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Conditions Flashcards

1
Q

Symptoms and signs of liver disease

Be able to explain each

A
  • Compensated signs: Xanthelasmas, parotid involvement, spider naevi, gynaecomastia, small/large liver, splenomegaly, Palma erythema, clubbing, Dupuytren’s contracture, xanthomas, testicular atrophy, purpura pigmented leg ulcers
  • General signs: Rapid onset of jaundice, Fever, loss of body hair, nausea, anorexia
  • Decompensated signs: neurological i.e. Disorientation, drowsiness and confusion (hepatic encephalopathy), hepatic flap, fetor hepaticus, ascites, dilated veins on abdomen, oedema, haematemesis and melaena (bleeding oesophageal varices)
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2
Q

Investigations for alcoholic liver disease

A

FBC: Neutrophilia - leucocytosis and thrombocytopenia (due to bone marrow hypoplasia and/or hypersplenism associated with hypertension)

SERUM ELECTROLYTES: often abnormal with hyponatraemia

LFTs: elevated - with AST:ALT > 2. Elevated bilirubin. Low serum albumin. Elevated INR (prolonged prothrombin time).

Microscopy and culture

USS

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3
Q

Management of ALD

A

Supportive - adequate nutrition, corticosteroids (contraindicated in renal failure)

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4
Q

What is anaemia?

A

Normal physiology= blood= made up of different cells with different functions= rbc- for taking O2 from the air we breathe in to all the different areas of the body that need it to work, wbc to fight infection, platelets to help clot blood if we hurt ourselves so that we don’t bleed continuously, and proteins with different functions- can help with transport if hormones and drugs around the body.

RBC produced by bone marrow- region of our bones, and these need to be released continuously into blood to replace those which are lost through breakdown- must break down rbc when no longer able to carry out their function effectively. rbc contain a protein known as Hb and it is this which binds O2 for transport. for constant rbc production, the bone marrow must be working effectively and nutrients such as iron and vitamins are needed.

Anaemia means that the amount of this important protein haemoglobin in the blood is less than normaly, which may mean there is less of it in each rbc, or that there is less rbc. Both of these mean that less O2 can carried to the different areas of the body as Hb needed to carry it and is reduced.

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5
Q

Signs & symptoms of anaemia

A

Will depend on severity and speed of onset - older adults role rate anaemia less well than young people

Fatigue, faintness and breathlessness

Pale skin and mucous membranes

May be a tachycardia and systolic flow murmur

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6
Q

Ddx iron deficiency

A

Blood loss eg menses
Increased demands eg growth, pregnancy, breast feeding
Decreased absorption eg small bowel disease or post-gastrectomy
Poor intake

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7
Q

Treatment for iron deficiency anaemia

A

Find and treat underlying cause

Oral iron - ferrous sulphate or ferrous gluconate

Parenteral iron (deep intramuscular or intravenous infusion (eg severe malabsorption)

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8
Q

Baseline investigations in a patient with atrial arrhythmia

A

ECG
TFT
Transthoracic echocardiogram

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9
Q

Causes of atrial arrhythmia?

A 
Ischaemic heart disease
Rheumatic heart disease
Thyrotoxicosis
Cardiomyopathy 
Wolf-Parkinson White syndrome
Pneumonia
Atrial septal defect
Carcinoma of the bronchus
Pericarditis
Pulmonary embolus
Acute & chronic alcohol use
Cardiac surgery
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10
Q

Epidemiology and signs of AF

A

Most common arrhythmia - 5-10% of pts over 65 years

Atrial activity is chaotic and mechanically ineffective

Irregularly irregular pulse

Can be asymptomatic or present with range of symptoms from palpitations and fatigue to heart failure.

No clear p waves on ECG

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11
Q

Treatment of AF

A

1) Treat underlying cause (chest infection, alcohol toxicity, hyperthyroidism)
2a) Haemodynamically unstable pt: heparin and electrical cardioversion. IV Amiodorone if unsuccessful.
2b) Stable patient: rate control and rhythm control.

Rate - Preferably beta blockers and calcium antagonists (Virapamil/ Diltiazem). However digoxin in sedentary pts.

Rhythm - appropriate in

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12
Q

Epidemiology and risk factors for a thromboembolic stroke or TIA?

