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OSCE Flashcards

1
Q

What is acute kidney injury?

A

-Significant decline in renal function over hours or days manifesting as an abrupt and sustained increase in serum urea and creatinine

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2
Q

What are pre-renal causes of AKI?

A
  • Shock

- Renalvascular compromise eg NSAIDs, ACE I, renal artery stenosis

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3
Q

Give the main causes of renal AKI

A
  • Acute tubulonecrosis caused by ischeamia, hypertension, thrombotic thrombocytopenia purpura
  • Interstitial nephritis by drugs (NSAIDs, Abx) and toxins
  • Nephritic syndrome
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4
Q

Post Renal causes of AKI

A

-Stones, neoplasm, stricture, prostate

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5
Q

Describe some possible clinical signs of an AKI

A
  • Oedema
  • Altered BP
  • Raised JVP
  • Postural hypotension
  • Raised Urea, creatinine, low urine output, acidosis/hyperkalaemia
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6
Q

What investigations would you do in AKI?

A
  • Bloods -> FBCs, U+Es, LFTs, glucose, Ca, clotting, ESR
  • ABG to look for acidosis, hypoxia and hyperkalaemia
  • urine dip
  • ECG, CXR and renal US
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7
Q

Describe the ECG features in order of hyperkalaemia

A
  • Peaked T waves
  • Flattened P waves
  • Increased PR interval
  • Widened QRS
  • VF
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8
Q

Describe the stages of alcoholic liver disease. At what stage is it irreversible?

A
  • Fatty liver -> hepatitis -> cirrhosis

- Cirrhosis

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9
Q

Which liver enzymes are commonly raised in alcoholic liver disease?

A
  • GGT

- AST:ALT >2

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10
Q

What is liver cirrhosis?

A

-Hepatocellular damage producing areas of nodular regeneration separated by fibrous septae

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11
Q

List some clinical signs of Alcoholic liver disease

A
  • Hands -> Clubbing, leuconychia (low albumin), dupytens contracture, palmar erythema,
  • Face -> pallor (ACD)
  • Trunk -> Spider naevi, gynaecomastia (decreased liver metabolism)
  • Abdo -> hepatosplenomegaly, caput medusa, ascites
  • General -> jaundice, bruising (coagulopathy), anorexia
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12
Q

What is portal hypertension? Describe the main features

A
  • Raised portal blood pressure >20mmHg

- SAVE (splenomegaly, ascites, varices (oesophageal, caput medusa, worsening piles) and encephalopathy

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13
Q

Describe portosystemic shunting in portal hypertension. Give the vessels involved in all 3 varices

A
  • Raised portal pressure causes a backflow and increased pressure of blood as blood cannot enter portal system. portal vessels become engorged and dilated causing shifting of blood from the portal system into the systemic system.
  • Oesophageal -> Left gastric vein to inferior oesophageal veins
  • Caput medusa -> peri-umbilical to superficial abdo
  • Haemorrhoids -> superficial rectal to inferior/middle rectal
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14
Q

What can be confused for caput medusa on the abdomen and how do you tell these apart?

A
  • IVC obstruction
  • blood flow down below umbilicus = portal hypertension
  • Blood flow up below umbilicus = ivc obstruction
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15
Q

Why does portal hypertension cause encephalopathy?

A
  • Decreased blood flow through liver decreases detoxification of blood.
  • Build up of toxins in systemic system including ammonia ->cross bbb -> astrocytes clear causing glutamate to glutamine -> osmotic imbalance -> cerebral oedema
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16
Q

Describe the pathophysiology of ascites in liver disease

A

-Back pressure due to accumulation of blood causes increased hydrostatic pressure leading to fluid exudation. This causes a decrease in circulating volume and RAAS activation which enters a cycle of increased exudation and further RAAS activation. Also decreased albumin and impaired aldosterone metabolism

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17
Q

In broad terms what is anaemia? What general symptoms/signs does it produce?

A
  • Decreased capacity of the haemoglobin to carry oxygen

- Fatigue, pallor, palpitations, light headedness

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18
Q

What are the causes of microcytic anaemia?

