  • nausea
  • gastric irritation
  • weight gain
  • thrombocytopenia
443
Q

What should be considered when prescribing lamotrigine?

A

25mg OD for 14 days

  • increase dose gradually
  • maintenance dose: 100-200mg daily
  • monitory for signs of hypersensitivity syndrome
444
Q

When is lamotrigine contraindicated?

A
  • myoclonic seizures

- hepatic/renal impairment

445
Q

What are the side effects associated with lamotrigine?

A
  • nausea and vomiting
  • diarrhoea
  • dry mouth
  • aggression, agitation
  • headache, drowsiness, dizziness
  • tremor, insomnia, blurred vision, rash
446
Q

What are COMMON INTERACTIONS with anticonvulsants?

A

1) WARFARIN
2) OCP
3) MACROLIDE ANTIBIOTICS
4) SSRIs
5) STATINS

447
Q

What should be done in an annual review for an epileptic patient?

A
  • seizure control
  • adverse effects and compliance with treatment
  • appropriate anti-epileptic drug prescribing
  • any social or psychological issues
  • carer’s skills in managing seizures
  • contraception needs and pregnancy planning
448
Q

What is the management for a tonic-clonic seizure lasting >5mins?

A
  • look for epilepsy card/ jewellry
  • protect them from injury: cushion their head; remove harmful objects from nearby
  • do not restrain them or put anything in their mouth
  • when seizure stops, check airway and put them in the recovery position
  • observe them until they have recovered
  • examine for and manage any injuries
  • arrange emergency admission if it is their first seizure
449
Q

What is the management for status epilepticus seizure lasting >5mins or >3 seizures in 1hr?

A
  • ABCDE
  • Treat with buccal midazolam or rectal diazepam
  • IV lorazepam if in hospital
  • urgent hospital admission if do not respond promptly
450
Q

What is a stroke?

A

Clinical syndrome caused by disruption of blood supply to the brain, characterized by rapidly developing signs of focal/global disturbance of cerebral functions, lasting for >24hrs or leading to death.

451
Q

What is a TIA?

A

Transient ischemic attack which solves in <24hrs.

452
Q

How are strokes classified?

A

1) ISCHAEMIC (85%)

2) HAEMORRHAGIC (15%)

453
Q

What are the features of ischemic stroke?

A
  • THROMBOTIC: a blood clot spontaneously forms in an artery in the brain- a common complication of atherosclerosis
  • EMBOLIC: part of the fatty material from an atherosclerotic plaque or a clot in a larger artery or heart travels downstream.
    Common complications of AF and atherosclerosis of the carotid arteries.
454
Q

What are the features of haemorrhagic stroke?

A
  • INTRACEREBRAL: bleeding from a blood vessel within the brain (HTN main cause)
  • SUBARACHNOID: bleeding from blood vessel between the surface of the brain and the arachnoid tissues that cover the brain
455
Q

What are the risk factors associated with stroke?

A
  • HTN
  • smoking
  • excess alcohol
  • obesity
  • DM
  • heart disease
  • past TIA/ stroke
  • contraceptive pill
  • hyperlipidemia, hypercholestrolaemia
  • polycythemia
  • clotting disorders
456
Q

What are the 4 main presenting areas for stroke in the brain?

A

1) TACS
2) PACS
3) POCS
4) LACUNAR STROKE

457
Q

Where does a TACS affect?

A

TOTAL ANTERIOR CIRCULATION stroke

  • large cortical stroke
  • MCA/ACA territory
458
Q

How does a TACS present clinically?

A
  • unilateral weakness and/or sensor disturbance of arm/leg
  • homonymous hemianopia
  • higher cerebral dysfunction (dysphasia, visuospatial disorder)
459
Q

Where does a PACS affect?

A

PARTIAL ANTERIOR CIRCULATION stroke

  • cortical stroke
  • MCA/ACA territory
460
Q

How does a PACS present clinically?

A

TWO of:

  • unilateral weakness and/or sensor disturbance of arm/leg
  • homonymous hemianopia
  • higher cerebral dysfunction (dysphasia, visuospatial disorder)
461
Q

Where does a POCS affect?

A

POSTERIOR CIRCULATION stroke

  • brain stem
  • cerebellum
  • occipital lobe
462
Q

How does a POCS present clinically?

A

ONE of:

  • cerebellar or brainstem syndrome
  • loss of conciousness
  • isolated homonymous hemianopia
463
Q

Where does a LACS affect?

A

LACUNAR stroke

- subcortical stroke

464
Q

How does a LACS present clinically?

A

ONE of:

  • unilateral weakness and/or sensory deficit to face and arm, arm and leg, or all three
  • pure sensory stroke
  • ataxic hemiparesis
465
Q

What are the clinical features associated with stroke?

A
  • facial weakness (one side 2/3 forehead spared)
  • unilateral weakness
  • sensory loss
  • speech problems
  • visual defects (amaurosis fugax)
  • perception and balance
  • coordination disorder
466
Q

Match the clinical feature to the corresponding structure involved:
HEMIPARESIS/ TETRAPARESIS

A

CORTICOSPINAL TRACTS

467
Q

Match the clinical feature to the corresponding structure involved:
SENSORY LOSS

A

MEDIAL LEMNISCUS AND SPINOTHALAMAIC TRACTS

468
Q

Match the clinical feature to the corresponding structure involved:
DIPLOPIA

A

OCULOMOTOR SYSTEM

469
Q

Match the clinical feature to the corresponding structure involved:
FACIAL NUMBNESS

A

5TH NERVE NUCLEI

470
Q

Match the clinical feature to the corresponding structure involved:
FACIAL WEAKNESS

A

7TH NERVE NUCLEUS

471
Q

Match the clinical feature to the corresponding structure involved:
NYSTAGMUS, VERTIGO

A

VESTIBULAR CONNECTIONS

472
Q

Match the clinical feature to the corresponding structure involved:
DYSPHAGIA, DYSARTHRIA

A

9TH AND 10TH NERVE NUCLEI

473
Q

Match the clinical feature to the corresponding structure involved:
DYSARTHRIA, ATAXIA, HICCUPS, VOMITING

A

BRAINSTEM AND CEREBELLAR CONNECTIONS

474
Q

Match the clinical feature to the corresponding structure involved:
HORNERS SYNDROME

A

SYMPATHETIC FIBER

475
Q

Match the clinical feature to the corresponding structure involved:
COMA, ALTERED CONSCIOUSNESS

A

RETICULAR FORMATION

476
Q

Match the clinical feature to the corresponding structure involved:
LOCKED IN

A

BRAINSTEM

477
Q

Match the clinical feature to the corresponding structure involved:
PURE MOTOR/SENSORY

A

LACUNAR

478
Q

What are the features of an UPPER neurone stroke?

A

tone: INCREASED
atrophy: ABSENT
fasciculation: ABSENT
reflex: HYPERACTIVE
babinski: PRESENT

479
Q

What are the features of a LOWER neurone stroke?

A

tone: DECREASED/ABSENT
atrophy: PRESENT
fasciculation: PRESENT
reflex: DECREASED/ABSENT
babinski: ABSENT

480
Q

What are the differential diagnoses associated with stroke symptoms?

A
  • MS
  • Migraine with/without aura
  • Epilepsy
  • Syncope
  • Hypo/hyperglycaemia
  • Hypercalcaemia
  • Subdural haemorrhage
  • Beauty parlor syndrome (bending neck back occluding blood vessels at base of the neck)
481
Q

When should brain imaging be performed IMMEDIATELY with acute stroke?