A

Second most common cause of death world wide

Major risk factors are those for atheroma - hypertension, diabetes, cigarette smoking, hyperlipidaemia, obesity, alcohol consumption, AF,

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13
Q

Define stroke

A

Rapid onset of neurological deficit (often focal) as the result of - vascular lesion and associated with infarction of nervous tissue.

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14
Q

Describe the Pathophysiology of a completed stroke

A

Most (85%) due to cerebral infarction as a result of arterial embolism or thrombosis. Thrombosis occurs at site of an atheromatous plaque in carotid, vertebral or cerebral arteries. Emboli arise from atheromatous plaques in carotid/vertebrobasilar arteries, or from cardiac mural thrombi or left atrium AF

15% - intracranial or subarachnoid haemmorhage

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15
Q

Describe a TIA

A

Usually result of microemboli arising from atheromatous plaques or cardiac mural thrombi. May also be caused by temporary drop in cerebral perfusion (eg cardiac dysrhythmia, hypo or hyper perfusion).

Rarely tumours of Subdural haematomas may present similar clinical picture.

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16
Q

Investigations for acute stroke

A

Brain CT (or MRI)

Bloods - FBC, ESR, U&Es, cholesterol, INR

Carotid artery imaging (particularly in TIA)

ECG - look for AF/ MI

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17
Q

Treatment of stroke

A

Aspirin 300mg daily

Thrombolysis - IV alteplase, improves functional outcome if given within 4.5h of onset in ACUTE stroke where haemorrhage has been excluded.

Hypertension - reduce

Supportive - stroke unit, SALT, hydration, avoid pressure sores, TED stockings.

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18
Q

List the indications for fibrinolytics

A

Acute MI - within 12 hours of symptom onset

Massive PE with hypotension

Acute Ischaemic stroke

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19
Q

ADRs and contraindications of fibrinolytics

A

Risk of haemorrage, hypotension, allergic reaction with streptokinase.

Contra: GI/ GU bleeding, aortic dissection, uncontrolled hypertension.

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20
Q

Common site and Clinical features of a cerebral hemisphere infarct

A

Internal capsule (due to occlusion of MCA)

Contralateral hemiplegia, hemisensory loss, UMN facial weakness & hemianopia

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21
Q

Artery and Presentation of brainstem infarction

A

Lateral medullary syndrome - occlusion of PCA. Sudden vomiting and vertigo, ipsilateral Horner’s syndrome, facial numbness, cerebellar signs and reduced gag reflex.

Coma - Retucular activator system

Locked in syndrome

Pseudobulbar palsy

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22
Q

Outline the pathophysiology of COPD

A

Chronic bronchitis -> narrowing: hypertrophy and hyperplasia of mucus secreting glands of bronchial tree. Bronchial wall inflammation & mucus oedema. Loss of ciliated epithelium.

Emphysematous changes –> loss of surface area and elastic recoil (which normally keeps airways open during expiration): destruction of alveolar walls.

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23
Q

Clinical features of COPD

A

Cough & sputum
Wheeze & breathlesness
Frequent infective exacerbations

Hyperinflated lungs (barrel shaped chest)
Use of accessory muscles, pursed lip breathing
Thin with loss of muscle mass

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24
Q

What are the features of CO2 retention?

A

Warm peripheries, Bounding pulse, flapping tremor.

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25
Q

Investigations for COPD

A

History, physical exam and lung function testing:

Peak flow
CO transfer factor
CXR
CT
Haemoglobin
ABG
Alpha1 antitrypsin levels
ECG
26
Q

Management of COPD

A 
Multidisciplinary and stepwise approach
Smoking cessation
Bronchodilators
Corticosteroids
Immunisations and prompt antibiotic treatment
Oxygen
27
Q

What drug is used in acute exacerbations of COPD for pts not responding to treatment?

A

Aminophylline - lots of ADRs; given IV with cardiac monitoring

BIPAP - bilevel positive airway pressure

Low molecular weight heparin

28
Q

Clinical features of diabetes

A

Polydipsia, polyuria, weight loss, infection

29
Q

Investigations for diabetes

A

Fasting plasma glucose > 7.0 mmol/L
Random plasma glucose >11.1 mmol/L
HbA1c > 48mmol/mol
FBCs, U&Es, LFTs, cholesterol and triglyceride levels

30
Q

Outline treatment pathway for type 2 diabetes (and recall the mechanism and ADRs for each)

A

Lifestyle changes

Metformin (or sulfonylurea for people who are not overweight)

Metformin + sulfonylurea

Add thiazolidinedione or insulin

31
Q

What is epilepsy?

