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Longterm conditions Flashcards

1
Q

What are the types of lung cancers?

A

Non-small cell lung cancer, small cell cancer, mesothelioma, carcinoid tumour

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2
Q

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

A

Adenocarcinoma, squamous cell carcinoma, large cell carcinoma, large cell neuroendocrine carcinoma

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3
Q

Which is the most common type of lung cancer?

A

Non-small cell cancer

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4
Q

What is the most common type of non-small cell lung cancer?

A

Adenocarcinoma

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5
Q

WHat is an adenocarcinoma?

A

A cancer that arises from glandular tissue

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6
Q

What is an adenocarcinoma in situ?

A

An adenocarcinoma arising from alveolar cells

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7
Q

What is squamous cell carcinoma?

A

Cancer arising from the squamous cells

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8
Q

What is a large cell cancer?

A

Cancer that is too poorly differentiated to tell what parent tissue it originated from

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9
Q

What is a neuroendocrine tumour?

A

Tumour that releases hormones

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10
Q

What are the signs and symptoms of a non-small cell lung cancer?

A

Cough, chest pain, SOB, haemoptysis, recurrent chest infections, lethargy, fever, malaise, weightloss, appetitie loss, wheezing, hoarseness, bone pain, spinal impingement, signs of a space occupying lesion

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11
Q

What are the radiological signs of a non-small cell lung cancer?

A

Hilar enlargement, pulmonary nodule, mass or infiltrate, mediastinal widening, pleural effusion, atelectasis

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12
Q

What is atelectasis?

A

Partial or complete of lung or lung lobe, occurs when alveoli deflate

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13
Q

What are the the diagnostic tests for a non-small cell lung cancers?

A

CXR, bronchoscopy, sputum cytology, mediastinoscopy, thoracentesis, thorascopy, thransthoracic needle biopsy

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14
Q

WHat are the treatments available for a non-small cell lung cancer?

A

Surgery (lobectomy, pneumonectomy, Wedge resection), chemo, radio

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15
Q

What is small-cell lung cancer?

A

An aggressive subset of cancer that is fatal within weeks if not treated, of a neuroendocrine origin and associated with distinct paraneoplastic syndromes

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16
Q

What is the pathophysiology of small cell lung carcinoma?

A

Arises in peribronchial locations and infiltrates into bronchial submucosa.
Widespread metastasis occurs via lympnodes to spread into liver, mediastinum, bones, adrenal glands and the brain

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17
Q

what are the indications of poor prognosis in small-cell lung cancer?

A

Relapse, weightloss of greater than 10%, hyponatremia, poor performance status

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18
Q

What are paraneoplastic syndromes?

A

Rare disorders that occur due to the triggering of the immune system in response to a neoplasm
A collection of symptoms arising due to the secretions of a neoplasm

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19
Q

Name 10 symptoms that can occur due to paraneoplastic syndromes

A

Cachexia, fever, dysgeusia, polymyositis, dermatomyositis, secondary kidney amyloidosis, chronic anaemia, rhrombocytopenia, maranteric endocarditis, itching, hypercalcermia

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20
Q

what is hepatocellular carcinoma?

A

Primary malignancy of the liver occurring in patients with pre-existing chronic liver cirrhosis and disease

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21
Q

How do hepatocellular carcinomas usually present?

A

Either in routine screeining or when they become sympptommatic

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22
Q

What are the presentations of hepatocellular carcinoma?

A

Jaundice, weightloss, anaemia, thrombcytopenia, hyponatremia, bleeding disorderscachexia, abdominal pain, abdominal mass/swelling

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23
Q

What lab tests and results can be seen iin hepatocellular carcinoma?

A

Anaemia, low PT, thrombocytopenia, raised serum creatinine, hyponatremia, Raised LFTs, hypoglycemia, raised bilirubin

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24
Q

What imaging studies are done on patients with hepatocellular carcinoma?

A

US, CT, MRI

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25
Q

Who is the typical patient of laryngeal cancer?

A

50-70, male

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26
Q

What are the risk factors for laryngeal cancer? Name 10

A

Smoking, obesity, reflux, alcohol, male, HPV, increasing age, exposure to paint, asbestos, radiation, diesel and gasoline fumes, metal or plastic workers, diets low in leafy greens and high in salt preserved meats and dietary fats

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27
Q

Which type of laryngeal tumour is usually discovered first?

A

Glottic tumours because they alter voice and are therefore symptomatic early

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28
Q

Which laryngeal tumours are usually discovered late?

A

Supraglottic tumours because the first symptom is usually obstruction, which only occurs if the tumour has grown to a large size

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29
Q

What type of cancer is laryngeal carcinoma usually?

A

Squamous cell carcinoma

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30
Q

What are the signs and symptoms of laryngeal carcinoma

A

Dysphonia, aphonia, dysphagia, dysnea, neck mass, otalgia, Blood tinged sputum, aspiration, cachexia, fatigue, weakness, pain, halitosis, expectoration of tissue

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31
Q

WHat is otalgia?

A

Ear pain

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32
Q

What can be seen in the history of a patient with laryngeal carcinoma?

A

weightloss, fatigue, hoarseness, dysphagia, dysnea, ear pain, pain, coughing up blood or solid matter

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33
Q

Which scan is used to diagnose laryngeal carcinoma?

A

CT scan

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34
Q

What is the therapy for early stage laryngeal cancer?