A
  • indications for thrombolysis or early anticoagulation treatment
  • on anticoagulant
  • known bleeding tendency
  • depressed level of consciousness (GCS<13)
  • unexplained progressive/fluctuating symptoms
  • papilloedema, neck stiffness or fever
  • severe headache at onset of stroke symptoms

IN ABSENCE OF THESE IMAGE WITHIN 24hrs

482
Q

What other investigations should be done in someone presenting with stroke symptoms?

A
  • FBC
  • BM (glucose)
  • ESR
  • U+Es
  • BP
  • ECG
483
Q

What is the stroke risk assessment tool used in patients with TIA?

A

ABCD2 score

484
Q

What is the ABCD2 score?

A

A- Age: >60 (1pt)

B- Blood pressure: >140/90mmHg (1pt)

C- Clinical features: unilateral weakness (2pts), speech disturbance without weakness (1pt)

D- Duration of symptoms: >60mins (2pts), 10-59mins (1pt)

D- Diabetes (1pt)

485
Q

What is classified as HIGH risk of an early stroke?

A
  • ABCD2: >4
  • AF
  • More than one TIA in one week
  • A TIA whilst on an anticoagulant
486
Q

What is the management for a TIA patient at high risk for an early stroke?

A
  • ASPIRIN 300mg immediate
  • Refer for specialist assessment TIA clinic within 24h
  • Carotid ultrasound
487
Q

What is classified as LOW risk of an early stroke?

A
  • ABCD2: <3

- Present >1 week after their last symptoms have resolved

488
Q

What is the management for a TIA patient at low risk of an early stroke?

A
  • ASPIRIN 300mg immediate

- Refer for a specialist assessment within one week

489
Q

What is the overall management for TIA patients?

A
  • MRI
  • Assess risk factors
  • CLOPIDOGREL 300mg loading dose
  • CLOPIDOGREL 75mg daily
  • STATIN (ATORVASTATIN 40mg)
  • ## If patient has GI disease, prescribe a PPI
490
Q

What should be done in the follow up after TIA?

A
  • Follow up should be arranged within 1 month
  • Annually in primary care
  • Check and optimise lifestyle measures
  • annually check and record BP and lipid profile
  • arrange pre winter flu jab
491
Q

What is the acute management for a stroke?

A
  • Ensure patient airway
  • Monitor blood glucose (maintain 4-11mmol)
  • Monitor BP
  • Give O2 if sats fall <95%
  • NBM until swallowing assessed
  • Keep hydrated: IV fluid
  • FBC, U+E, cholesterol, glucose, TFT, INR
492
Q

What medication should be used in ischaemic stroke?

A

THROMBOLYSIS- Alteplase

ASPIRIN 300mg- orally, rectally, enteral tube

493
Q

When should alteplase be prescribed?

A
  • treatment 4.5 hours of onset of stroke symptoms
  • intracranial haemorrhage has been excluded
  • calculated 0.9mg/KG up to 90mg
  • cardiac monitoring
  • regular BP
  • 24hr after finishing course, CT to check for bleeding
494
Q

What are the contraindications for alteplase?

A
  • WARFARIN

- MEDICAL PROCEDURE IN THE LAST 10 DAYS

495
Q

What is the medical management for an embolic stroke?

A
  • Full dose anticoagulation treatment
  • Give a PPI if previous dyspepsia
  • Statin: 48 hours after acute stroke
  • Carotid imaging and carotid endarterectomy
  • Control BP and cardiovascular risk factors
496
Q

What is the medical management for a haemorrhagic stroke?

A
  • Refer to neurosurgery
  • Decompressive hemicraniectomy for MCA involvement
  • Always consider subarachnoid haemorrhage if thunderclap headache
497
Q

What is the conservative management associated with stroke?

A
  • Stop smoking
  • Cardioprotective diet, including reducing salt intake
  • regular exercise
  • reduce alcohol consumption
  • achieving and maintain a satisfactory BMI
498
Q

What is the definition of chronic kidney disease?

A

CKD= GFR <60 for >3months

OR

GFR>60 together with the presence of kidney damage, present for >3months

499
Q

What are the causes of CKD?

A

1) Diabetic nephropathy
2) Congenital and inherited disease (PCKD)
3) Glomerular disease
4) Vascular disease
5) Tubulointerstitial disease
6) Urinary tract obstruction (e.g. prostatic disease)
7) Cardiovascular causes (HTN, heart failure)
8) Nephrotoxic drugs (NSAIDs)
9) Unknown

500
Q

What are the risk factors associated with CKD?

A
  • DM
  • Age >60
  • recurrent UTIs
  • urinary obstruction
  • systemic illness that effects the kidneys
501
Q

What are the clinical features associated with CKD?

A

often ASYMPTOMATIC but picture often shows common symptoms when Urea >40mmol/l

  • Urea >60mmol/L- there are severe uremic symptoms and CNS involvement
  • incidental finding
  • Monitoring at risk individuals
502
Q

What are the clinical signs of uremia?

A
  • short stature
  • brown discoloration of the nails
  • fluid overload: pleural effusion
  • pericardial friction rub
  • mitral regurgitation
  • glove and stocking peripheral sensory loss
  • High BP
503
Q

What are the clinical signs associated with CKD?

A
  • impalpable kidneys unless PCKD, tumour, obstruction
  • cutaneous vasculitic lesions in systemic vasculitis
  • retinopathy in diabetes
  • evidence of PVD
  • evidence of spinal bifida or other causes of neurogenic bladder
  • hydration status- JVP, cap refill, turgor
504
Q

What are the complications of CKD?

A

1) Anaemia
2) Renal osteodystrophy
3) Pruritis
4) Nephrogenic systemic fibrosis
5) fluid overload
6) GI problems
7) Gout and DM
8) Endocrine
9) Muscles
10) Nervous system: seizures
11) CV: increased risk of MI, HF, sudden death
12) Malignancy

505
Q

What are examples of nephrotoxic drugs (DIAMOND H)?

A 
D- Diuretics
I- Iodine
A- Aminoglycosides (gentamicin)
M- Metformin
O- Opiates
N- NSAIDs
D- Digoxin

H- Heparin

506
Q

What BLOOD investigations should be done in CKD?

A

BLOODS

  • FBC (low Hb, normocytic, normochromic), eosinophilia
  • ESR (raised)
  • U+E (low eGFR)
  • metabolic acidosis
  • immunology
507
Q

What should be checked for in URINALYSIS for CKD?

A
  • haematuria
  • proteinuria
  • urinary ACR
508
Q

What other investigations should be done in CKD?

A
  • ECG
  • US
  • AXR: renal stones
  • CT: retroperitoneal fibrosis
  • RENAL BIOPSY
  • bone scan
509
Q

How is CKD diagnosed?

A
  • eGFR persistently <60 and/or ACR persistently <3
510
Q

What is the normal function of the kidney?

A 
EXCRETE
- inorganic substances (potassium, phosphate)
- organic substances (urea, creatinine)
- larger molecules
HOMEOSTASIS
- fluid balance etc
PRODUCE- erythropoetin- makes RBCs
Helps bone formation
Affects blood pressure (renin)
511
Q

What is the conservative management for CKD?

A

MONITOR eGFR REGULARLY AND PROTEINURIA ANNUALLY

  • Manage CVD risk factors
  • Treat underlying cause
  • Slow progression
  • Treat complications
  • Refer to specialist at stage 4
  • Stop nephrotoxic drugs
512
Q

What are the other forms of management for CKD?

A

1) HAEMODIALYSIS
2) HAEMOFILTRATION
3) PERITONEAL DIALYSIS
4) KIDNEY TRANSPLANT
5) CONSERVATIVE/PALLIATIVE CARE

513
Q

What are the GFR stages of kidney disease?

