Week 2 Flashcards

1
Q

Causes of cardiac arrhythmia

A

Coronary artery disease, htn, cardiomyopathy, valve disorders, electrolyte imbalance, injuries from MIs, post-surgical healing.

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2
Q

left sided heart failure: causes what, signs, reasons: murmur, cough, pndysp+dizzy (5)

A

Lshf makes blood pool in lungs > inc pressure > oedema and resp symp from lack of reception of o2 blood.

Crackles heard in bases but everywhere if pulmonary oedema. Cyanosis, dsypnoea, Orthopnea, laterally displaced apex beat if cardiomegaly/ left vent hypertrophy or dialation.

Murmur indicate valve disease- aortic stenosis as a cause or mitral regurgitation as a result.

Cough and wheeze can come from congestive failure. Paraoxysmal nocturnal dyspnea attacks can indicate left sided heart failure

Compromise of left sided systemic flow makes dizzy, confused, cool extremities. Often on exertion.

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3
Q

Right sided heart failure signs (5)

A

Associated with issues of pulmonary circulation- eg pulmonary htn/stenosis.

fixed pitting oedema

Ascites, effusion, liver and spleen enlargement. Raised JVP sometimes.

Rvent pressure inc can give a parasternal heave.
Sacral oedema
nocturia
Liver issues go to congestive heart failure, jaundice and coagulation issues.

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4
Q

High output failure + causes (2)

A

Hf from more blood circulating than the heart can cope with.

Transfusion, kidney disease, severe chronic anaemia, vitamin B, hyperthyroidism, cirrhosis, pagets disease multiple myeloma, arteriovenous fistula or malformation

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5
Q

Pericarditis signs, cause, treatment (4)

A

Symptoms include stabbing chest pain, pain in neck spreading to shoulders/arms, fever, nausea, shortness of breath.

Worse when lying down and better when leaning forward.

Mostly idiopathic. Some causes are viral/bacterial infection, an autoimmune disease, myocarditis rubbing against pericardium eg after surgery or MI.

Diagnose anti inflammatory drugs like colchicine, painkillers, pericardial window surgery.

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6
Q

Pericardial effusion, cause, signs, treatment (4)

A

Build up of fluid in the pericardial space. Too much can put pressure of the heart known as cardiac tamponade, restricting heart expansion and O2 delivery.

Causes include metastasised cancer, bacterial or viral infection or inflammation of the pericardium, immune disease, kidney failure with uremia, medication reaction and radiation.

Symptoms are chest pain, enlarged jvp, fainting, tachycardia, nausea, urq pain, short of breath, limb swelling, hypotension if severe.

Antibiotics or pericardiocentresis

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7
Q

Pleural effusion, signs, causes, treatment, association (6)

A

Build up of fluid in pleural space. Dense white on X-ray.

Can be transudate ultra filtered plasma from eg heart failure or cirrhosis. Or can be exudate from inflammation which is difficult to treat. Stuff like pneumonia, lung cancer.

Signs are dyspnea, fast breathing, chest pain on inspiration/exhalation and cough.

Major causes: congested heart failure, kidney failure, pulmonary embolism, hypoalbuminemia, cirrhosis, trauma

Exudate looks like ldh > 0.45 of upper limit norm blood value, protein > 2.9g/dl and cholesterol > 45mg/dl (all in the pleural fluid)

Can give thoracentresis, surgery to separate tissue, or pleural desis

Congestive heart failure is associated to atherosclerosis, htn,thyroid bc blood x be pumped out. Backflowmakes swelling and vessels leak

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8
Q

Pulmonary oedema, causes c or not, symptoms, flash po. (5)

A

Also pulmonary congestion, liquid accumulation in the bronchioles. Makes impaired gas exchange and possible resp failure or cardiac arrest

Cardiogenic/left ventricular or non cardiogenic
Cardiogenic = congestive heart failure eg valve to ventricular failure, arrhythmia, fluid overload eg kidney failure, hypertensive crisis

Non cardiogenic = from negative pressure eg inhaling against an upper airway obstruction rupturing capillaries. Also caused by pe, acute lung injury or seizure

Symptoms are dyspnea, pink sputum, sweating, orthopnea, and paroxysmal nocturnal dyspnea, peripheral oedema, raised jvp, hepatomegaly, crackles, third heart sound

Flash pulmonary oedema is caused by acute MI, aortic regurgitation, raised left vent pressure, htn, renal artery stenosis

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9
Q

Direct acting oral anticoagulant names, reversals, MU, contraindicated (5)

A

Risk of bleeding. Includes apixaban, dabigatran, edoxaban and rivaroxaban.