A

Radiation or surgical techniques that preserve anatomical function
Transoral laser microsurgery

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35
Q

What is the therapy for late stage laryngeal cancer?

A

laryngectomy, reconstruction and post-op chemo

open partial laryngectomy

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36
Q

What are the signs and symptoms of oesophageal cancer?

A

Dysphagia, bleeding, weightloss, fatigue, bone pain, hoarseness, persistent cough, hepatomegaly, lymphadenopathy

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37
Q

What is the pathophysiology of oesophageal adenocarcinoma?

A

Reflux > Barret’s oesophagus > Adenocarcinoma

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38
Q

What are the investigations used for oesophageal cancer and why?

A

Oesophagogastroduodenoscopy (visualization and biopsy), endoscopic US and PET scan (staging), bronchoscopy and CT (for metastasis)

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39
Q

What is the treatment for early (stage I) oesophageal cancer?

A

Endoscpic therapy

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40
Q

What is the treatment for intermediate (stage II-III) oesophageal cancer?

A

Chemo and surgery

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41
Q

What is the treatment for end stage (stage IV) oesophageal cancer

A

Chemo or supportive and symptomatic care

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42
Q

What arethe options for surgery in oesophageal cancer?

A 
Transhiatal esophagectomy (THE)
Transthoracic esophagectomy (TTE)
Minimally invasive esophagectomy
Endoscopic mucosal resection (EMR)
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43
Q

What type of cancer is oral cancer usually?

A

Squamous cell carcinoma

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44
Q

WHat do oral cancers typically look like?

A

Speckled/verrocous (premalignant, white lesions (non-malignant) velvety red plaques (malignant)

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45
Q

What can oral cancers manifest as?

name 8

A

A red lesion (erythroplakia)
A granular ulcer with fissuring or raised exophytic margins
A white or mixed white and red lesion
A lump sometimes with abnormal supplying blood vessels
An indurated lump/ulcer (ie, a firm infiltration beneath the mucosa)
A nonhealing extraction socket
A lesion fixed to deeper tissues or to overlying skin or mucosa
Cervical lymph node enlargement, especially if hardness is present in a lymph node or fixation

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46
Q

What are the causes of oral cancer?

A

Smoking, alcohol, oral health, socioeconomic status, diet low in fresh fruit and veg, infective agents

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47
Q

What are the tests in oral cancer usually for?

A

to rule out metastasis

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48
Q

WHat are the advantages and disadvantages of using radiotherapy fororal cancers?

A

ADvantages: no need for anaesthesia, salvage surgery available, function maintained
Disadvantages:Side effects, not commonly curative, subsequent surgery is more difficult

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49
Q

What are the side effects of mouth cancer therapy?

A

Mucositis, oral ulceration, infections, bleeding, pain, taste loss, trismus, caries, xerostomia

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50
Q

What is the most common bone cancer?

A

Osteosarcoma

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51
Q

What is the major cause of death due to osteosarcoma?

A

pulmonary metastatic disease

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52
Q

What tests are used for diagnosis in patients with metastatic bone disease?

A

Serum alkaline phosphatase (marker of bone destruction)

Serum protein electrophoresis, urinalysis, urine protein electrophoresis

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53
Q

What imaging studies are used for evaluating metastatic bone disease and why?

A

Radiography (assessment of extent of tumour and degree of cortical erosion), CT (bone destruction), MRI (anatomic assessment of lesion), Bone scan (activity of lesion), angiography (devascularization of vascular metastasisi)

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54
Q

What treatments are used for metastatic bone disease?

A

Radiotherapy, surgery, surgical fixation of ling bones, monoclonal antibody antineoplastic agents, calcium metabolism modifiers

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55
Q

What are the most common sites of metastatic bone disease?

A

Spine, pelvis, ribs, limb girdles

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56
Q

WHat are the signs and symptoms of bladder cancer?

A

Painless gross haematuria, irritative bladder symptoms (dysuria, urgency, frequency), palpable mass, pelvic or bony pain

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57
Q

What are the diagnostic tests available for bladder cancer?

A

Urinalysis, urine culture to rule out infection, voided urine cystology, urinary tumour marker testing

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58
Q

what is the treatment of non muscle invasive bladder cancer?

A

transurethral resection of bladder tumour, followed by intravesical BCG vaccine, postop chemodose, repeat resection if necessary

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59
Q

How is muscle invasive bladder cancer treated?

A

radical cystoprostatectomy, ant. pelvic exenteration (in women), bbilateral pelvic lymphadenectomy, creation of urinary diversion, chemo

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60
Q

What is the most common type of bladder cancer?

A

Transitional cell carcinoma

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61
Q

WHat are the signs and symptoms of colon cancer?

A

Iron deficiency anarmia, rectal bleeding, abdo pain, change in bowel habit, intestinal obstruction or perforation, fatigue, malaise, weight loss, palpable abdo mass, hepatomegaly, ascities

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62
Q

What lab tests and procedures can be done to diagnose colon cancer?

A

FBC, LFTs, serum carcinoembryonic anitgen

Colonoscopy, Sigmoidoscopy, Biopsy of suspicious lesions, Double-contrast barium enema

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63
Q

What radiological studies can be used for colorectal cancer?

A

Chest radiography
Chest computed tomography
Abdominal barium study
Abdominal/pelvic CT
Contrast ultrasonography of the abdomen and liver
Abdominal/pelvic MRI
Positron emission tomography, including fusion PET-CT scan

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64
Q

What is the management of colon cancer?