A 
G1- >90 (normal)
G2- 60-89 (mild reduction)
G3a- 45-59 (mild-moderate reduction)
G3b- 30-44 (moderate-severe reduction)
G4- 15-29 (severe reduction)
G5- <15 (kidney failure)

(Above 60 is essentially normal unless they have associated kidney disease)

514
Q

What are the ACR stages of kidney disease?

A

A1- <3 (normal- mildly increased)
A2- 3-30 (moderately increased)
A3- >30 (severely increased)

515
Q

What are the risk factors associated with coronary heart disease?

A
  • hypercholesterolaemia
  • smoking
  • hypertension
  • diabetes
  • age
  • low blood LDL
  • high blood triglyceride
  • insulin resistance
  • overweight
  • physical inactivity
  • diet high in fat, sodium and sugar
  • stress, lack of social support, depression, anxiety
  • alcohol
  • social class
516
Q

What are the clinical features associated with coronary heart disease?

A
  • chest pain radiating to the neck, left shoulder and arm
  • exertion dyspnoea
  • fatigue on exertion
  • arrhythmias
  • heart failure
  • stable angina
517
Q

What investigations should be done in coronary heart disease?

A
  • BMI, BP, CV examination
  • ECG (normal at rest, pathological Q waves, LBBB, ST depression/elevation, T-wave flattening/elevation)
  • Bloods: FBC, HDL, LDL, cholesterol, U+Es, TFTs, troponin
  • ECHO
518
Q

What is the management for coronary heart disease?

A
  • Assess lifestyle
  • Explain angina
  • GTN spray
  • Beta blocker (ATENOLOL)
  • ASPIRIN/CLOPIDOGREL 75mg
  • ACEi
  • STATIN
  • Angioplasty
519
Q

How should a GTN spray be taken?

A
  • When an attack occurs, stop and rest
  • Use GTN spray/tablet
  • Take a second dose after 5 mins if not setled
  • Call 999 if not settled 5 mins after 2nd dose
  • Take third dose
520
Q

What are the side effects associated with GTN spray?

A
  • Transient hypotension
  • Headache
  • Burning/stinging/ tingling in the mouth
521
Q

What are the main interactions associated with GTN?

A

PHOSPHODIESTERASE INHIBIOTS (sildenafil/tadalafil/vardenafil)

  • can produce excessive hypotension
  • may precipitate myocardial infarction
522
Q

What should be done in an CHD review in primary care?

A
  • ongoing symptoms of angina (at rest or with exercise)
  • Assess CVD risk and any modifiable CV risk factors
  • Any complications of angina treatment and provide information
  • Review medication
  • Mood
523
Q

What is AF?

A

A cardiac arrhythmia with:

  • irregular RR intervals
  • no distinct P waves on the surface ECG
  • rapid and chaotic atrial activity
524
Q

How is AF classified?

A

1) INITIAL
2) PAROXYSMAL
3) PERSISTENT
4) LONG STANDING PERSISTENT
5) PERMANENT

525
Q

What are the features of initial episode of AF?

A

AF >30s diagnosed by ECG

526
Q

What are the features of paroxysmal AF?

A

recurrent >2 episodes that terminate within 7 days

527
Q

What are the features of persistent AF?

A
  • continuous >7 days

- AF> 48h which decision made to perform CV

528
Q

What are the features of longstanding persistent AF?

A

Continuous AF of >12 months duration

529
Q

What are the features of permanent AF?

A
  • Where a joint decision has been made by patient and clinician to stop further attempts to restore/maintain sinus rhythm
530
Q

What are the clinical features of AF?

A
  • Palpitations
  • SOB
  • fatigue
  • dizziness
  • syncope
  • decreased exercise capacity
  • left ventricular function
531
Q

What are associated conditions with AF?

A
  • HTN
  • HF
  • diabetes, obesity
  • sleep apnea, chronic lung disease
  • valvular heart disease
  • congenital heart disease
  • coronary artery disease
  • hyperthyroidism
  • chronic kidney disease
  • infection
  • atrial flutter and SVT
532
Q

What is the purpose CHADSVASC?

A

A score to aid in stroke prevention

533
Q

What is CHA(2)DS(2)VASC?

A 
C- Congestive hear failure
H- HTN
A- Age >75
D- Diabetes
S- Stroke/TIA
V- vascular disease
A- Age 65-74
Sc- Sex Category (F)
534
Q

What are the objectives of treatment of AF?

A
  • Stroke prevention
  • Symptom relief
  • Ventricular rate control
  • Correction of rhythm disturbance
  • Optimal management of cardiovascular disease
535
Q

What are the investigations associated with AF?

A
  • ECG: 24h ambulatory
  • Bloods: FBC, U+Es, TFTs, LFTs, coagulation screen
  • Transthoracic ECHO if murmur
536
Q

What is the management of AF?

A

1) ANTICOAGULATION
2) RATE CONTROL
3) RHYTHM CONTROL

537
Q

What is the anticoagulation treatment for AF?

A
  • warfarin

- NOAC (APIXABAN, DABIGATRAN, RIVAROXABAN

538
Q

What is used for rate control in treatment for AF?

A

BETA BLOCKERS

  • BISOPROLOL
  • ATENOLOL
  • PROPRANOLOL

RATE LIMITING CCB

  • DILTIAZEM 60mg TDS
  • DIGOXIN (only in non-paroxysmal AF)
539
Q

What are the side effects associated with beta blockers?

A
  • bradycardia
  • cold extremities
  • sleep disturbance
  • fatigue
  • sexual dysfunction
540
Q

What are the side effects associated with CCBs?

A
  • dizziness
  • AV block
  • palpitations
  • GI disorders
  • erythema
  • malaise
  • fatigue
541
Q

What methods are used for rhythm control?

A
  • BETA BLOCKERS (amiodarone, flecainide, propafenone)
  • CARDIOVERSION
  • CATHETER LEFT ATRIAL ABLATION
542
Q

What is heart failure?

A

A complex syndrome resulting from a structural or functional cardiac disorder that impairs the pumping ability of the heart and the heart’s ability to maintain the circulation of blood

  • inadequate cardiac output
  • peripheral under perfusion
543
Q

What are the three main classifications of heart failure?

A

1) LEFT VENTRICULAR SYSTOLIC DYSFUNCTION
2) RIGHT VENTRICULAR FAILURE
3) CONGESTIVE CARDIAC FAILURE

544
Q

What are the cardiac muscle causes of heart failure?

A
  • Coronary artery disease
  • hypertension
  • cardiomyopathies
  • toxins
  • DM, hypo/hyperthyroidism, Cushing’s
  • Adrenal insufficiency, excessive growth hormone
  • Sarcoidosis, amyloidosis, hemochromatosis
545
Q

What are the low cardiac output causes of heart failure?

A
  • hypertension
  • arrhythmias
  • pericardial diseases
  • aortic stenosis
546
Q

What are the high cardiac output causes of heart failure?

A
  • anaemia
  • thyrotoxicosis
  • septicaemia
  • liver failure
  • AV shunts
  • paget’s disease
  • Thiamine deficiency
547
Q

What are the clinical features associated with heart failure?

A
  • BREATHLESSNESS (orthopnea, PND)
  • FATIGUE
  • FLUID RETENTION
  • NOCTURIA, cold peripheries
  • nocturnal cough
  • chest pain, tightness and palpitations
548
Q

What are the clinical signs associated with heart failure?