Dabigatran reversal = idarucizumab
Apixaban/rivaroxaban = andexanet alfa

Anticoagulant. Prevents MU when with acetylsalylic acid (+ clopidogrel or ticlipidine)

X for antiphospholipid syndrome or prosthetic heart valves

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10
Q

Vitamin K antagonist, contracondition, risks (4)

A

Eg warfarin. Don’t use with hep c now either, not many antibiotics or antivirals. Risk of bleed. Risk bacterial endocarditis

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11
Q

Verapamil hydrochloride uses, contraind (3)

A

Is a calcium channel blocker for htn and arrhythmia like supra ventricular, paroxysmal tachy, angina. Also for prevention of cluster headaches, acute porphyria ( aflut or afib with accessory pathway), bradycardia, hf with red ef, 2/3rd degree heart block

Not good for postural hypotension nor early on MI

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12
Q

Procainamide uses, risks (2)

A

Anti arrhythmia for ventricular ectopy, tachycardia, supra ventricular arrhythmia, reentry tachycardia,afib. Sodium channel blocker

Risk bradycardia, hypotension, shock, drug lupus erythema

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13
Q

Isoprenaline/isoproterenol uses, when, not (4)

A

Treatment for bradycardia, asthma and heart block. Beta agonist. Adjunct treatment for hypovolemic and septic shock.

Not good tachy arrhythmia.

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14
Q

What does the congenital and perinatal infection acronym ToRCHeS stand for?

A
Toxoplasmosis 
Rubella
Cytomegalovirus 
Herpes simplex 
Syphilis
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15
Q

Necrotising enterocolitis, treatment, abx, xray, symptoms (5)

A

Too little o2 or perfusion to the intestine at birth or later. The intestinal wall becomes damaged and it is eroded by the growth of bacteria or viruses.

Treatment is for stage one or two. Involves stopping enteral feedings, giving nasogastric decompression and broad spectrum antibiotics.

Ampicillin, gentamicin and metronidazole

X-ray shows multiple small bubbles on the wall of the intestine

Symptoms abdominal pain, swelling, bloody diarrhoea, green or yellow vomit, lethargy and no appetite

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16
Q

Retinopathy of prematurity/retrolental fibroplasia RLF/ Terry syndrome (3)

A

Prem baby after o2 therapy have disordered growth of retinal vessels leading to scarring and detachment sometimes. Main treatment is peripheral retinal ablation

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17
Q

Cerebral palsy, risk, 3 classes

A

Group of movement disorders presenting at childhood

Poor coordination, stiff or weak muscles, tremors, sensory and speech impairment. Often don’t roll or sit at their milestones. Can have seizures.

Risk is preterm, being a twin, infection in pregnancy, hard delivery or early head trauma

Can be spastic, ataxic or dyskinetic

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18
Q

Perinatal asphyxia, dates, signs, risk, treatment (5)

A

Being o2 deprived at birth or in the womb enough to cause harm usually to the brain. Sometimes specific organs. From 28th week gestation to 7 days old
Shows hypoxia damage and metabolic acidosis

Can sometimes lead to hypoxia ischemia encephalopathy or intraventricular haemorrhage

Adrenaline and a to e

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19
Q

Perinatal cord prolapse signs and treat

A

C section treats with cord decompression. Signs are low fetal heart rate that doesn’t resolve

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20
Q

Anticoagulant vs antiplatelet

A

Anticoagulants interfere with clotting factors in the blood. Eg stops thrombin from working by binding to antithrombin, or inhibiting vitamin k.