A

Colectomy primarily

Cryotheraby, radiofrequency ablation, chemo,

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65
Q

What is the most common type of colon and rectal cancer?

A

Adenocarcinoma

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66
Q

What are the signs and symptoms of bowel cancer?

A

Change in bowel habit, occult bleeding, abdo pain, back pain, urinary symptoms, malaise, pelvic pain, emergencies like peritonitis

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67
Q

What are the diagnostic tests for rectal cancer?

A

DRE, rigid proctoscopy

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68
Q

What blood tests are diagnositic for rectal cancer?

A

Bloods, serum chemistries, liver and renal function test, carcinoembryonic antigen, cancer antigen assay

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69
Q

What screening tests are diagnositic for rectal cancer?

A

Guaiac-based FOBT, stool DNA screening, fecal immunochemical test, rigid protoscopy, flexible sigmoidoscopy, combined glucose based \FOBT and flexible sigmoidoscopy, double-contrast barium enema, CT colonography, fiberoptic flexible colonoscopy

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70
Q

What is the treatment of rectal cancer?

A

Surgery (transanal excision, transanal endoscopic microsurgery, endocavity radiotherapy, sphincter-sparing procedures), radiation, chemo, radioembolization, vaccines, antineoplastic agents

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71
Q

What are the three pathways for rectal cancer pathophysiology?

A

APC gene
Hereditary nonpolyposis colorectal cancer pathway
UC dysplasia

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72
Q

What is the definition of chronic bronchitis?

A

Presence of a chronic productive cough for 3 months during each of 2 consecutive years

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73
Q

What is the definition of emphysema?

A

abnormal. permanent enlargement of air spaces distal to the terminal bronchioles, accompaned by wall destruction without obvious fibrosis

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74
Q

What are the symptoms of COPD?

A

Productive cough, breathlessness, wheeze, chest illness

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75
Q

What are the signs of COPD?

A

Tachypnea, bronchial breathing, cyanosis, raised JVP, peripheral oedema, use of accessory muscles to breathe, hyperinflated chest, hyperresonant chest, wheezing, reduced breath sounds, prolonged expiration, coarse inspiratory crackles

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76
Q

How many stages of COPD are there?

A

4

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77
Q

What are the risk factors of COPD?

A

Smoking, asbesotos, coal mining, alpha-1-antitrypsin deficiency, IV drug use, immunodeficiency, vasculitis, connective tissue disorder

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78
Q

What are the common CXR findings in COPD?

A

Hyper inflation of chest, flattening of diaphragm, increased retrosternal air space, long, narrow heart shadow, rapidly tapering vascular shadow, hyperlucency of lungs, cardiomegaly, hyperlucency of lungs

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79
Q

What examinations should be used to investigate COPD?

A

Spirometry, ABG, CXR, CT chestsodium retention (serum sodium), alpha1antitrypsin (patients belo 40), sputum, BNP (differentiate from CHF)

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80
Q

What ABGs indicate respiratory acidosis?

A

pH<7.35

CO2>45

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81
Q

What can cause respiratory acidosis?

A

Acute- failure of ventilation (resp depression, airway obstruction, neuromuscular disease, myasthenia, lateral sclerosis, guillan-barre)
Chronic (COPD due to reduced responsiveness to hypoxia and hypercapnia, increased VQ mismatch, dereased diaphragmatic function)

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82
Q

What ABGs indicate respiratory alkosis?

A

pH>7.45

CO2<35

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83
Q

What ABGs indicate metabolic acidosis?

A

pH<7.35

HCO3<22

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84
Q

What ABGs indicate metabolic alkosis?

A

pH>7.45

HCO3>26

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85
Q

What values in spirometry are diagnostic for COPD?

A

FEV1/FVC < 70%

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86
Q

What is the normal range for blood pH?

A

7.35-7.45

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87
Q

What are the causes of respiratory alkalosis?

A

CNS causes (meningitis, pain, hyperventilation, anxiety, panic disorders, fever, tumour, trauma, encephalitis, psychosis) high altitude, right-to-left shunts, progesterone, drug toxicity, catecholamines, nicotine

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88
Q

What are the causes of metabolic acidosis?

A

Ketoacidosis, lactoacidosis, renal failure, toxic ingestions, impaired renal secretion, GI or renal HCO3- loss

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89
Q

What are the causes of metabolic alkalosis?

A

Hypokalemia, hypomagnesia, diuretics, gastric acid loss (vomitting, villous adenoma), hyperaldosteronism

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90
Q

What is pulmonary rehabilitation?

A

Pulmonary rehabilitation includes patient education, exercise training, psychosocial support and advice on nutrition.
Pulmonary rehabilitation has been shown to improve exercise capacity, reduce breathlessness, improve health-related quality of life, and decrease healthcare utilisation.

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91
Q

How is COPD treated?

A

Bronchodilation (beta agonists and anticholinergics), tiotropium (long acting beta agonist), Umeclidinium bromide(bronchial muscle relaxant, antimuscarinic), phosphodiesterase inhibitors (bronchodilation)

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92
Q

What are the medications used for smoking cessation?

A

Varenicline, nicotine replacement, bupropion

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93
Q

What medications are used for sputum lysis in COPD?