A

One can experience recurrent seizures or fits= experience a short episode of symptoms- few s to a few min, that is due to nerves in the brain becoming too active, too electrically excitable, so the brain loses it’s ability to control the body e.g. when someone becomes really excited and hyperactive, and they may start running around and will try to tell you something but may not be able to get it out properly, and you can’t understand what they’re trying to tell you, so this is what is happening in the brain- brain controls everything we do, and it does this by having special cells- your nerves, which talk to one another to control the body, but in seizures, the nerves become overactive, so they’re trying to talk to one another but the nerves just can’t understand what they’re being told to do, so they don’t have any control and the brain loses its control over the body.

Nerves not able to talk and listen to one another which they normally do by having electrical activity, now too electrically excitable, so they are setting off lots and lots of electrical impulses, too many too be understood, nerves are all talking to one another at once.
depending on which part of the brain these nerves become too active and excitable will determine your symptoms. may have abnormal movements, sensations- may smell something, may have a feeling of deja vu.

brain normally tells us to stay awake, so if lose control over that, we may lose consciousness.

32
Q

How are seizures classified?

A

1) Generalised tonic-clonic (grand mal) seizures - sudden onset, rigid tonic phase followed by convulsion. Loss of consciousness, may be associated with tongue biting and/or incontinence. Followed by drowsiness for several hours.
2) Typical absence seizures (petit mal) - trance like state, common in childhood which become grand mal in adulthood.
3) Partial seizures - electrical activity starts in one area. They can be simple (not affecting memory or consciousness) or complex(affecting memory before during or after). Todd’s paralysis. Temporal lobe seizures associated with deja-vu or aura

33
Q

What is status epilepticus and how is it treated?

A

Medical emergency - continuous seizures without recovery of consciousness.

In hospital:

  • O2, secure large vein (many AEDs cause phlebitis), cardio respiratory monitoring and pulse ox

1) lorazepam (ADRs inc. resp depression and hypotension)
2) phenytoin (ADRs inc. dysthymias - requires cardiac monitoring)
3) phenobarbital

  • URGENT: blood glucose, electrolytes inc Ca and Mg, drug screen, anticonvulsant levels
  • consider CT, lumber puncture and blood cultures.
34
Q

What advice do you give someone with epilepsy?

A

Restrict life as little as possible but avoid swimming alone, avoid dangerous sports eg rock climbing, leave door open when taking a bath.

EU driving - seizure free for a year
Heavy goods - seizure free for 10 years.

35
Q

What are the first line treatments for generalised tonic clinic seizures? Include possible ADRs

A

Sodium valproate (avoid in women of child bearing age) - weight gain, hair loss, liver damage

Lamotrigine - toxic epidermal necrosis (TEN)

Carbemazepine - rashes, leucocytopenia, TEN

Phenytoin (in developing countries) - rashes, SLE, TEN, gum hypertrophy, hirsuitism

36
Q

First line treatment (and ADRs) for petit mal seizures?

A

Sodium valproate (ADRs include weight gain, hair loss, liver damage)

37
Q

First line treatments (and ADRs) for partial seizures?

A

Lamotrigine (toxic epidermal necrolysis) and Carbemazepine (rashes, leucocytopenia, and toxic epidermal necrolysis)

Sodium valproate

Phenytoin

38
Q

What is the aim of AED treatment?

A

Monotherapy with the dose increased until seizure control achieved or tolerance exceeded.

39
Q

Describe the epidemiology of gallstones. What are the two different types of gallstones? Describe their Pathophysiology and symptoms

A

1) present in 10-20% of the population. Most common in women, risk increases with age and obesity. Increased levels or oestrogen (contraceptive or HRT) may increase risk.
2) cholesterol gallstones (80% of all gallstones) and pigment gallstones
3) Gallstones are small stones, usually made of cholesterol, that form in the gallbladder. In most cases they don’t cause any symptoms and don’t need to be treated. However, if a gallstone becomes trapped in a duct (opening) inside the gallbladder it can trigger a sudden intense abdominal pain that usually lasts between one and five hours. This type of abdominal pain is known as biliary colic.