For people with prior history of blood clots like dvt, coronary artery clots, PE and atrial fibrillation which gives high risk of clots.

Side effects are haemorrhage, high potassium levels, thrombocytopenia. Examples include heparin, warfarin, rivaroxaban, apixaban and dabigatran.

Antiplatelets stop platelets sticking in the blood stream. Good for those who had ischemic strokes, coronary artery issues, heart valve surgery, bypass surgery, stents and those presently having a heart attack, angina, TIA and PAD.

Side effects are haemorrhage, GI upset and dizziness. Examples include aspirin, clopidogrel dipyridamole and abciximab

Prophylaxis or stable cvd- anticoagulant. Secondary prev or very high risk- both
NV Afib- 2antip+antic, 6 m then one of each for 6m then antip
Valve disease- antic or both if super high clot risk
Dvt- both then after 3m antic

Lower dose antic when with antip

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21
Q

What is hepatitis, symptoms (3)

A

Acute parenchymal liver damage caused by drugs, bugs, autoimmune disorders and metabolic disorders

Alcoholic liver disease is one of the most common causes for alcoholic cirrhosis and alcoholic hepatitis that leads to cirrhosis also. This leads to hepatocellular carcinoma

Symptoms of alcoholic liver disease include asymptomatic elevated transaminases. Steatosis disappears after 3 months of alcohol abstinence.

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22
Q

Presentation of alcoholic hepatitis

A

Jaundice and hepatomegaly. 1/3 die in acute presentation, particularly if has hepatic encephalitis or prolonged prothrombin time. If abstain, 70% survive to 5 yrs.

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23
Q

Presentation of alcoholic cirrhosis, cells, leads to

A

Only presents with complications: varceal haemorrhage or ascites. If presents with severe complications, 50% survive to 5 yrs. There’s also inc risk of hepatocellular carcinoma.

Cirrhosis includes diffuse fibrosis, distorted hepatic vasculature. Can give portal htn and affects enzymes, clotting and filtration functions.

Leads to: dec factors, hepatic encephalopathy (confusion with raised icp from neurotoxins not metabolised), ascites, varices, hepatorenal syndrome - renal vasoconstriction due underfilled systemic circulation when there’s portal htn and ascites.

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24
Q

Acute liver disease: causes, presentation and cell changes.

A

Acute liver disease is likely Hep A or E enterally transmitted.

Presents malaise, nausea, anorexia, couple weeks in jaundice. Also hepatomegaly and lymphadenopathy. Will have raised AST and ALT before jaundice.

Hepatocytes swell, vacuolate, cytoplasmic granulation and necroses. Patchy and multiacinar all over but worst on the outside of the organ at periphery.

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25
Q

Bugs of liver disease

A

Hep A B C D E, EBV, CMV, Herpes simplex, Toxoplasmosis and yellow fever

26
Q

Chronic hepatitis: cause, presentation and cellular change

A

Hepatitis lasting 6m+. Presents similar to acute but less severe. Has relapses and chronic raised transaminases.

Within the liver lymphocytes and plasma cells congregate. There’s a distorted portal plate, love change with the necrosis joined by fibrosis and often then cirrhosis. Usually caused by hep B/D and hep C.

Can be treated with peg interferon.

27
Q

Chronic hepatitis D

A

Can’t replicate without Hep B. A superinfection of D can flare hep B. Having D with B brings cirrhosis faster. Fewer are responsive to peg interferon treatment too.

28
Q

Hep C

A

Often in iv drug users and was in haemophiliacs before blood screening. Not often sexually transmitted. Most are asymptotic unless chronic. Can get flu and jaundice.

Extrahepatic symptoms can be arthritis, photo sensitivity, rash, diabetes, lichen planus.

When severe or chronic there’s minimally raised Alts

29
Q

Autoimmune liver disease

A

Most common in women and associated with diseases like coeliacs, pernicious anaemia, thyroiditis and AIHA.

Two types. ANA and anti SLA is the first and antiLKM is the second. Second o sets earlier eg teens.