A

Mucolytic(N-acetylcysteine)

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94
Q

What are the contents of a COPD rescue pack?

A

Predinsalone and amoxicillin?

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95
Q

What are COPD rescue packs used for?

A

Exacerbation of COPD

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96
Q

Define heart failure

A

Failure of the heart to pump enough blood to fulfill the needs of the body

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97
Q

What should be asked about in the history of patients with suspected heart failure as co-morbidites or risk factors? (name 10)

A

Myopathy, alcohol, smoking diabetes, familial valve problems, valve problems, previous MI, hyperlipidaemia, hypertension, sleep-disordered breathing, rheumatic fever, PVD, chemotherapy to chest, thyroid disease

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98
Q

WHat are the symptoms of heart failure? Name 10

A

Dyspnea at rest, exertional dysnea, orthopnea, PND, pleural oedema, chest pain, palpitations, fatigue, nocturia, oligouria, cerebral symptoms (elderly patients w/ advanced HF)

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99
Q

What causes orthopnea?

A

When lying down, blood pools in the thoracid compartment. The failing LV cannot pumpthe excess blood without dilating. This increases pulmonary venous and capillary pressure, causing pulmonary oedema

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100
Q

What are the mechanisms of dysnea at rest in HF?

A

Decreased pulmonary function due to decreased compliance and increased airway resistance
Increased ventilatory drive secondary to hypoxemia due to ventilation/perfusion (V/Q) mismatching
Respiratory muscle dysfunction, with decreased respiratory muscle strength, decreased endurance, and ischemia

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101
Q

What causes nocturia and oligouria in HF?

A

Recumbency reduces the deficit in cardiac output in relation to oxygen demand, renal vasoconstriction diminishes, and urine formation increases.

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102
Q

What signs can be seen in the examination of a patient with HF?

A

Ascites, raised JVP, cardiomyopathy, orthopnea, cyanosis,icterus,malar flush, diminished pulse, dusky skin, tachycardia, diaphoresis, crackles in the lung bases, cardiac wheeze, frothy pink sputum, S3 gallop, pulsus alternans, cachexia

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103
Q

What are the underlying causes of HF?

A

Structural abnormalities that effect circulation, pericardium, or valves, leading to increased haemodynamic burden or myocardial or coronary insufficiency

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104
Q

What investigations should be done in a patient with suspected HF?

A

ECG, BNP, FBC, CXR, Echocardiogram, LFTs, U & Es, TSH, treadmill testing, lipid profile

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105
Q

What is the surgical treatment for HF?

A

Electrophysiological intervention, revascularization, ventricular assist devices,heart transplant, artificial heart, valve repair/replacement, ventricular restoration, extracirporeal membrane oxygenation

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106
Q

What is the pharmacological treatment for HF?

A

Diuretics, vasodilatorsm inotropic agents, anticoagulants, beta blockes, digoxin

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107
Q

What are the non pharmacological treatments for HF?

A

Attention to weight gain, reduced sodium, O2, noninvasive positive pressure ventilation, fluid restriction, exercise

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108
Q

What are the percipitating causes of HF?

A

Underlying heart disease (eg valvular stenosis), other conditions (feverm anemia, infection) or medications (chemo, NSAIDs) that alter homeostasis of patient

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109
Q

What are the fundamental causes of HF?

A

biochemical or physiological processes

110
Q

What are the underlying causes of systolic HF?

A

Coronary artery disease, HTN, DM, arrhytmia, valvulardisease, myocarditis, congenital, idiopathic, cardimyopathy

111
Q

What are the underlying causes of diastolic HF?

A

Coronary artery disease, DM, HTN, valvular disease, hypertrophic cardiomyopathy, restricive cardiomyopathy, constrictive pericarditis

112
Q

Whhat are the underlying causes of acute HF?

A

Drugs, sepsis, MI, myocarditis, acute valvular regurgitation, arrythmia

113
Q

what are the underlying causes of right sided heart failure?

A

LVF, cor pulmonale, coronary artery disease, pulmonary hypertension, pulmonary valve stenosis, pulmonary embolism, chronic pulmonary disease, neuromuscular disease

114
Q

WHat are the precipitating causes of HF?

A

profound anaemia, myxoedema, thyrotoxicosis, paget’s, cor pulmonale, obesity, pregnancy, nutritional deficiencies, glomerunephritis

115
Q

What are the signs and symptoms of angina pectoris?

A

Retrosternal chwst discomfort localized to epigastrium, back, neck, jaw or shoulders, percipitated by exertion, eating, cold or emotional stress

116
Q

What tests are used for diagnosing Angina pectoris?

A

ECG, coronary angiography, treadmill tests, CXR, BNP, troponin

117
Q

How is angina pectoris treated?

A

Managing risk factors (smoking, obesity, hyperlipidaemia, HTN,
sublingual GTN

118
Q

What are the surgical treatments available for angina pectoris?

A

Revascularization, treatment of underlying cause

119
Q

WHat is the criteria for diabetes testing?

A

Diabetes symptoms plus:a random venous plasma [glucose] ≥ 11.1 mmol/l or
a fasting plasma [glucose] ≥ 7.0 mmol/l (whole blood ≥ 6.1 mmol/l) or
two hour plasma [glucose] ≥ 11.1 mmol/l two hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT).

120
Q

What is the pathophysiology of t2diabetes?