Some people with gallstones can also develop complications, such as inflammation of the gallbladder (cholecystitis), which can cause:
persistent pain, jaundice, fever

40
Q

Management of gallstones

A

Analgesia and low fat diet

Elective cholecystectomy (laparoscopic)

41
Q

How would you explain heart failure and symptoms to a patient?

A

Heart failure is a condition caused by the heart failing to pump enough blood around the body at the right pressure.

It usually occurs because the heart muscle has become too weak or stiff to work properly.

If you have heart failure, it does not mean your heart is about to stop working. It means your heart needs some support to do its job, usually in the form of medicines.

Breathlessness, feeling very tired and ankle swelling are the main symptoms of heart failure. But all of these symptoms can have other causes, only some of which are serious.

The symptoms of heart failure can develop quickly (acute heart failure). If this happens, you will need to be treated in hospital. But they can also develop gradually (chronic heart failure).

42
Q

Causes of heart failure

A

Ischaemic heart disease
Heart muscle weakness - Cardiomyopathy (genetic or infective)
Hypertension

43
Q

Investigations in heart failure

A

CXR
ECG
Blood tests
Echocardiography

44
Q

Signs and symptoms of HF

A

Exertional dyspnoea, orthopneoa, fatigue, cardiomegaly with displaced apex beat, 3rd and 4th heart sounds, tachycardia, crackles, ankle oedema

45
Q

Treatment of HF - general measures

A

Education
Physical activity (reduce during exacerbations, low level)
Diet and social (reduce weight, salt, alcohol)
Sexual activity - pts on nitrates not to take phosphodiesterase inhibitors

46
Q

What are the three pathological changes associated with alcohol intake?

A

1) Fatty liver (steatosis); gamma GT elevated.
2) Alcoholic hepatitis; Mallory bodies (amorphous eosinophilic material) surrounded by neutrophils
3) Alcoholic cirrhosis; destruction of architecture and fibrosis - nodules

47
Q

Pharmacological treatment of HF

A 
ACE inhibitor
Beta blocker
Diuretic 
Spironolactone 
Digoxin
Vasodilator so
Inotropic agents
48
Q

Why is high blood pressure important?

A

High blood pressure (hypertension) rarely has noticeable symptoms, but if untreated it increases your risk of heart attack, heart failure, kidney disease, stroke or dementia.

49
Q

Pharmacological treatments for hypertension

A

ACE inhibitors
Calcium channel blockers
Thiazide type diuretic

Add further diuretic therapy or beta blocker

50
Q

Symptoms of IBD

A

Pain, swelling or cramping in the tummy
recurring or bloody diarrhoea
weight loss
extreme tiredness

Not everyone has all of these symptoms, and some people may experience additional symptoms, including vomiting, anaemia and high temperature (fever).

The symptoms of IBD can come and go. People may experience periods of severe symptoms (flare-ups), and go through long periods when they have few or no symptoms at all (remission).

51
Q

What is ulcerative colitis? What symptoms?

A
  • Ulcerative colitis is a long-term condition, where the colon and rectum become inflamed.

The colon is the large intestine (bowel), and the rectum is the end of the bowel where stools are stored.

Small ulcers can develop on the colon’s lining, and can bleed and produce pus.

Ulcerative colitis is thought to be an autoimmune condition. This means the immune system – the body’s defence against infection – goes wrong and attacks healthy tissue.

The most popular theory is that the immune system mistakes harmless bacteria inside the colon for a threat and attacks the tissues of the colon, causing it to become inflamed.

Exactly what causes the immune system to behave in this way is unclear. Most experts think it is a combination of genetic and environmental factors.

52
Q

What is crohns, what are the symptoms?

A

Crohn’s disease is a long-term condition that causes inflammation of the lining of the digestive system.
Inflammation can affect any part of the digestive system, from the mouth to the back passage, but most commonly occurs in the last section of the small intestine (ileum) or the large intestine (colon).