A
  • TAILS
  • Thalassaemia
  • Anaemia of chronic disease
  • Iron deficiency Anaemia
  • Lead Poisoning
  • Sideroblastic anaemia
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19
Q

Describe causes of normocytic anaemia

A
  • Recent blood loss
  • Bone marrow failure
  • Early ACD
  • Pregnancy
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20
Q

What are causes of macrocytic anaemia?

A
  • Vit B12 deficiency
  • Folate deficiency
  • Reticulocytosis
  • liver disease
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21
Q

Give some causes of haemolytic anaemia

A
  • Autoimmune
  • Malaria
  • Hereditary spherocytosis/elliptosis
  • burns
  • G6PD deficiency
  • Destruction by mechanical heart valves
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22
Q

Give 3 differentials for causes of iron deficiency anaemia

A
  • Poor diet
  • Menorrhagia
  • Coeliac
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23
Q

Give 2 signs specific for iron deficiency anaemia

A
  • Koilonychia

- Angular stomatitis

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24
Q

What are the causes of b12 deficiency?

A
  • Bacterial overgrowth syndrome (increased use of b12)
  • Crohns
  • Pernicious anaemia
  • Veganism
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25
Q

What are the causes of folate deficiency?

A
  • Pregnancy
  • Poor diet
  • Haemolysis
  • Malignancy
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26
Q

What are the specific symptoms in b12 deficiency?

A
  • Glossitis

- Peripheral neuropathy

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27
Q

Describe the pathophysiology of asthma

A

-Bronchial hypersensitivity causing an exaggerated response to normally non-allergenic non-noxious stimuli resulting in mucosal oedema, mucus hypersecretion and bronchoconstriction which leads to reversible airway narrowing. Over time this lead to goblet cell hyperplasia, smooth muscle hypertrophy and airway remodelling .

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28
Q

What cellular/immune components are involved in asthma

A
  • Histamine release from mast cells
  • IgE and eosinophils
  • Lymphocytes
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29
Q

Name some precipitants of asthma

A
  • Atopy -> t1 hypersensitivity to dust, pollen, animals
  • Stress -> cold air, viral urti, exercise, emotion
  • Toxins -> smoking, hairspray
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30
Q

What are the signs and symptoms of asthma

A
  • Cough +/- sputum
  • Wheeze
  • Dysponea
  • Diurnal variation
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31
Q

What things would you want to illicit in a history to point towards asthma?

A
  • Precipitants
  • diurnal variation
  • Exercise tolerance
  • Life Effects
  • Other Atopy
  • Home/job environment
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32
Q

Give 2 differentials for asthma

A
  • COPD
  • Pulmonary oedema
  • Bronchiectasis
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33
Q

Differentials of acute severe asthma

A
  • Pneumothorax
  • Pulmonary embolism
  • Pulmonary oedema
  • Acute exacerbation of COPD
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34
Q

What is atrial fibrillation? Give common signs and symptoms

A
  • Recurrent uncoordinated contraction of the atria, normally at over 300bpm. Most beats filtered out by avn allowing ventricles to not beat at 300bpm
  • Asymptomatic, chest pain, palpitations, dysponea, faintness
  • Signs = irregularly irregular pulse/loss of pulse
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35
Q

Give some causes of AF

A
  • Alcohol
  • Ischaemic heart disease
  • Thyrotoxicosis
  • Hypertension
  • PE/Pneumonia
  • Rheumatic heart disease
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36
Q

What is the treatment for acute AF?

A

-Electrical or pharmacological cardioversion
1st line->flecainide or diltiazem
2nd line -> amiodarone
-LMWH

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37
Q

What does AF look like on ECG

A
  • Narrow complex tachycardia
  • Loss of P waves
  • Loss of isoelectric baseline
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38
Q

What is cerebrovascular disease and how does it commonly present? State the main risk factor and how it causes cerebrovascular disease

A
  • A disease of the arteries which supply the brain often resulting in a stroke of TIA.
  • Often caused by hypertension which damages the blood vessels lining exposing collagen causing platelet aggregation and thrombus formation
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39
Q

Give 3 risk factors of cerbrovascular disease

A
  • Hypertension
  • Diabetes mellitus
  • Smoking
  • Family History
  • Hyperlipidaemia
  • AF
  • Peripheral vascular disease
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40
Q

What are the symptoms of a total anterior stroke? Which vessel(s) is most likely involved?