A
  • laterally displaced apex beat
  • raised JVP
  • hepatomegaly
  • third/fourth heart sound (gallop rhythm)
  • tachycardia
  • pulmonary crepitations
  • dependent oedema: legs, sacrum, ascites
  • anorexia, cachexia
549
Q

What is the New York Classification system of heart failure symptoms?

A

CLASS 1- no limitations
CLASS 2- slight limitation of physical activity
CLASS 3- marked limitation of physical activity
CLASS 4- symptoms of heart failure are present even at rest

550
Q

What are the investigations for heart failure if there has been previous MI?

A

ECHO to assess:

  • LV systolic function
  • diastolic function (HFPEF)
  • LV wall thickness
  • Valvular disease
  • pulmonary artery systolic pressure
  • BNP
551
Q

What are the investigations for heart failure if there has been NO previous MI?

A
  • BNP and NT-proBNP
  • if BNP >100 refer and assess <6 weeks
  • if BNP>400 refer and ECHO <2 weeks
12 lead ECG
Bloods: FBC, U+E, creatinine, TFT, LFT
Urinalysis
Lung function tests (peak flow, spirometry)
CXR
552
Q

What can be seen on chest X ray of heart failure patients (ABCDE)?

A 
A- Alveolar oedema (bat wings)
B- kerley B lines
C- Cardiomegaly
D- Dilated prominent upper lobe vessels (tram lines)
E- pleural Effusion
553
Q

What is the conservative management for heart failure?

A
  • weight control
  • reduce salt intake
  • restrict alcohol
  • restrict fluid intake
  • aerobic exercise
  • smoking cessation
  • sexual activity
  • flu vaccine
  • heart failure nurses
554
Q

What is the pharmacological treatment for heart failure?

A

1) DIURETIC
2) ACEi
3) BETA BLOCKER
4) ALDOSTERONE ANTAGONIST
5) IVABRADINE
6) DIGOXIN
7) AMIODARONE
8) AMLODIPINE
9) WARFARIN
10) ASPIRIN

555
Q

What should be considered when prescribing diuretic in HF?

A
  • LOOP diuretics are preferred
  • FUROSEMIDE 40mg
  • BUMETANIDE 1mg

Monitor renal function and serum electrolytes before starting treatment and 1-2 weeks after starting treatment

556
Q

What are the interactions with diuresis in HF Management?

A
  • Lithium
  • digoxin
  • phenytoin
  • theophylline
557
Q

What are the adverse effects associated with HF?

A
  • orthostatic hypotension
  • dehydration
  • renal dysfunction
  • electrolyte imbalances
  • hyperuricaemia
  • precipitate/ aggravate gout
558
Q

What should be considered when starting ACEi for HF?

A

It is the FIRST line therapy

  • RAMIPRIL 2.5mg OD
  • ENALAPRIL, LISINOPRIL, TRANDOLAPRIL

START LOW AND TITRATE UP

Monitor renal function and serum electrolytes before starting treatment and 1-2 weeks after starting treatment
monitor 1-2 weeks after increased dose
monitor every 6 months when stable

559
Q

What are the adverse effects associated with ACEi in HF?

A
  • orthostatic hypotension

- dry cough

560
Q

What should be offered as an alternative in a chronic cough?

A

ARB

  • candesartan
  • losartan
  • valsartan

hydralazine if ARB not tolerated

561
Q

What should be considered when prescribing a beta blocker in HF?

A

FIRST line in combination with ACEi
BISOPROLOL 1.25mg-10mg, (carvedilol, nebivolol)

start on low dose and aim to increase

Monitor clinical status for symptoms and signs of HF

562
Q

What are the associated adverse effects of beta blockers in HF?

A
  • Deteriorating symptoms of heart failure
  • hypotension
  • bradycardia
  • sexual dysfunction
  • cold extremeties
  • paraesthesia
  • asthenia
  • sleep disturbance
  • depression
563
Q

When should aldosterone antagonist be added?

A

If diuretic+ ACEi + BB is not effective

564
Q

What aldosterone antagonist should be used?

A

SPIRONOLACTONE 25mg-50mg OD
or
EPLERENONE

565
Q

What are the adverse effects associated with aldosterone antagonist?

A
  • HYPERKALAEMIA
  • GYNACOMASTIA
  • fatigue
  • GI disturbances
  • menstrual disruption
  • skin symptoms
  • blood disorders
566
Q

What is Ivabradine?

A
  • heart rate lowering drug

- to be considered when beta-blockers are contraindicated

567
Q

What are the doses used for digoxin?

A

125 micrograms to 250 micrograms

568
Q

What are the non pharmacological treatments for HF?

A
  • revascularisation (CABG or PCI)
  • surgical repair of valves
  • cardiac resynchronization therapy
  • LVADs
  • heart transplant
  • ICDs
569
Q

What should be covered in the annual review for heart failure?

A
  • Assess functional capacity (NYHA)
  • Assess fluid status
  • Assess cardiac rhythm
  • Assess mood for signs of depression/anxiety
  • FBC, U+Es, LFTs, clotting, TFTs
  • ADLs and level of social support
  • Review management plan
  • Discuss palliation and end of life if appropriate
570
Q

When should an urgent referral be made in LUNG cancer?

A
  • haemoptysis
  • > 3wk history of significant resp. signs
  • persistent hemoptysis in smokers/ex-smokers >40
  • CXR suggestive of lung cancer
571
Q

When should an urgent referral be made in BREAST cancer?

A
  • lump: discrete, hard with fixation, with/without skin tethering
  • > 30 with discrete lump
  • <30 with lump that enlarges
572
Q

When should an urgent referral be made in PROSTATE cancer?

A
  • Hard, irregular prostate felt on DRE

- LUTS symptoms and high PSA

573
Q

When should an urgent referral be made in TESTICULAR cancer?

A
  • any patient with a swelling or mass in the body of the testis
574
Q

When should an urgent referral be made in COLORECTAL cancer?

A
  • > 40, rectal bleeding, change in bowel habit, increased frequency >6weeks
  • > 60, rectal bleeding for >6 weeks OR change in bowel habit without anal symptoms
  • palpable rectal mass
  • any man with unexplained iron deficiency anaemia and <11g/100ml
  • non-menstruating woman with unexplained iron deficiency anaemia and Hb <10
575
Q

What is the pathophysiology of MS?

A
  • DEMYELINATION of neurones causes scar tissue to form, allowing or blocking signals to and from the brain and spinal cord affecting movement and sensation
576
Q

What are the patterns of MS?

A
  • RELAPSING/REMITTING
  • Secondary progressive MS
  • Primary progressive MS
  • Acute attacks are followed by periods of remission when there is remyelination but this process fails
577
Q

What is the clinical presentation of MS?

A
  • MONOSYMPTOMATIC
  • disturbances in vision, hearing, balance, sensation
  • deteriorating mental health
  • numbness
  • weakness
  • bladder (incontinence/ urinary retention)
578
Q

How is the diagnosis of MS made?

A
  • clinical
  • MRI can exclude other causes and show plaques
  • CSF: oligoclonal IgG can indicate CNS inflammation
  • MOG/MBP antibodies
579
Q

What is the management of MS?

A
  • INTERFERON BETA (reduces relapses and reduces lesion accumulation)
  • MONOCLONAL ANTIBODIES (Natalizab
  • METHYLPREDNISOLONE 1g OD IV/PO
580
Q

What is the pathophysiology for MND?

A

Degenerative condition affecting the ANTERIOR HORN CELLS of the SPINAL CORD and MOTOR CRANIAL NUCLEO
Affects both upper and lower motor neurones

581
Q

What is the clinical presentation of MND?

A
  • weakness, stiffness, cramping
  • often focal onset, limb, bulbar or respiratory
  • LMN signs tend to be predominant with a mixed picture
582
Q

What is the management of MND?