A 
increased glucose production caused by increased hepatic glucose production, increased carb intake, redusced peripheral glucose uptake and decreased insulin production
Beta cell dysfunction
Insulin resistance
Genetic factors
Amino acid metabolism
121
Q

What are the complications of t2 diabetes?

A

CV risk due to hyperlipidaemia, cognitive decline, diabetic retinopathy, diabetic neuropathy, poor healing, depression, vasculopathy, end stage renal disease, cancer

122
Q

What are the RF of T2 diabetes?

A

Overweight, obesity, race, family historym history f gestational diabetes, polycystic ovarian syndrome, hypertension, hyperlipidaemia

123
Q

What are the symptoms of t2D?

A

polyuria, polydipsia, weightloss, polyphagia, blurred vision, paraesthesia, yeast infections

124
Q

What are the signs of T2DM?

A

Mostly asymp, can have blurred vision, reduced touch sensation, acanthosis nigricans, eye haemorrhages

125
Q

What are the tests done for T2D

A

Impaired glucose tolerance test, glycated hemoglobin studies, urinary albumin tests, BM,

126
Q

What tests are used to differentiate T2DM and T1DM?

A

fasting C-peptide level, autoantibodies

127
Q

What are the treatments available for T2D?

A

Biguanides, sulfonylureas, Alpha-glucosidase inhib, meglitinide derivatives, thiazolidinediones, glucagonlike peptides, dipeptidyl peptidase IV inhib, selective na-glucose transporter 1 inhib, insulins

128
Q

Name a biguanide

A

Metronidazole

129
Q

How does metronidazole work?

A

lowers basal plasma [glucose] by decreasing hepatic glucaneogenesis and interstinal glucose absorption
improves insulin sensitivity by increasing peripheral glucose uptake

130
Q

Name some sulfonylureas

A

Glyburidem glipizide, glimepiride

131
Q

How do sulfonylureas work?

A

insulin secretagogues that stimulate insulin release from pancreatic beta cells

132
Q

What is a common side effect of sulfonylureas?

A

hypos

133
Q

How do meglitinide derivatives work?

A

Shorter acting insulin secretagogues

134
Q

How do alpha-glucosidase inhibitors work?

A

Prolong carb absorbtion, Prevent post food glucose surges

135
Q

What is a common side effect of alpha-glucosidase inhibitors?

A

Farting

136
Q

How do thiazolidinediones work?

A

Insulin sensitizers, require insulin to work

137
Q

How does DPP-4 inhib work>

A

Prolong the action of incretin hormones

138
Q

How do SGLT2 inhibss work?

A

Lowers renal glucose threshold, increasing renal glucose excretion

139
Q

What is the pathophysiology if T1DM?

A

Lack of insulin caused by autoimmune attack of pancreatic beta cells

140
Q

What are the common symptoms of T1DM?

A

Polyuria, polydispsia, polyphagia, lassitude, nausea, blurred vision and fatigue

141
Q

What causes fatigue in t1DM?

A

Muscle weakness from catabolic state of insulin deficiency, hypovolemia and hypokalemia

142
Q

What causes polyuria in t1DM?

A

Osmotic diueresis due to hypo

143
Q

What causes blurred vision in T1DM?

A

Effect of hypoosmolar state on lens and vitreous humour (glucose causes swelling, altering the shape and therefore focus of the lens)

144
Q

What are the common complications of diabetes?

A

Infections, visual blurring, senile cataracts, diabetic retinopathy, nephropathy, neuropathy, coronary atherosclerosis, gangrene

145
Q

What is Atopic dermatitis?

A

Chronic, pruritic, inflammatory skin disease of unknown arigin, associated with IgE

146
Q

What is atopic dermatitis associated with?

A

Food allerfy, asthma, allergic rhinitis

147
Q

What are the classic features of atopic dermatitis?

A

Pruritis, early onset, ecxema, atopy, xerosis

148
Q

Describe a lesion of atopic dermatitis

A

Erythematous, lichenified and possibly exudative plaque. crusting is common

149
Q

What are the causes of atopic dermatitis?

A

Genetics, infection, hygiene, food allergy, climate, tobacco

150
Q

Name 5 possible differentials for atopic dermatitis

A

Allergic contact dermatitis, scabies, immunodeficiency, plaque psoriasis, zinc deficiency, tinea corporis, seborrheic dermatitis,

151
Q

What is the treatment of atopic dermatitis?

A

Moisturizers topical steroids and immunomodulators if necessary

152
Q

What is a seizure?

A

Physical symptoms manifesting due to electrical overexcitement of the brain

153
Q

WHat are the causes of seizures?

A

Genetic predisposition, alcohol withdrawal, hypo, head trauma, stroke, space occupying lesions

154
Q

What is required in the diagnosis of epilepsy?

A

Occurence of at least 2 unrpovoked seizures

155
Q

Describe an absence seizure

A

Type of generalized seizure with impaired awareness, with childhood onset and a history of ‘staring spells’

156
Q

Describe a compllex partial seizure

A

A seizure affecting only a part of the brain but with impaired awareness

157
Q

Describe a tonic clonic seizure

A

A genralized seizure characteristic of it’s tonic phase (where all the muscles clench) and clonic phase (where the body undergoes rhythmic jerks). Often precededed by a high pitched whine caused by the diaphragm pushing air through a closed glottis

158
Q

What diagnostic tests can be done on a patient with a seizure?