A
  • Contralateral Hemiparesis and/or sensory deficit to >2 face, arm and leg
  • Contralateral homonymous hemianopia
  • Higher cortical dysfunction eg dysphasia, hemispatial neglect
  • Large infact in carotid/MCA
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41
Q

What are the symptoms of a PACS?

A

-2/3 of TACS usually contralateral hemiparesis and higher cortical function but deficit is less dense or incomplete

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42
Q

What are the symptoms of a POCS and which vessels are involved?

A 
-One of:
Cerebellar syndrome
Brainstem syndrome
Contralateral homonymous hemianopia
-Vertebrobasilar territory
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43
Q

What are the symptoms of a lacuna stroke and what vessels are involved?

A
  • Depends on where lesion is
  • Pure motor (commenest) or pure sensory or mixed sensorimotor or dysarthria/decreased coordination or ataxic hemiparesis
  • Involves perforating arteries around basal ganglia, thalamus, pons and internal capsule
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44
Q

Give 3 differential diagnoses of stroke

A
  • SOL
  • Head injury
  • Altered glucose
  • Infection eg encaphalitis, abscess
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45
Q

What is the difference between a stroke and a TIA?

A

-Sudden onset focal neurology which lasts less than 24 hours due to temporary occlusion of part of the cerebral circulationm Mainly caused by atherothromboelbolism from carotids

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46
Q

What is the ABCD2 score used for?

A

-Predict the risk of a stroke following a TIA

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47
Q

Describe how predicted FEV1 is used to assess severity

A

All categories are FEV/FVC<70% and symptomatic

  • Mild = FEV1>80%
  • Mod = FEV1 50-79%
  • Sev = FEV1 30-49%
  • Very Sev = FEV1<30%
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48
Q

What 2 conditions does COPD generally encompass? Briefly describe each

A
  • Emyphysema -> destruction of alveolar walls producing enlarged air spaces
  • Chronic bronchitis -> smooth muscle hypertrophy and mucus hypersecretion causing airway narrowing and a productive cough
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49
Q

What are the major causes of COPD?

A
  • Smoking

- A1-antitrypsin deficiency

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50
Q

Describe the signs and symptoms of COPD. What are pink puffers and blue bloaters

A
  • Symptoms = cough, sputum, wheeze, dysponea,
  • Signs = tachyponea, hyperinflation, cyanosis, cor pulmonale,
  • Pink puffer -> emphysema causing breathlessness but not cyanosis -> progressing to T1 respiratory failure
  • Blue bloater -> chronic bronchitis -> Cyanosed but not breathless, rely on hypoxic drive -> type 2 resp failure
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51
Q

What is the MRC Dysponea score? describe its classification

A
  • A systematic approach to grading breathlessness
    1) only on vigorous exercise
    2) On hurrying/walking up stairs
    3) Walking slowly/has to stop
    4) stops after a few mminutes
    5) In normal ADLs/struggles to leave the house
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52
Q

Name some complications associated with COPD

A
  • Acute exacerbations +/- infection
  • Pneumothorax
  • Cor Pulmonale
  • Lung Carcinoma
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53
Q

What investigations would you perform if you suspected COPD?

A
  • Bloods (FBCs, A1-antitrypsin, ABG)
  • CXR
  • ECG
  • Spirometry
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54
Q

What signs may you see on a CXR of someone with COPD

A
  • Hyperinflation -> >6 ribs anteriorly
  • Flattened diaphragm
  • Cardiomegaly
  • Prominent pulmonary arteries
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55
Q

State the main differences between COPD and asthma

A
  • COPD nearly always smoker
  • COPD commonly presents over 35 asthma is under
  • COPD common to have chronic productive cough
  • COPD persistent and progressive breathlessness, asthma is variable
  • Asthma wakes from nightime cough and wheeze
  • Asthma has diurnal symptom pattern or day-day variability
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56
Q

How is an acute COPD exacerbation treated?