Fatigue, acute hepatitis, jaundice, high aminotransferases, cirrhosis, hepatosplenomegaly and things like poly arthritis

30
Q

Wilson’s disease

A

Disorder of copper metabolism. Copper is transported to the liver bound to albumin to become caeruloplasmin. Doesn’t happen in Wilson so copper is deposited into liver, basal ganglia, cornea and gives kaiser fleisher rings. Serum copper and caeruloplasmin will be low. Signs are liver and neuro based. Can lead to cirrhosis.

31
Q

Haemochromatosis

A

In this disease there’s inc risk of diabetes and pancreatic cancer. Iron deposits in the liver leading to hepatomegaly and increased liver enzymes. RUQ pain and risk of fibrosis, cirrhosis and cancer.

Iron can also damage liver joints pancreas heart. 30-60 years old.

Might show fatigue, weight loss, joint pain,erectile dysfunction, irregular periods. Treat with phlebotomy or chelation iron reducing drugs

32
Q

Which liver diseases often show palmar erythema?

A

Cirrhosis, Wilson’s and haemochromatosis

33
Q

Treatment for oesophageal varices

A

Terplipressin.

34
Q

Primary biliary cholangitis

A

(Not primary sclerosing cholangitis - large bile duct inflammation and scarring)

It’s a chronic liver disorder mostly seen in middle aged women. Inflammation of small bile ducts in the liver leading to scarring. It can give jaundice and cirrhosis. Stages 1-4. Symptoms = fatigue, pruritus, jaundice. Complications can be portal htn, fat malabsorption, fat deposits, osteoporosis.

Patient may be comorbid with thyroid disease, sjogrens, celiacs.

Will have high ALP and anti mitrochondrial antibody

35
Q

Primary biliary sclerosis/primary sclerosing cholangitis

A

Chronic disease of bile ducts that become blocked because of inflammation, scarring and fibrosis. This causes bile to accumulate in the liver where in damages cells making fibrosis and cirrhosis. Very Gradual onset. Can also lead to cholangiocarcinoma or gallstones.

36
Q

Gilbert syndrome

A

Genetic liver disease where body can’t process bilirubin leading to hyperbilirubinemia. The body lacks an enzyme for its elimination. May be asymptomatic until teens and present with jaundice.

Bilirubin increases with stress, exertion, dehydration, alcohol consumption, fasting and infection.

If symptomatic: fatigue, nausea, abdominal pain and diarrhoea. More common in men

37
Q

Cholangiocarcinoma

A

Cancer occurring in any part of the bile drainage system so can be intrahepatic or extrahepatic.

Symptoms: jaundice, weight loss, bloating, abdominal pain, itching, dark urine, light stool. But may not be symptomatic until metastasis. It can occur from psc, ulcerative cholitis, hepatitis, cirrhosis.

38
Q

G6PD deficiency / glucose 6 phosphate dehydrogenase deficiency

A

Hereditary condition with hemolysis when body is exposed to foods like fava beans, infection or stress.

Symptoms during an episode: haemolytic anaemia, pallor, jaundice, dark urine, fatigue, splenomegaly and tachycardia

Heinz bodies appear when there’s damage to haemoglobin from thiosulfate compounds.

39
Q

What can itching in liver disease be?

A

Primary biliary cirrhosis, primary sclerosing cholangitis, intrahepatic cholestasis of pregnancy

40
Q

How ascites is formed and how to treat

A

Peripheral arterial dialation from splanchnic arterial vasodilation from high NO levels makes intravascular underfilling that stimulates raas and sns releasing vasopressin. More sodium and water retention leads to more fluid accumulation in the peritoneal cavity.

Also caused by heart failure, TB, pancreatitis, blockage of the hepatic vein.

Treated via paracentesis restricting sodium and diuretics. Treat underlying disease too.

41
Q

Crigler najjar syndrome

A

Types 1 and 2; bud orders of bilirubin conjugation with consecutive indirect hyperbilirubinemia of different severity. Mutation in the UGT1A1 gene.