A

Prolactin (usually raised 3-4x in generalised seizure), CT or MRI to eliminate structural abnormalities, EEG, phenytoin levels (to establish control of previously diagnosed epileptic patient)

159
Q

What does an EEG show during an epileptic attack

A

Many and wild squiggly lines

Epileptiform changes
focal sslowing
diffuse background slowing
intermittent diffuse intermixed slowing

160
Q

What is the first line treatment of focal seizures?

A

Carbamazepine, Iamotrigine

161
Q

What’s the first line treatment of generalized seizures?

A

Sodium valproate, Iamotrigine

162
Q

What’s the first line treatment of absence seizures?

A

Ethosuximide, sodium valproate

163
Q

What’s the first line treatment of myoclonic seizures?

A

sodium valproate

164
Q

What’s the first line treatment of tonic seizures?

A

sodium valproate

165
Q

What’s the first line treatment of atonic seizures?

A

sodium valproate

166
Q

What are the causes of falls?

A

Medication, vasovagal syncope, cough, defaecation or micturition syncope, orthostatic hypotension, autonomic dysfunction, , epilepsy, confusion, epilepsy, environmental

167
Q

what are the risk factors for falls?

A

polypharmacy, osteoporosis, epilepsy, dementia, delirium, vision or hearing impairment, parkinsons, thyroid problems, vertigo,

168
Q

What is the definition of syncope

A

Transient loss of consciousness due to hypoperfusion of the brain

169
Q

What investigations can be done on a patient presenting with syncope?

A

FBC, ECQ CXR, BM, BNP, CK, U & E, urine dipstick, CT head, tilt table

170
Q

What drugs can increase falls risk?

A

Antihypertensives, diuretics, B blockers, sedatives, hypnotics, tricyclics, benzos,

171
Q

What can cause orthostatic hypotension?

A

autonomic dysfunction, mediction

172
Q

What test can be done to diagnose autonomic dysfunction?

A

lying and standing BP

173
Q

Where is the femur most likely to be fractured?

A

Neck

174
Q

What is the division between intracapsular and extracapsular?

A

Intertrochanteric line

175
Q

How many grades of femoral neck fractures are there?

A

4

176
Q

Describe a grade I neck of femur fracture

A

incomplete or valgus impacted fracture

177
Q

Describe a grade II neck of femur fracture

A

Complete fracture without bone displacement

178
Q

Describe a grade III neck of femur fracture

A

Complete fracture with partial bone displacement

179
Q

Describe a grade IV neck of femur fracture

A

Complete fracture with total displacement of fracture fragments

180
Q

What is the classic clinical presentation of a neck of femur fracture?

A

Little old lady who fell down and was unable to get up, shortened and externally rotatated leg

181
Q

What can occur due to long periods of immobility?

A

Rhabdomyolysis

182
Q

What can rhabdomyolysis cause?

A

Acute kidney injury

183
Q

How can rhabdomyolysis be diagnosed?

A

Raised creatinine kinase

184
Q

How can a neck of femur fracture be diagnosed?

A

Xray pelvis

185
Q

What is the treatment for an intracapsular NOF fracture

A

Total or partial hip replacement,

Hip screw in the young

186
Q

What is the treatment for an extracapsular NOF fracture?

A

Hip screw

187
Q

WHy is there a difference in the surgical management of intra and extracapsular NOF fractures?

A

An intracapsular fracture interrupts the blood supply to the head of the femur, causing avascular necrosis

188
Q

What are the indications for a joint replacement surgery?

A

Moderate to severe joint arthritis that causes pain and/or interferes with daily living

189
Q

What are the contraindications for a joint surgery?

A

Severe osteoporosis, increased falls risk (dementia or alcoholism), Infection, nicotine. Weight is not an exclusion criteria, but obesity reduces the life span of a hip joint

190
Q

What are the parts of the prosthesis seen in a hip replacement?

A

Cup (socket) and beall (femoral stem of hip replacement)

191
Q

What happens after hip replacement surgery?

A

Patient recuperates in hospital for 3-5 days,
Patient is encouraged to walk
Patient must avoid certain movements

192
Q

What types of movement must be avoided in patients with a recent hip replacement?

A

Crossing legs, deep hip bends, extreme rotating or bending of the hip joint.
Patients may sleep with a special pillow for a few weeks

193
Q

What is the focus of physio in patients with a hip replacement?

A

Promoting blood flow to the joint, incresing range of motion, increasing muscle strength, reducing scar tissue formation

194
Q

What are the complications of a total hip replacement?

A

Complications due to analgesia, hip dislocation, different leg lengths, infection, hip stiffness (due to scar tissue formation), damage to surrounding tissue, allergic reaction to bone cement, increased pain

195
Q

What are the complications of knee replacement surgery?

A

Wounds, PE, stiffness, pain, haematoma, bleeding, blood clots, surrounding tissue damage, infection, dislocation

196
Q

How long does a knee replacement last?

A

20 for a total, 10 for a partial

197
Q

What are the types of knee replacement surgery?

A

Total knee replacement, patellofemoral replacement, complex or revision knee replacement, partial knee replacement

198
Q

What is multiple sclerosis?

A

Immune-mediated (T-cell) demylinating disease of the CNS. Causes significant physical disability within 20-25 years

199
Q

What is characteristic of an episode of MS?

A

Symptomatic episodes seperate in location and time

200
Q

What is the classic pattern of MS?