A
  • O2 (titrated be careful of hypoxic drive)
  • Salbutamol
  • Hydrocortisone or prednisolone
  • Ipratropium
  • Thephylline
  • Abx
  • Physiotherapy
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57
Q

What bacterium is associated with pneumonia in a COPD patient?

A

-Haemophilus influenzae

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58
Q

What is diabetes?

A
  • Multisystem disorder due to an absolute or relative lack of endogenous insulin resulting in metabolic and vascular complications
  • T1 -> autoimmune destruction of b cells causing absolute insulin deficiency, onset is usually before puberty with polyuria, polydipsia and weightloss
  • T2 -> insulin resistance resulting in b cell dysfunction causing a relative insulin deficiency, onset is in older patients with polyuria, polydipsia or coplications
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59
Q

What are the diagnostic tests and criteria for DM?

A

-Symptomatic with fasting plasma glucose >7, random plama glucose >11.1 or OGTT >11.1

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60
Q

What is first line teatment in T2 DM? What is its mechanism of action? Give some side effects of metformin

A
  • Metformin
  • Inhibits hepatic gluconeogenesis and increases insulin sensitivity
  • NV, abdo pain, lactic acidosis
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61
Q

What is the second step in managing T2 DM? How does this drug work?

A
  • Add a sulphonylurea eg gliclazide
  • Stimulates B cells to produce insulin by binding to closed ATP sensitive K channels. This prevents K from exiting the cel causing depolarisation and a rise in intracellular calcium. This causes increased insulin vesicle fusion and subsequent release
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62
Q

How do thiazolidinediones work and give an example?

A
  • Pioglitazone
  • Stimulates PPAR-g which ultimately reduces insulin resistance by regulating adipose, muscle and liver gene expression. Also decreases hepatic gluconeogenesis,
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63
Q

What are GLP-1 agonists? Give an example

A
  • Exenatide
  • Stimulates GLP-1 receptors in order to enhance insulin secretion, promote satiety, slow gastric emptying and suppress glucagon secretion
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64
Q

What is sitagliptin?

A

-DPP4 inhibitor. DPP4 usually breaks down incretins which are gut hormones which increase peripheral utilisation of glucose, decrease glucagon secretionand reduce hepatic glucose output

65
Q

What is acarbose?

A

-a-glucosidae inhibitor which delays glucose load into gut

66
Q

How do SGLT2 inhibitors aim to reduce blood glucose?

A

-Cause it to remain in renal tubule lumen and be excreted in urine

67
Q

What are the common adverse effects of insulin?

A
  • Weight gain
  • Lipid dystrophy
  • Hypoglycaemia
68
Q

Briefly explain ketogenesis and dehydration diabetic ketoacidosis

A
  • Ketogenesis = Absolute lack of insulin causes an increase in lipolysis and fatty acid oxidation due to mobilising of other energy sources and a decreased insulin:glucagon ration causing the acetyl-CoA pathway to switch to ketone production.
  • Dehydration = extreme hyperglycaemia causes an osmotic diuresis leading to dehydration, also possible vomiting due to ketonuria.
69
Q

How may DKA present?

A
  • Abdo pain and vomiting
  • Gradual drowsiness
  • Slow ventilation
  • Dehydration
  • Ketotic breath
70
Q

What is epilepsy?

A

-A condition where there is recurrent and spontaneous abnormal electrical activity in the brain which manifests as seizures

71
Q

Name 3 causes of epilepsy

A
  • Idiopathic
  • SOL
  • Vascular accident
  • Scar tissue from infection
72
Q

Give 3 differentials of seizures

A
  • Epilepsy
  • Infection eg meningitis, encephalitis
  • Metabolic eg glucose, Na, Urea
  • Raised ICP eg tumour, trauma
  • Eclampsia
73
Q

What should you illicit from a seizure history?

A
  • before = Prodrome (mood/behaviour), aura, autonomic changes
  • During = tongue biting, foaming, incontinence, unconsciousness,
  • After = amnesia, how long did it take to recover
  • Previous episodes, length, witnessed?
74
Q

Which epilepsy drug should be taken in pregnancy? How does this work?