A

RILUZOLE may prolong life by 2-4 months
- muscle cramps can be treated with diazepam/beclofen

survival usually 3-5 years

583
Q

What is the pathophysiology of Parkinson’s disease?

A
  • Movement disorder due to degeneration of the DOPAMINERGIC NEURONES in the SUBSTANTIA NIGRA which causes decrease in striata dopamine levels
584
Q

What are the risk factors of Parkinson’s disease?

A
  • Increasing prevalence with age
  • Slightly more common in males
  • Smoking
  • Pesticide exposure
585
Q

What are the clinical features associated with Parkinson’s disease?

A
  • insidious onset
  • reduced dexterity
  • fixed facial expression
  • quiet voice
  • tremor
  • rigidity
  • bradykinesia
586
Q

What is the classic triad of signs:

A

1) TREMOR: worse at rest, pin-rolling action of thumb over fingers
2) RIGIDITY: increased tone ‘cogwheel rigidity’
3) BRADYKINESIA/HYPOKINESIA: slowness of movement initiation- reduced arm swing and shuffling steps in gait

587
Q

What are the non-motor features associated with Parkinson’s disease?

A
  • Anosmia
  • Depression
  • Dementia
  • Visual hallucinations
  • Dribbling saliva
  • Postural instability
  • REM behavioural sleep disorder
  • mild urinary frequency and urgency
588
Q

What investigations should be done in Parkinson’s disease?

A

Diagnosis based on clinical history and examination

- investigations can be used to exclude alternative diagnosis: CT or MRI

589
Q

What is the management for Parkinson’s disease?

A
  • LEVODOPA (sine met, madopar)
  • DOPAMINE AGONISTS (pramipexole, bromocrpitine, cabergoline)
  • MAOBIs (selegiline, rasagiline)
590
Q

What is the progression for Parkinison’s disease?

A
  • Festinating gait, worsening of earlier symptoms
  • Parkinson’s related dementia now more common
  • mean duration: 15 years
591
Q

What is the pathophysiology of osteoarthritis?

A
  • joint pain associated by varying degrees of physical limitation
  • peripheral joints are more affected
  • occurs in synovial joints and is characterized by LOSS OF CARTILAGE with accompanying PERIARTICULAR BONE response
  • inflammation to the articular and periarticular bones
592
Q

What are the risk factors of OA?

A
  • GENETIC FACTORS
  • Ageing
  • female sex
  • obesity
  • bone density
  • joint injury
  • occupation/recreational stresses
593
Q

What are the clinical symptoms associated with OA?

A

JOINT PAIN

  • exacerbated by exercise
  • relieved by rest
  • pain worse at the end of the day
  • rest and night pain can occur in advance OA
  • knee pain due to OA is usually bilateral
  • hip pain felt in groin and anterior/lateral thigh

JOINT STIFFNESS in the morning or after rest
- reduced joint function

594
Q

What are the clinical signs associated with OA?

A
  • reduced range of movement
  • joint swelling/synovitis
  • periarticular tenderness
  • crepitus
  • joint instability
  • muscle weakness/ wasting around the affected joint
  • Bony swelling and deformities due to osteophytes:
  • HEBERDEN’S NODES: DIP swelling
  • BOUCHARD’S NODES: PIP swelling
595
Q

What are the investigations associated with OA?

A
  • Clinical examination
  • Plain x-rays LOSS (Loss of joint space, Osteophytes, Subarticular sclerosis, Subchondral cysts)
  • Blood tests: CRP slightly raised
  • MRI
  • Arthroscopy
  • Aspiration of synovial fluid
596
Q

What is the conservative management of OA?

A
  • weight loss
  • exercises to improve muscle strength and joint stability
  • keep active
  • physiotherapy, hydrotherapy
597
Q

What is the pharmacological management of OA?

A
  • paracetamol
  • topical NSAIDs
  • Opioid analgesics (codeine)
  • Oral NSAIDs (co-prescribe PPI)
  • intraairticular steroid injections
  • surgical: joint replacement
598
Q

What is the pathophysiology of RA?

A
  • RA is a common chronic inflammatory autoimmune disease characterized by an inflammation of the synovial joints leading to joint and periarticular tissue destruction
  • Causes chronic symmetrical polyarthritis with systemic involvement due to synovial inflammation
  • Rheumatoid factor self aggregate and form immune complex and result in synovitis
599
Q

What are the causes of rheumatoid arthritis?

A
  • HLA DR4 AND DR1 have a strong association
600
Q

What are the risk factors associated with rheumatoid arthritis?

A
  • women before menopause
  • smoking
  • possible infective aetiology
  • onset is more common in winter
601
Q

What are the clinical symptoms associated with rheumatoid arthritis?

A
  • symmetrical swollen, painful, stiff small joints of the hands and feet
  • worse in the MORNING
  • NORMOCYTIC NORMOCHROMIC ANAEMIA
  • Joint inflammation: heat, redness, pain, swelling, stiffness
602
Q

What are the early clinical signs of rheumatoid arthritis?

A
  • inflammation, no joint damage
  • swollen MCP, PIP, wrist, MTP joints
  • look for tenosynovitis or bursitis
603
Q

What are the late clinical signs of rheumatoid arthritis?

A
  • joint damage and deformity
  • Ulnar deviation of the fingers and dorsal wrist sublaxation
  • Boutonniere’s deformities of the fingers: flexed PIP, extended DIP
  • Swan neck deformities of the fingers: hyperextended PIP, flexed DIP
  • Z- deformities of thumbs
  • Hard extensor tendons
  • foot changes
  • muscle wasting and tendon rupture
604
Q

What are the extra-articular signs of rheumatoid arthritis?

A
  • Rheumatoid nodules
  • lymphadenopathy
  • vasculitis
  • fibrosis alveolitis
  • pleural and pericardial effusion
  • Raynaud’s disease
  • carpel tunnel syndrome
  • peripheral neuropathy
  • splenomegaly
  • scleritis, episcleritis
  • osteoporosis
  • amyloidosis
605
Q

What are the blood test investigations associated with rheumatoid arthritis?

A
  • Rheumatoid factor is positive in >70%
  • NORMOCYTIC NORMOCHROMIC ANAEMIA in chronic disease
  • Raised ESR, CRP, platelets and plasma viscosity
  • Anti-cyclic citrulinated peptide antibodies (anti-CCP)
606
Q

What can be seen on Xray in rheumatoid arthritis?

A
  • soft tissue swelling
  • juxta-articular osteopenia
  • reduced joint space
  • erosions, sublaxation or complete carpal destruction
607
Q

How is rheumatoid arthritis diagnosed?

A

4 OUT OF 7

1) Morning stiffness (>1hr lasting >6wks)
2) Arthritis of >3 joints
3) Arthritis of hand joints
4) Symmetrical arthritis
5) Rheumatoid nodules
6) Positive RhF
7) Radiographic changes

608
Q

When should a 2 week referral be made for rheumatoid arthritis?

A
  • small joints of the hands or feet are affected
  • more than one joint is affected
  • there was a delay of >3months between onset of symptoms and medical advice
609
Q

What is the management for rheumatoid factor?

A

INITIAL: pain relief with paracetamol (+/- codeine)

  • if pain is not controlled, add an NSAIDs (plus PPI)
  • DMARDS (methotrexate, sulfasalazine)
  • TNF-ALPHA INHIBITORS (infliximab, entanercept, adalimumab)
  • CORTICOSTEROIDS: rapidly reduce symptoms and inflammation
  • regular exercise, physiotherapy, OT
  • surgery: joint prosthesis, may relieve pain and improve function.
610
Q

What are the red flags associated with chronic back pain?