Type 1 is rarer, shows high levels of bilirubin shortly after birth >20-50mg/dl. There are no bilirubin glucuronides in bile. It’s associated with bilirubin encephalopathy and death unless managed with photo therapy and plasma exchange transfusions. Risk for kernicterus continues into adulthood. Phenobarbital x work.

Type 2 Arias syndrome has reduced UGT1A1 and is recessive. Levels don’t exceed 20mg/dl and glucuronides are present in bile. Rarely kernicterus. Responds to phenobarbital to reduce bilirubin by ~30%. Type 2 should avoid drugs that displace unconjugated bilirubin from plasma binding sites eg sulfonamides, salicylates and penicillin.

Both show jaundice. Type 2 gets it often after infection, anaesthesia or drugs. Type 1 accumulates and kernicterus presentation can show hypotonia, deafness, oculomotor palsies and death by 2 if untreated.

42
Q

Rotor syndrome

A

Is recessive mixed conjugated and unconjugated hyperbilirubinemia leading to non haemolytic jaundice. Less than 20mg/dl bilirubin. Gene mutation impairs clearance of bilirubin .

43
Q

Dubin Johnson syndrome

A

Recessive isolated raise in conjugated bilirubin in serum as an inability to excrete into the bile for clearance. Condition causes a black liver due to deposits of a melanin like pigment. It’s asymptomatic and often doesn’t need treating. Has raised urine coproporphyrin like Rotor syndrome but with proportion of isomer that’s 80% instead of 25% of what is there.

44
Q

Intrahepatic cholestasis of pregnancy

A

Raised oestrogen and progesterone slows the flow of bile causing buildup. Can cause itchy jaundice. Treated with ursodiol. The condition is a risk factor for preterm birth.

45
Q

Pellagra and Niacin

A

Pellagra is caused by lack of niacin B3. Symptoms include peeling inflamed skin , diarrhoea, dementia, sores in the mouth. Skin is uv sensitive.

Primary pellagra is from diet without niacin and tryptophan. Secondary is poor niacin ingestion and utilisation from the diet. Can result from alcoholism, long term diarrhoea, carcinoid syndrome, Hartnup disease and medications like isoniazid (TB antibiotic).

Diagnosis from presentation and Urine+Electrolytes. Treat with niacin or nicotinamide. Disease occurs in developing countries the most.

Niacin can also be used to treat high cholesterol. May flush as a side effect- then take with aspirin.

46
Q

Symptoms of Parkinson’s

A

Psychosocial: depression, anxiety, cognitive impairment including dementia, OCD behaviour, psychosis as delusions and hallucinations.

Physical: tremors, slow movements, stiff and inflexible muscles

47
Q

Symptoms of Huntington’s disease

A

Early symptoms: lack of concentration, poor memory, depression, clumsiness, mood swings.

Later symptoms: chorea (involuntary jerking) dystonia (rigid or contracting muscles), abnormal eye movements, impaired gait, posture and balance, difficulty speaking and swallowing.

Onset 30-50

48
Q

What does INR measure

A

Measure of coagulation + monitored on those taking warfarin. Low vitamin k can raise the INR

If a large bleed is indicated- stop warfarin and give k as fresh frozen plasma or prothrombin complex

Small bleed- stop warfarin and give k + 24hrs take INR

INR 8+ : stop warfarin and give k + 24hrs take INR

INR 5+: stop 1-2 doses of warfarin then review maintenance dose at clinic

49
Q

Presentation of meningitis

A

Lethargy, headache (stiff neck) fever (not always) rigours, vomiting, non blanching rash

Give im benzyl penicillin

50
Q

What causes slapped cheer syndrome

A

Parvovirus b19

Gives a fever

51
Q

Hand foot and mouth is what

A

Comes with the common cold. Blisters/ulcers on hands, feet and mouth with a fever

Coxsackie a16

52
Q

Presentation of scarlet fever

A

Course red rash, sore throat, headache, fever, red tongue

Give phenoxymethylpenicillin
Infectious until 24 hrs after treatment dose 1/10days

53
Q

Measles symptoms

A

Red blanching maculopapular rash and crust over to form blisters that can be itchy. ALSO fever, cough, runny nose, conjunctivitis and kopliks spots before.