A
  • Lamotrigine
  • Na channel blocker which is use dempendant and leads to stabilisation of neuronal membranes by prolonging inactivation state preventing spontaneous neuronal firing
75
Q

Which epileptic medication are cyp inducers? Why can this be an issue in young women?

A
  • Carbamezapine
  • Phenytoin
  • Induce the metabolism of OCP making less effective and the drugs are strong teratogens
76
Q

What are the common side effects of lamotrigine?

A
  • Skin rash

- Diplopia

77
Q

What are some common side effects of valproate?

A
  • Appetite increase and weight gain
  • Liver failure
  • Pancreatitis
  • Reversible hair loss
  • Oedema
  • Ataxia
  • Teratogen, tremor, thrombocytopaenia
  • Encephalopathy due to liver failure
78
Q

List some side effects of carbamazepine

A
  • Leukopenia
  • Diplopia
  • SIADH ->hyponatraemia
79
Q

List some side effects of phenytoin

A
  • Gingival hyperplasia
  • Hirsuitism
  • Cerebellar syndrome
  • Peripheral sensory neuropathy
  • Diplopia
  • Tremor
80
Q

What is status epilepticus? How is it treated?

A
  • Prolonged seizure which lasts for more than 30 mins or repeated seizures without a recovery interval of consciousness
  • Barbituates and IV phenytoin
81
Q

What are gall stones?

A

-Components of bile eg pigments, cholesterol which precipitate out and form stones

82
Q

Describe the common presentation of gall stones

A
  • Right upper quadrant or epigastric pain which is cramping and intermittent in nature
  • Can have associated fever, vomiting, local peritonism
83
Q

Give 3 differentials of Acute cholecystitis

A
  • Biliary colic
  • Ascending cholangitis
  • Liver abscess
84
Q

What is the difference between acute cholecystitis and biliary colic?

A
  • AC -> gallstones are in neck of gall bladder and there is local peritonitis, and the pain may be refered to the right shoulder, fever is present
  • Biliary colic is physical contraction of cystic duct
85
Q

What is charcots triad?

A
  • Suggestive of ascending cholangitis

- Jaundice, RUQ pain, fever

86
Q

What is heart failure? What is the difference between systolic and diastolic failure?

A
  • When the cardiac output is insufficient to maintain the bodys requirement due to defects in systole, diastole or both
  • Systolic failure is when the contraction of the heart is insufficient to eject an efficient ejection fraction
  • Daistolic failure is when the heart fails to relax fully and there is a reduced end diastolic volume, which in turn reduces the stroke volume
87
Q

Give the symptoms of left and right heart failure

A
  • Left = Pulmonary oedema, dyspnoea, orthopnoea, paroxysmal nocturnal dysponoea, fatigue, reduced exercise tolerance, wheeze (cardiac asthma)
  • Right = sacral, thigh and ankle oedema, hepatosplenomegaly, ascites, raised JVP, nausea
88
Q

What investigations would you undertake if you suspect hf?

A
  • Bloods -> FBCs, U+Es, BNP, TFTs, glucose, lipids
  • CXR -> Cardiothoracic ratio, alveolar oedema (bats wing), prominant upper pulmonary veins, pleural effusion
  • ECG -> AF, ischaemia, hypertrophy
  • Echo
89
Q

What is the difference between acute and chronic heart failure?

A
  • Acute is new onset or decompensation of chronic characterised by pulmonary/peripheral oedema with or without signs of peripheral hypoperfusion -> medical emergency
  • Chronic is stable heart failure which is developing slowly and arterial pressure being maintained.
90
Q

Which drugs are avoided in patients with heart failure?