A
  • recent violent trauma/minor trauma in people with osteoporosis
  • age at onset <20 or >50 years
  • history of cancer, drug abuse, HIV immunocompromised
  • constitutional symptoms
  • recent bacterial infection e.g. UTI
  • Pain that is worse when supine, severe at nighttime, thoracic
  • non-mechanical without relief from bed rest or postural modification
  • unchanged despite treatment for 2-4 weeks, accompanied by severe morning stiffness
  • accompanied by saddle anaesthesia, urinary retention, incontinence
611
Q

What is bronchiectasis?

A

A permanent dilatation and thickening of the airways characterized by:

  • chronic cough
  • excessive sputum production
  • bacterial colonisation
  • recurrent acute infection

It can be diffuse (widespread) or focal (more localized)

612
Q

What are the morphological classifications of bronchiectasis?

A

1) CYLINDRICAL: bronchi are enlarged and cylindrical
2) VARICOSE: bronchi are irregular with areas of dilatation and constriction
3) SACCULAR/CYSTIC: dilated bronchi form clusters of cysts

613
Q

What is the pathophysiology of bronchiectasis?

A
  • The affected airways are inflamed and easily collapse
  • There is an impairment of airflow and drainage of secretions, leading to accumulation of a large amount of mucus in the lungs
  • The mucus collects bacteria, predisposing to frequent and often severe LRTIs
614
Q

What is the cause of bronchiectasis?

A
  • CHRONIC INFLAMMATION of the airways
  • associated with: lung infections, immunodeficiency, cystic fibrosis, connective tissue disease, asthma, allergic bronchopulmonary aspergillosis, gastric aspiration, congenital defects
615
Q

What are the clinical features of bronchiectasis?

A
  • chronic cough
  • excessive sputum production
  • bacterial colonisation
  • recurrent acute infections
  • dyspnoea
  • chest pain
  • haemoptysis
616
Q

What are the clinical signs of bronchiectasis?

A
  • coarse crackles (heard in early inspiration and often in the lower zones)
  • large airway rhonchi (low-pitched snore-like sounds)
  • wheeze
  • clubbing (infrequent)
617
Q

What investigations are done in suspected bronchiectasis?

A
  • CHEST X RAY

- High Resolution Computed Tomography (HRCT)

618
Q

What is the management of bronchiectasis?

A

CANNOT BE CURED

  • therefore treatment is to manage symptoms and slow down further deterioration
  • treatment of underlying causes
  • LIFESTYLE: dietary, smoking cessation, immunisations
  • PHYSIOTHERAPY: airway clearance techniques and exercise
  • ANTIBIOTICS: AMOXICILLIN 500mg TDS, CLARITHROMYCIN 500mg BD 14days
619
Q

What pulmonary fibrosis?

A

A group of diseases which produce interstitial lung damage and ultimately fibrosis and loss of elasticity in the lungs

620
Q

What are the three types of lung fibrosis?

A

1) REPLACEMENT FIBROSIS :secondary to lung damage e.g. infarction/TB/pneumonia
2) FOCAL FIBROSIS: in response to irritants e.g. coal dust and silica
3) DIFFUSE PARENCHYMAL LUNG DISEASE: occurs in fibrosis alveoli’s and extrinsic alveoplitis

621
Q

What are the risk factors associated with lung fibrosis?

A
  • Occupational causes
  • Smoking
  • GORD
  • infectious agents
  • genetic factors
622
Q

What are the clinical features associated with pulmonary fibrosis?

A
  • gradual onset dyspnoea
  • chronic cough (non productive)
  • wheezing
  • haemoptysis
  • chest pain
623
Q

What are the clinical signs associated with pulmonary fibrosis?

A
  • central cyanosis
  • fine and expiratory pulmonary crackles
  • low-grade fever and myalgia
  • finger clubbing
  • late signs: pulmonary hypertension, RHF
624
Q

What investigations should be done in suspected pulmonary fibrosis?

A
  • Detailed history: OCCUPATIONAL (asbestos?)
  • Bloods: FBC, ESR/CRP (raised), LFTs, autoantibodies
  • ABG (O2 desats)
  • lung function tests
  • CXR: honeycombing
  • CT scan
  • bronchoalveolar lavage
625
Q

What is the definitive investigation for pulmonary fibrosis?

A

OPEN/ THORACOSCOPIC LUNG BIOPSY

626
Q

What is the management for pulmonary fibrosis?

A
  • treatment of underlying cause
  • smoking cessation
  • O2 therapy
  • pulmonary rehabilitation
  • corticosteroids, cytotoxic drugs (AZATHIOPRINE)
  • lung transplantation
627
Q

What is Crohn’s disease?

A

A chronic inflammatory GI disease characterized by:

  • TRANSMURAL GRANULOMATOUS INFLAMMATION
  • autoimmune disease of unknown aetiology
  • Can affect any part of the gut but favors terminal ileum and proximal colon
  • There is UNAFFECTED BOWEL (skip lesions) between areas of active disease
628
Q

What are the risk factors associated with Crohn’s disease?

A
  • Genetic susceptibility: mutations of NOD2/CARD15 gene
  • Environmental
  • Smoking
  • Oral contraception
  • Appendectomy
629
Q

What are the clinical features associated with Crohn’s disease?

A
  • diarrhoea (may be bloody)
  • abdominal pain (colicky)
  • weight loss/ failure to thrive in children
  • fever/ malaise and anorexia in active disease
630
Q

What are the clinical GI signs associated with Crohn’s disease?

A
  • right iliac fossa mass
  • abdominal tenderness
  • apthous ulcerations
  • perianal abscesses/ fistulas, skin tags
  • anal/ rectal strictures
631
Q

What are the extra intestinal signs associated with Crohn’s disease?

A
  • Clubbing
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Conjunctivitis
  • episcleritis
  • iritis
  • large joint arthritis
  • fatty liver/ liver granulomas
  • cholangiocarcinoma
  • renal stones
  • osteomalacia
  • malnutrition
  • amyloidosis
  • anaemia/leukocytosis/thrombocytosis
632
Q

What are the bio investigations for Crohn’s disease?

A
  • FBC (low Hb, high WCC)
  • ESR (high)
  • CRP (high)
  • U+E
  • LFT
  • Blood culture
  • stool MC+S
633
Q

What are the imaging investigations for Crohn’s disease?

A
  • sigmoidoscopy
  • rectal biopsy
  • small bowel enema
  • barium enema (cobble stoning)
  • colonoscopy
  • MRI
634
Q

What are the complications associated with Crohn’s disease?

A
  • Small bowel obstruction
  • Toxic dilatation
  • abscess formation
  • fistulae
  • perforation
  • rectal haemorrhage
  • colonic carcinoma
  • toxic megacolon
  • stricture
  • small bowel syndrome
635
Q

What is the conservative management for Crohn’s disease?

A
  • smoking cessation

- enteric nutrition (low fat ad low linoleic content for 28 days)

636
Q

What is the pharmacological management for mild attacks in Crohn’s disease?

A
  • LOPERAMIDE
  • CODEINE PHOSPHATE
  • PREDNISOLONE
637
Q

What is the pharmacological management for severe attacks in Crohn’s disease?

A
  • HYDROCORTISONE 100mg/6h IV

- METRONIDAZOLE 400-500mg/8h PO or IV

638
Q

What are additional pharmacological managements for Crohn’s disease?