Common symptoms can include:
diarrhoea
abdominal pain
fatigue (extreme tiredness)
unintended weight loss
blood and mucus in your faeces (stools)
53
Q

Ddx IBD (other causes of Chronic diarrhoea, Malabsorption and malnutrition)

A

TB

Infection

54
Q

Non- pharm treatment of IBD

A

Nutrition and diet

Surgery

55
Q

Pharmacological treatment of CD

A 
Oral 5-ASA
Steroids
Liquid enteral nutrition
thioprine drugs - azathioprine
Metronidazole
Methotrexate
Anti-TNF antibodies
56
Q

Pharm treatments of UC

A

5-ASA (oral or rectal)
Steroids (oral or rectal)
Azathioprine

Systemic features - hydrocortisone, ciclosporin, infliximab

57
Q

Ischaemic heart disease

A

The heart
The heart is a muscle about the size of your fist. It pumps blood around your body and beats approximately 70 times a minute. After the blood leaves the right side of the heart, it goes to your lungs where it picks up oxygen.

The oxygen-rich blood returns to your heart and is then pumped to the body’s organs through a network of arteries. The blood returns to your heart through veins before being pumped back to your lungs again. This process is called circulation.

The heart gets its own supply of blood from a network of blood vessels on the heart’s surface called coronary arteries.

What causes coronary heart disease?
Coronary heart disease is the term that describes what happens when your heart’s blood supply is blocked or interrupted by a build-up of fatty substances in the coronary arteries.

Over time, the walls of your arteries can become furred up with fatty deposits. This process is known as atherosclerosis and the fatty deposits are called atheroma.

Atherosclerosis can be caused by lifestyle factors and other conditions, such as:
smoking
high cholesterol
high blood pressure (hypertension)
diabetes
58
Q

Pharmacological treatment of IHD

A

Nitrates
Beta blockers
Calcium antagonists

59
Q

Peptic ulcer

A

Stomach ulcers, also known as gastric ulcers, are open sores that develop on the lining of the stomach.

Ulcers can also occur in part of the intestine just beyond the stomach – these are known as duodenal ulcers.

Both stomach and duodenal ulcers are sometimes referred to as peptic ulcers. Here the term “stomach ulcer” will be used, although the information applies equally to duodenal ulcers.

Signs and symptoms
The most common symptom of a stomach ulcer is a burning or gnawing pain in the centre of the abdomen (tummy).
However, stomach ulcers aren’t always painful and some people may experience other symptoms, such as indigestion, heartburn and feeling sick.

60
Q

Thromboembolism

A

Thromboembolism: Formation in a blood vessel of a clot (thrombus) that breaks loose and is carried by the blood stream to plug another vessel. The clot may plug a vessel in the lungs (pulmonary embolism), brain (stroke), gastrointestinal tract, kidneys, or leg. Thromboembolism is a significant cause of morbidity (disease) and mortality (death), especially in adults. Treatment may involve anticoagulants (blood thinners), aspirin, or vasodilators (drugs that relax and widen vessels).

61
Q

Under active thyroid

A

An underactive thyroid gland (hypothyroidism) is where your thyroid gland doesn’t produce enough hormones.

Common signs of an underactive thyroid are tiredness, weight gain and feeling depressed.

An underactive thyroid can often be successfully treated by taking daily hormone tablets to replace the hormones your thyroid isn’t making.

There’s no way of preventing an underactive thyroid. Most cases are caused either by the immune system attacking the thyroid gland and damaging it, or by damage to the thyroid that

62
Q

Over active thyroid

A
  • Overactive thyroid (also known as hyperthyroidism) is a relatively common hormonal condition that occurs when there is too much thyroid hormone in the body.
    Excess levels of thyroid hormones can then speed up the body’s metabolism, triggering a range of symptoms, such as:
    nervousness and anxiety
    hyperactivity – where a person can’t stay still and is full of nervous energy unexplained or unplanned weight loss
    swelling of the thyroid gland, which causes a noticeable lump, known as a goitre, to form in the throat

What causes an overactive thyroid gland?
The thyroid gland is found in the neck. It produces hormones that are released into the bloodstream to control the body’s growth and metabolism. These hormones are called thyroxine and triiodothyronine.
They affect processes such as heart rate and body temperature, and help convert food into energy to keep the body going.
In hyperthyroidism, the thyroid gland produces too much thyroxine or triiodothyronine, which speeds up the body’s metabolism.
There are several possible underlying causes, the most common being Graves’ disease, in which the body’s immune system targets the thyroid gland and causes it to produce too much of the thyroid hormones.

Examinations (15 decks)

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