A

Relapsing and remitting

201
Q

What occurs in the CNS due to MS

A

Myelin loss, plaque formation, oligodendrocyte destruction, relative axon sparing, reactive astrogliosis

202
Q

What is optic neuritis?

A

One of the common presentations of MS, characterized by rapidly developing visual impairment in 1 or both eyes, recovering with little defect. Some changes to colour and contrast may be permanent

203
Q

What are the risk factors of MS?

A

Genetics, geography, lack of vitamin D, viral infection

204
Q

Name 10 classical MS presentations

A

sensory loss, spinal cord symptoms ( motor or autonomic), spasticity, heat intolerance, fatigue, trigeminal neuralgia, optic neuritis, depression, frank dementia, bipolar disorder, euphoria, cerebellar signs (ataxia, dysarthria, tremor), facial myokymia, pain, subjective cognitive difficulties

205
Q

What is facial myokymia?

A

Irregular twitching of facial muscles

206
Q

What eye symptoms can occur due to MS?

A

Diplopia, optic neuritis (pain on movement of eye, usually unilaterally, that presents acutely)

207
Q

What are the spinal cord symptoms that can occur with MS?

A

Bladder, bowel and sexual dysfunction, muscle cramping secondary to spasticity

208
Q

What is acute transverse myelitis?

A

Acuteloss of motor, sensory, autonomic, reflex and sphincter function below the level of the lesion

209
Q

What type of transverse myelitis usually occurs in patients with MS?

A

Partial

210
Q

WHat does the typical MS patient look like?

A

young, white and female

211
Q

Name some examination findings in a patient with MS

A

Increased tone or stiffness, hyperreflexic, localised weakness, focal sensory disturbance

212
Q

What are the types of MS?

A

Relapsing remitting,
primary progressive
secondary progressive,
Progressive-relapsing

213
Q

Which type of MS has the poorest prognosis?

A

Primary progresive

214
Q

What is the best test to confirm MS diagnosis?

A

MRI to show evidence of fibrosis

215
Q

What is used to treat MS?

A

Interferons and antibodies

Steroids can increase the rate of recovery but don’t modify disease

216
Q

What are the two common neurological findings in parkinsons?

A

Lewy bodies and loss of pigmented dopaminergic cells in the substantia niagra

217
Q

What is the most common presenting feature of Parkinsons’?

A

Tremor

218
Q

Name some other causes of a tremor?

A

Cerebellar lesions, dystonic tremor, essential tremor, anxiety

219
Q

Which part of the body is affected by parkinson’s?

A

The basal ganglia (substantia niagra) of the brain

220
Q

What does the basal ganglia regulate?

A

Cortical output for normal movemet

221
Q

What is the general pathophysiology of parkinson’s?

A

Decreases ( through direct and indirect pathway), the inhibition of the globus pallidus internus and the substantia niagra. increasing the inhibition of the cortex

222
Q

What are the risk factors of parkinsons’?

A

WHO THE FUCK KNOWS?

TBH, they think its genetic and environmental, but no one can figure out the triggers

223
Q

What can predict more rapid rate of motor progression in parkinnsons’?

A

Older age of onset, initial rigidity/hypokinesia, male, postural instability/gait dificulty

224
Q

Whatcan predict a slower progression course and longer therapeutic benefit from Levadopa?

A

Presentation with a tremor

225
Q

What is the parkinsons triad?

A

tremor, bradykineasia, rigidity

226
Q

What are the non motor symptoms of parkinsons?

A

Hyposmia, constipation, urinary urgency, forgetfulness, excessive saliva

227
Q

What are the initial clinical symptoms of parkinsons?

A

Tremor, reduced dexterity, sleep disturbances, decreased facial expression, soft voice, slowness of thinking, depression, weakness, malaise

228
Q

What type of tremor does parkinsons cause?

A

A pill rolling, resting tremor

229
Q

How can brady kinaesia present?

A

Decreased facial expression,softer speech, drooling, slowness in rising from bed, falls, small, effortful hand writing, decreased dexterity

230
Q

What are the four cardinal signs of Parkinsons’ dsease?

A

resting tremor, rigidity, postural instability, bradykinaesia

231
Q

How can rigidity be tested?

A

Presence of cog wheeling or lead piping

232
Q

What is the diagnostic test for Parkinsons?

A

It is a clinical test. MRI and CT are usually unremarkable. Tests tend to exclude differentials

Reduced intake of flurodopa can be seen in PET imaging in the basal ganglia

233
Q

What is the treatment for Parkinsons?

A

Levodopa with carbidopa
MOA-B inhibitors
Dopamine agonists

234
Q

What signs and symptoms suggest parkinsons plus?

A

Early onset of dementia, postural instability and hallucinations. Impaired vertical gaze, nystagmus, unexplained pyramidal tract signs, symmetriccal signs, postural hypotension and urinary incontinence

235
Q

What is psoriasis?

A

A complex, multifactorial inflammatory disease involving the hyperproliferation of keratinocytes in the epidermis (with increased epidermal cell turnover)

236
Q

What are the types of psoriasis?

A

Nail, pustular, guttate, arthritis, scalp, plaque, chronic stationary, oral, eruptive, erythrodermic

237
Q

What is chronic stationary psoriasis?