A 
- INFLIXIMAB
(to maintain remission)
- AZATHIOPRINE
- 6-MERCAPTOPURINE
- MYCOPHENOLATE
- MOFETIL
639
Q

What are the surgical options for the management of Crohn’s disease?

A
  • Panproctocolectomy and end-ileostomy
  • Stricturoplasty
  • Resection of the worst areas
640
Q

What is ulcerative colitis (UC)?

A
  • inflammatory disorder of the colonic mucosa
641
Q

Where does UC spread?

A
  • RECTUM (proctitis 50%)
  • LEFT SIDED COLITIS (30%)
  • ENTIRE COLON (pancolitis 20%)

-UC “never” spreads proximal to the ileocaecal valve

642
Q

What is the common histological feature of UC?

A
  • hyperaemic/haemorrhagic granular colonic mucosa +/- pseudo polyps formed by inflammation
  • punctuate ulcers may extend into the lamina propriety, but inflammation is not typically transmural
643
Q

What are the risk factors associated with UC?

A
  • non-smokers
  • stress and depression
  • oral contraceptives
  • APPENDECTOMY IS PROTECTIVE
644
Q

What are the clinical features associated with ulcerative colitis?

A
  • gradual onset of diarrhoea
  • cramps abdominal discomfort
  • bowel frequency is related to severity of disease
  • systemic symptoms during attacks (fever, malaise, anorexia, weight loss)
  • urgency and tenesmus
  • constipation
  • rectal bleeding
  • anaemia
645
Q

What are the clinical signs associated with ulcerative colitis?

A
  • fever
  • tachycardia
  • tender, distended abdomen
646
Q

What are the extra-intestinal signs associated with ulcerative colitis?

A
  • Clubbing
  • apthous ulcers
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Conjunctivitis
  • episcleritis
  • iritis
  • large joint arthritis, sacroilitis, ankylosing spondylitis
  • fatty liver
  • cholangiocarcinoma
  • malnutrition
  • amyloidosis
  • nutritional deficits
647
Q

What are the complications associated with ulcerative colitis?

A
  • colorectal cancer
  • perforation
  • haemorrhage
  • toxic dilatation of the colon
  • venous thrombosis
  • colonic cancer
  • stricture
648
Q

What are the bio investigations associated with ulcerative colitis?

A
  • FBC
  • ESR
  • CRP
  • U+E
  • LFTs
  • blood cultures
  • stool MC+S
649
Q

What imaging investigations are associated with ulcerative colitis?

A
  • ABDOMINAL X-RAY: no faecal shadows, mucosal thickening, colonic dilation
  • ERECT CHEST XRAY
  • SIGMOIDOSCOPY: inflamed friable mucosa
  • RECTAL BIOPSY: inflammatory infiltrate, goblet cell depletion, glandular distortion, mucosal ulcers, crypt abscesses
  • COLONOSCOPY
650
Q

What is the management for mild UC?

A
  • if <4 motions per day and systemically well: PREDNISOLONE, MESALAZINE
  • mild distal disease: PR STEROID FOAMS (predsol, colifoam)
651
Q

What is the management for moderate UC?

A
  • 4-6 motions per day but systemically well:
  • PREDNISOLONE
  • 5-AMINOSALYCILIC ACID
652
Q

What is the management for severe UC?

A

Systemically unwell and passing >6 motions a day

  • admit for NBM and maintenance hydration
  • HYDROCORTISONE 100mg/6h IV
  • RECTAL STEROIDS e.g. HYDROCORTISONE 100mg in 100ml saline PR
  • daily bloods
653
Q

What is the surgical management for UC?

A
  • PROCTOCOLECTOMY
  • TERMINAL ILEOSTOMY
  • COLECTOMY WITH LATER ILEO-ANAL POUCH
654
Q

What is coeliacs disease?

A

Disorder of the small intestine causing malabsorption

- T CELL MEDIATED immune disease in which prolamin intolerance causes villous atrophy and malabsorption.

655
Q

What are the risk factors for coeliacs disease?

A
  • HLA DQ2
  • HLA DQ8
  • Rotavirus infection in infancy
656
Q

What are the clinical features of Coeliacs disease?

A
  • Steatorrhoea
  • Diarrhoea
  • Abdominal pain
  • Bloating
  • Nausea and vomiting
  • Apthous ulcers
  • angular stomatitis
  • weight loss
  • fatigue
  • weakness
  • iron deficiency anaemia
  • osteomalacia
  • failure to thrive
  • dermatitis herpetiformis
657
Q

When should coeliac disease be suspected?

A

ALL THOSE WITH DIARRHOEA AND WEIGHT LOSS

658
Q

What investigations should be done in coeliac disease?

A
  • ANTIBODIES: alpha gliadin, transglutaminase and anti-endomysial
  • DUODENAL BIOPSY: done at endoscopy
  • HISTOLOGY: subtotal villous atrophy, increased intra-epithelial WBCs and crypt hyperplasia, reversing on gluten free diet
  • HLA TYPING
659
Q

What is the management for Coeliacs disease?

A
  • GLUTEN FREE DIET
  • Verify diet by endomysial antibody testing
  • Replacement minerals and vitamins
660
Q

What are the complications associated with coeliacs disease?

A
  • Anaemia
  • secondary lactose intolerance
  • GI T-cell lymphoma
  • increased risk of malignancy
  • myopathies
  • neuropathies
  • hyposplenism
  • osteoporosis
661
Q

What is chronic liver disease?

A
  • liver loses the ability to regenerate or repair so that decompensation occurs.
662
Q

What is chronic liver disease marked by?

A
  • HEPATIC ENCEPHALOPATHY
  • ABNORMAL BLEEDING
  • ASCITES
  • JAUNDICE
663
Q

What are the toxic causes of chronic liver disease?

A
  • chronic alcohol abuse
  • paracetamol poisioning
  • drug toxicity
  • illicit drugs including ecstasy and cocaine
  • Reyes syndrome
664
Q

What are the infectious causes of chronic liver disease?

A
  • viral hepatitis
  • adenovirus
  • EBV
  • CMV
  • viral haemorhagic fevers
665
Q

What are the neoplastic causes of chronic liver disease?

A
  • Hepatocellular carcinoma

- metastatic carcinoma

666
Q

What are the metabolic causes of chronic liver disease?

A
  • Wilson’s disease
  • Alpha 1 anti-trypsin deficiency
  • galactosaemia
  • tyrosinaemia
667
Q

What are the pregnancy related causes of chronic liver disease?

A
  • acute fatty liver of pregnancy
668
Q

What are the vascular causes of chronic liver disease?

A
  • ischemia
  • veno-occlusive disease
  • Budd-Chiari syndrome
669
Q

What are other causes of chronic liver diseases?

A
  • Autoimmune liver disease

- Unknown 15%

670
Q

What should be assessed in chronic liver disease history?

A
  • haematemesis or melaena
  • date/onset of jaundice
  • alcohol use
  • full drug history
  • family history of liver disease
  • exposure risk factors (needles, sexual contact, occupation)
  • toxic ingestion (mushrooms, organic solvents)
  • past medical history
671
Q

What should be assessed on examination in chronic liver disease?

A
  • MSE may show drowsiness and possibly confusion
  • jaundice
  • abdominal distension
  • abdominal masses
  • hepatomegaly
  • splenomegaly
  • cerebral oedema with increased ICP
  • papilloedema, HTN, bradycardia
  • palmar erythema and hepatic flap
  • hepatic encephalopathy
672
Q

What bloods should be done on investigation of chronic liver disease?

A
  • FBC (thrombocytopenia)
  • raised INR
  • transaminases are very markedly raised
  • bilirubin raised
  • ammonia levels high
  • elevated lactate, hypoxia and raised creatinine
  • blood cultures
  • free copper for Wilson’s disease
  • paracetamol levels in case of posioning
673
Q

What is the imaging used in investigation for chronic liver disease?