54
Q

Roseola vs rubella

A

Roseola is herpes 6 and gives systemic red lace rash and a fever.

Rubella has posterior auricular lymphadenopathy and a rash that spreads head to chest

55
Q

Types of thyroid cancer

A

Papillary cancer = 70% and shows she 30-40. Can spread locally and compress trachea and also metastasise to bone and lung.

Follicular = in women and those with low I. Iodine. Presents 30-60. More likely to metastasise than stay local

Medullary cancer (associated with MEN) and anaplastic cancer presenting 55-80 years old. Often metastasise and spreads to lymphatics. Invasive.

Thyroid lymphoma: 10% and is non Hodgkin lymphoma for 50-80 years old and familiar with Hashimoto’s thyroiditis.

56
Q

Types of lung cancer (non small cell)

A

Non-metastatic manifestations of bronchial carcinoma
It is important to recognise non-metastatic complications of bronchial carcinoma, which can arise due to local invasion. These complications can include:
Shortness of breath: people with lung cancer can experience shortness of breath if the cancer invades major airways.
Haemoptysis: the invasion of cancer into the airways which is friable tissue may lead to bleeding.
Pain: advanced lung cancer may cause local invasion affecting the lining of pleural cavity or bone causing pain.
Pleural effusion: lung cancer can cause inflammatory reactions which lead to the accumulation of fluid in the pleural space.
Superior vena cava obstruction: the cancer may invade into surrounding tissues leading to compression of the drainage of the superior vena cava leading to dyspnea and facial plethora due to venous congestion.
Pneumothorax: invasion of the tumour may lead to a communication between the lung parenchyma and the pleural cavity resulting in the collapse of the lung.
Atelectasis (collapse of a lung or lobe): the invasion of a tumour may lead to total obstruction of the airway leading to collapse of that lobe.
Important Features of Squamous cell carcinoma
Most common type of lung cancer in the UK
Usually present as obstructive lesions of the bronchus leading to infection.
Occasionally cavitates (10% at presentation) Lung Ca that most commonly cavitates
On X-ray it is not possible to tell whether it is an abscess or a cancer (the border’s definition cannot be easily seen) but on the CT there is obviously a jagged border – indicating cancer.
Local spread is common, but metastasis are normally late (but frequent)
Often causes hypercalcaemia – by bone destruction or production of PTH analogues (PTHrp).
Also associated with clubbing and HPOA (Hypertrophic pulmonary osteoarthropathy)
Important Features of Adenocarcinoma
Arises from mucous cells in the bronchial epithelium
Commonly invades the mediastinal lymph nodes and the pleura, and spreads to the brain and bones
Does not usually cavitate
Proportionally more common in non-smokers, women and in the Far Eastleast likely to be related to smoking
Most likely to cause pleural effusion (as are mesotheliomas)

57
Q

Lung cancer- small cell

A

Important Features of Small cell carcinoma
Arise from endocrine cells (Kulchitsky cells). These are APUD cells, and as a result, these tumours will secrete many poly-peptides mainly ACTH.
They can also cause various presentations such as Addison’s and Cushing’s disease.
Small cell carcinoma spreads very early and is almost always inoperable at presentation.
These tumours do respond to chemotherapy, but the prognosis is generally poor.

58
Q

Symptoms of lung cancer

A
Symptoms
Cough
Haemoptysis
Dyspnoea
Chest Pain
Weight loss
Nausea and Vomiting
Anorexia
Signs
Cachexia
Finger Clubbing
Hypertrophic pulmonary osteoarthropathy
Anaemia
Horner's syndrome (if the tumour is apical)
Examination of the chest: consolidation (pneumonia); collapse (absent breath sounds, ipsilateral tracheal deviation); pleural effusion (Stony dull percussion, decreased vocal resonance and breath sounds)
Enlargement of supraclavicular and axillary lymph nodes
Paraneoplastic syndromes: Cushing's syndrome, SIADH, and Lambert-Eaton syndrome (suggest small-cell), hyperparathyroidism (suggests squamous cell)
59
Q

Lung cancer management

A

Non-small cell lung cancer (NSCLC) management
First-line: lobectomy
Curative radiotherapy can also be offered to patients with stage I, II and III NSCLC.
Chemotherapy should be offered to patients with stage III and IV NSCLC to control the disease and improve quality of life.
Small-cell lung cancer management
Generally palliative chemotherapy, as tumours are disseminated on presentation.