A

the most common type of psoriasis, involves scalp, extensor surfaces, genitals, umbilicus and lumbrosacral and retroauricular regions

238
Q

Where does plaque psoriasis usually affect?

A

Extensor surfaces of knees, elbows, scalp and trunk

239
Q

What is guttate psoriasis?

A

type of psoriasis that presents predominanyly on the trunk after a URTI with a group A beta-haemolytic streptococci. More itchy

240
Q

What is inverse psoriasis?

A

Occurs on flexor surfaces

241
Q

Where does pustular psoriasis usually develop?

A

palms or soles, or diffusely around the body

242
Q

What is erythrodermic psoriasis?

A

Typically encompasses nearly the entire body surface area with red skin and a diffuse, fine, peeling skin

243
Q

What is the pathophysiology of psoriasis?

A

Trigger causes an autoimmune, t cell mediated infiltration of the epidermis, inducing keratinocyte proliferation and cytokine production. Parakeratosis occurs, causes poorly adherent stratum corneum leading the flaking and scales
An increase in epidermal cell turnover

244
Q

What does psoriasis usually look like?

A

Erythamatous plaque, papules or macules, well demarcated, non coherent with silvery plaques and a glossy homogenous erythema

245
Q

How does plaque psoriasis present?

A

Raised inflamed lesions covered by white scale

246
Q

How does guttate psoriasis present?

A

Small salmon pink paules

247
Q

How does pustular psoriasis present?

A

Sterile pustules diffused around the body

248
Q

How does nail psoriasis present?

A

Thickened and yellowish nails, nail may separate from nail bed

249
Q

What are the complicationcs of psoriasis?

A

Secondary infections, psoriatic arthritis, mitral valve prolapse

250
Q

What lab studies should be done for psoriasis?

A

RF, ESR, check if fluid from pustules is sterile, perform fungal studies

251
Q

What is the treatment of psoriasis?

A

light therapy, stress reduction, climatotherapy
moisturizers and salicylic acid as scale removing agents, topical corticosteroids, keratolytics, vit D analogues, immunemodulators

252
Q

What is the typical presentation of rheumatoid arthritis?

A

Symmetrical swollen proximal joints, with stiffness, pain worst at morning,

253
Q

Name five less common presentations of rheumatoid arthritis

A

Widespread systemic arthritis,
Persistent monoarthritis of a single joint
Systemic illness with extra auricular symptoms
Recurrent soft tissue problems (eg carpal tunnel, frozen shoulder)
Recurrent mono/poly arthritis

254
Q

What are the early signs of rheumatoid arthritis?

A

Swollen and tender mcp, pip, wrist and mtp joints. Check for synovitis and tendinitis

255
Q

What are the late signs of rheumatoid arthritis?

A

Swan neck deformity, ulnar deviation, z thumb, dorsal wrist subluxation, with similar foot changes

256
Q

What are the extra articulate signs of rheumatoid arthritis?

A

Nodules, lymphadenopathy, vasculitis, scleritis, episcleritis, fibrosing alveolitis, obliterating bronchitis, carpal tunnel, splenomegaly, raynaud’s, peripheral neuropathy, amyloidosis, osteoporosis

257
Q

What blood tests can be done for RA?

A

ESR, CRP, RF,Anti CCP, ANA

258
Q

Which of the blood tests for RA is most diagnostic?

A

AntiCCP

259
Q

What can be seen in a radiograph for rheumatoid arthritis>

A

Soft tissue swelling, symmetric or concentric joint space narrowing, osteoporosis, marginal bone erosion

260
Q

What is the first line therapy for RA?

A

Methotrexate

261
Q

What is early RA treated with?

A

Disease modifying anti-rheumatic drugs

262
Q

What are the possible surgical treatments for RA?

A

Synovectomy, tenosynovectomy,, tendon realignment, recontructive surgery

263
Q

What types of medication are used for RA?

A

DMARDS steroids, NSAIDS, analgesics

264
Q

What signs are present in a TACS

A 
All three of the following:
1. Unilateral weakness (and/or sensory
deficit) of face, arm and leg
2. Homonymous hemianopia
3. Higher cerebral dysfunction (dysphasia,
visuospatial disorder)
265
Q

What signs are present in a PACS

A 
Two of:
1. Unilateral weakness (and/or sensory
deficit) of face, arm and leg
2. Homonymous hemianopia
3. Higher cerebral dysfunction (dysphasia,
visuospatial disorder)
266
Q

What signs are present in a POCS

A

One of

  1. Cerebellar or brainstem syndromes
  2. Loss of consciousness
  3. Isolated homonymous hemianopia
267
Q

What signs are present in a LACS

A

one of:
Unilateral weakness (and/or sensory deficit)
of face and arm, arm and leg or all three.
Pure sensory stroke.
Ataxic hemiparesis.

268
Q

Why is a CT Head important for a suspected stroke?

A

To identify haemorrhaagic strokes and treat ischaemic strokes and haemorrhagic strokes accordingly

269
Q

What are the four important stroke mimics?

A

Migraine, Hypothermia, hypoglycaemia, epilepsy

270
Q

What are the RF for strokes?

A

Anticoagulants, AF, age, sex, Cholesterol, HTN, family history,

271
Q

What is the acute management of haemorrhagic strokes?

A

Reversal of thrombolytic treatment - Vit K + serum plasma proteins

272
Q

What is the acute management of ischaemic strokes?

A

300mg aspirin

FOCP (12 decks)

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