A
  • DOPPLER ULTRASOUND: could detect patent hepatic vein, ascites, tumour
  • CT/MRI
674
Q

What is the management for chronic liver disease?

A
  • liver transplantation
  • monitor glucose
  • lactulose and neomycin to reduce ammonia production
  • fresh frozen plasma
  • platelet concentrates
  • antifibrinolytic drugs
  • prothrombin complex
  • recombinant activated factor VII
675
Q

What are the complications associated with chronic liver disease?

A
  • Spontaneous peritonitis
  • infection of access line
  • opportunistic infection
  • cerebral oedema
  • haemorrhage
  • AKI
676
Q

What is a diverticulum?

A
  • herniation of mucosa though the thickened colonic muscle.

common in the SIGMOID and DESCENDING COLON

677
Q

What is diverticulosis?

A

Presence of diverticula which are asymptomatic

678
Q

What is diverticular disease?

A

Diverticula associated with symptoms

679
Q

What is diverticulitis?

A

Evidence of diverticular inflammation with or without localized symptoms and signs

680
Q

What are the risk factors for diverticular diseases?

A
  • Age >50
  • Low dietary fibre
  • Obesity
  • smoking
  • NSAID
  • paracetamol use
681
Q

What is the presentation of uncomplicated diverticular disease?

A
  • Frequently an incidental finding
  • lower abdominal pain
  • pain exacerbated by eating and diminished with defecation/ flatus
  • bloating, constipation
  • rectal bleeding
682
Q

What is the presentation of diverticulitis?

A
  • generally present with left lower quadrant pain
  • pain may be intermittent or constant and associated with change in bowel habit
  • fever
  • tachycardia
  • anorexia
  • nausea
  • localized tenderness
  • palpable mass
  • reduced bowl sounds
683
Q

What investigations are done in diverticular disease?

A
  • colonoscopy

- Bloods: (WCC raised)

684
Q

What are the investigations specific to uncomplicated diverticular disease?

A
  • Barium enema
685
Q

What are the investigations specific to diverticulitis?

A
  • CHEST X-RAY: detection of pneumoperitoneum
  • ABDOMINAL X-RAYS: small/large bowl ileus, bowel obstruction on soft tissue densities
  • contrast enemas
  • CT scanning with contrast
686
Q

What is the management for diverticular disease?

A
  • No treatment for asymptomatic patients
  • prophylactic benefit of high fibre diet
  • adequate fluid intake
  • bulk forming laxatives
687
Q

What is eczema?

A

Characterized by papule and vesicles on erythematous base

688
Q

What are the risk/exacerbating factors of eczema?

A
  • family history of atopy
  • genetic defects in skin barrier function
    exacerbated by:
  • infections
  • allergens
  • sweating
  • heat
  • severe stress
689
Q

Way are the clinical features of eczema?

A
  • Commonly present as itchy erythematous dry scaly patches
  • more common on face and extensor limbs of infants
  • common on flexural spaces of children and adults
  • acute lesions: erythematous, vesicular and weepy
  • chronic scratching/rubbing can lead to excoriations and lichenification
690
Q

How is a diagnosis of eczema made?

A

A history of an itching condition and 3 of the following:

  • history of rash in skin folds
  • history of generally dry skin in the past year
  • onset under the age of 2 years
  • visible flexural dermatitis
  • personal history of asthma or hayfever
691
Q

What is the management for eczema?

A
  • avoid known exacerbating agents
  • frequent emollients
  • bandages
  • bath oil/ soap substitutes
  • topical steroid
  • topical immunomodulators (TACROLIMUS)
  • Antihistamines for symptomatic relief
  • Antibiotics for bacterial infections
  • Antivirals for herpes infections
  • Phototherapy and immunosuppresion
692
Q

What are the varying strengths of topic steroid for eczema?

A

MILD: HYDROCORTISONE 0.5%/1%/2.5%
MODERATE: BETNOVATE RD
POTENT: BETNOVATE N/C
VERY POTENT: DERMOVATE

693
Q

What is psoriasis?

A
  • Chronic inflammatory skin disease due to HYPERPROLIFERATION of KERATINOCYTES and inflammatory cell infiltration
  • T-ce;; mediated autoimmune disorder
694
Q

What are the different types of psoriasis?

A
  • Chronic plaque psoriasis
  • Guttate
  • Seborrhoeic
  • Flexural
  • Pustular
  • Erythrodermic
695
Q

What are the precipitating factors for psoriasis?

A
  • trauma (may induce Köebner’s phenomenon)
  • infection
  • drugs
  • stress
  • alcohol
  • smoking
  • postpartum hormonal changes
696
Q

What are the clinical features of psoriasis?

A
  • well demarcated erythematous scaly plaques
  • distribution is symmetrical and common on extensor surfaces of the body and scalp
  • itchy, burning/ painful lesions
  • Auspitz sign (bleeding under scales)
  • Nail changes (pitting, onycholysis)
  • psoriatic arthropathy
697
Q

How is diagnosis of psoriasis made?

A
  • clinical findings

- PASI score

698
Q

What is the management for psoriasis?

A
  • Avoid known precipitating factors
  • emollients to reduce scales
  • vitamin D analogues
  • topical corticosteroids
  • coal tar preparations
  • phototherapy
  • UVB and photochemotherapy
  • methotrexate
  • retinoids
  • ciclosporin
  • biologics (infliximab, etanercept)
699
Q

How does haemorrhage appear on CT?

A
  • white blob
700
Q

How does an infarct appear on CT?

A
  • darkened area (hypodense)
701
Q

What is malignant MCA syndrome?

A
  • Large MCA infarct leading to extracellular oedema and rise in ICP
  • Mass effect
  • Decompressive craniotomy is needed to relieve pressure
702
Q

What is agnosia?

A

Inability to process sensory information in the absence of sensory or memory impairment

703
Q

What is anosognosia?

A

lack of isight in to recognition of impairment

704
Q

What is apraxia?

A

disorder of motor planning; unable to perform tasks or movements when asked, despite understanding

705
Q

What is ideomotor apraxia?

A

Can explain and do action but can not mime it

706
Q

What is conceptual apraxia?

A

Inability to conceptualise a task, unable to complete multistep actions

707
Q

What is constructional apraxia?

A

Inability to draw figures

708
Q

What is hemineglect?

A

The inability to process and perceive a stimulus on one side, when that inability is not due to lack of sensation
typically due to RIGHT PARIETAL LOBE INJURY

709
Q

What are the various types of gait?

A
  • parkinsonian
  • frontal gait disorder
  • hemiparetic
  • cautious
  • paraparetic
  • scissor
  • Trendelenburg
  • Waddling
  • Dementia
  • Choreic
710
Q

What are the features of expressive aphasia?

A
  • BROCA’S AREA
  • stilted, difficult flow of speech
  • Difficulty finding words
  • reading, writing and comprehension relatively intact
  • e.g. MCA stroke
711
Q

What are the features of receptive aphasia?

A

WERNICKE’S AREA

  • neologisms
  • mistake closely related words
  • comprehension, reading, writing impaired
  • e.g. MCA stroke
712
Q

What is dysarthria?

A

MOTOR SPEECH PROBLEM

  • neuromuscular barin stem, cerebellum, cranial nerve nuclei
  • normal comprehension and content of speech
  • changes in voice quality: speech slurred
  • facial drooping or impaired movement of mouth
  • chewing or swallowing difficulty

YEAR 4 (5 decks)

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