60
Q

What are the paraneoplastic syndromes?

A
Paraneoplastic Syndromes in Lung Cancer
Neurological
Polyneuropathy (Antibodies against the myelin sheath)
Cerebellar degeneration
Lambert-Eaton Syndrome

Vascular and haematological complications: Anaemia and Thrombophlebitis migrans
HPOA (Hypertrophic pulmonary osteoarthropathy) this occurs in 3% of cases. There will be joint stiffness, and severe pain in the wrists and ankles, sometimes also gynaecomastia. On x-ray there will be proliferative periostitis at the ends of the long bones, which have an ‘onion skin’ appearance. This is also associated with finger clubbing where cancer is the cause. It is thought to be caused by a blood borne factor released by the tumour – when patients have the primary tumour removed, the pain goes away!

Finger clubbing: 30% of cases – caused by non-small cell carcinoma.
Carcinoid syndrome - This presents with hepatomegaly, flushing and diarrhea
Inappropriate ADH secretion – this can cause hyponatraemia
Ectopic ACTH secretion – causing Cushing’s syndrome
Hypercalcemia (squamous) – due to the secretion of parathyroid hormone related peptides (PTHrp).

61
Q

Large bowel obstruction

A

Abdominal pain – often cramping
Bloating
Absolute constipation – not passing wind and faeces
Nausea and vomiting – may occur, but occurs more commonly in small bowel obstruction. Vomiting is a later sign in large bowel obstruction.

Causes (in order of most common)
Colonic tumour
Strictures – secondary to diverticular disease, or other conditions such as inflammatory bowel disease or post-surgical anastomosis
Volvulus – sigmoid or caecal
Hernias
Adhesions

Investigations
Abdominal X ray – helps to establish diagnosis of large bowel obstruction
CT Abdomen can be useful to establish cause (e.g. malignancy), as well as provide other useful information such as transition point and distinguishing between caecal and sigmoid volvulus

Management
Supportive care – analgesia, IV fluids, anti-emetics
Decompression of sigmoid volvulus – using flexible sigmoidoscope
The majority of patients (70%) with large bowel obstruction require surgical intervention – laparoscopic or open colonic resection. This can involve a primary anastomosis or stoma formation.

62
Q

Causes of large bowel obstruction

A

Caecal volvulus
The caecum is the second most common site for a large bowel volvulus to occur at. A ‘caecal embryo sign’ may be seen as the dilated caecum resembles a mammalian embryo on AXR.

Small bowel obstruction
AXR of small bowel obstruction would show centrally located dilated loops of bowel, with valvulae conniventes present. The most common cause of small bowel obstruction is adhesions, secondary to abdominal surgery.

Sigmoid volvulus
The AXR shows a ‘coffee bean’ sign which is a feature of sigmoid volvulus. The twisted loop of dilated sigmoid colon is said to resemble a coffee bean. This patient systemically unwell and needs immediate decompression by sigmoidoscopy and insertion of a flatus tube. As this is a closed loop bowel obstruction, he is at high risk of perforation and/or bowel ischaemia.

Toxic megacolon
Toxic megacolon usually occurs as a complication of ulcerative colitis or ischaemic colitis. AXR would show a dilated large bowel of ≥6cm. There may also be thumbprinting observed, due to mucosal oedema. Pneumoperitoneum may also be present if perforation occurs.

Paralytic ileus
Paralytic ileus occurs due to adynamic bowel secondary to the absence of normal peristalsis. Patients usually present with symptoms that are similar to mechanical bowel obstruction. AXR may show distended small and large bowel loops that are filled with gas.