A
  • NSAIDs

- Verapamil (-ve inotropes)

91
Q

Describe the classes of drugs which are used in heart failure and why they are used

A
  • Loop Diuretics eg furosemide -> relieve symptoms by decreasing fluid volume
  • ACEi/ARB -> decrease effects of activated RAS system by preventing angiotensin II -> decreases vasoconstriction and aldosterone activation
  • B-blocker -> decreases heart rate to increase filling time -> starlings curve
  • Spironolactone -> antagonise effects of aldosterone in DCT preventing water resorption
  • Digoxin -> improve symptoms by increasing CO
  • Vasodilators
92
Q

Describe the compensatory mechanisms which occur in heart failure

A
  • Starling effect dilates the heart to enhance contractility
  • Hypertrophy to increase contractility
  • RAS in order to increase blood volume to try increase CO
  • ANP/BNP to decrease fluid volume due to stretch of atria and ventricles
  • Sympathetic activation to increase contranctility and CO
93
Q

What happens in decompensation of heart failure to cause presentation?

A
  • Heart cannot sustain contractility and loss of function causes decreased CO
  • Dilation of the heart due to remodelling leads to valve reguritation
  • Hypertrophy leads to relative cardiac ischaemia as too much heart tissue to perfuse
  • RAS activation causes excessive oedema due to venous congestion
  • Excessive sympathetic stimulation causes increased afterload which heart cannot overcome causing further decrease in CO
94
Q

Give the common causes of RVF?

A
  • LVF
  • Cor pulmonale
  • Tricuspid or pulmonary valve disease
95
Q

What are the most common causes of LVF?

A
  • IHD
  • Idiopathic dilated cardiomyopathy
  • Systemic HTN
  • Mitral/aortic valve disease
96
Q

Give some secondary causes of HTN

A
  • Glomerulonephritis (increased H2O retention)
  • Hyperthyroid, cushings, pheochromocytoma, Conn’s
  • Coarctation of aorta
97
Q

Describe the management pathway of hypertension

A
  • Under 55 -> Ace then +CCB then +Thiazide/like

- Over 55/black -> CCB then +ACEi then +Thiazide/like

98
Q

Describe how you illicit each heart murmur and what type of murmur they are

A
  • Mirtal regurg ->is herd in apex PSM
  • Aortic regurg -> 5th ICS with patient sat forward breath held on expiration -> EDM
  • Aortic stenosis -> Listen to carotids using bell -> ESM
  • Mitral stenosis-> listen out to axilla using bell with breath held on expiration, roll to exaggerate MDM
99
Q

What is murphys sign?

A
  • Test for acute cholecycstitis
  • Place 2 fingers over RUQ and ask pt to breathe in -> pain as gb touches fingers, only positive if same test in LUQ does not cause pain
100
Q

What are the two main types of IBD? State the common presentation of each

A
  • Crohns and UC
  • UC often presents with bloody diarrhoea with mucus, abdominal discomfort and tenesmus, may have a fever
  • Crohns presents with diarrhoea which is usually non-bloody, abdominal pain and weight loss, may have apthamous ulcers in mouth, RIF mass and perianal abscesses, anal strictures
101
Q

Give some common extra-abdominal signs seen with IBD

A
  • Clubbing and erythema nodosum
  • Iritis
  • Arthritis, ankylosing spondylitis
  • Primary Sclerosing Cholangitis and gallstones
102
Q

Give some complications of crohns and UC

A
  • UC -> toxic megacolon, bleeding, malignancy risk

- Crohns -> Fistulae, strictures, abscesses, malabsorption (fat, B12, Vit D, Protein)

103
Q

Give some pathological differences between UC and Crohns

A
  • UC occurs in the rectum and retreats through the colon +/- backwash ileitis, in a continuous fashion. The ulceration is superficial and crypt abscesses and pseudopolyps are present.
  • Crohns can affect anywhere from mouth to anus, especially terminal ileum, skip lesions are present and ulceration is transmural creating cobblestone appearance. Granulomas and fistulae are present
104
Q

Regarding IBD, in which disease is smoking protective/harmful?

A
  • Protective in UC

- Harmful in Crohns

105
Q

Suggest some drugs which can be used in the treatment of an acute flare of UC or Crohns and why

A
  • Hydrocortisone or oral prednisolone (immune suppression
  • Abx such as ciclosporin/metronidazole
  • Infliximab (anti TNF)
  • Sulfasalazine for maintenance
106
Q

What investigations may you do in IBD?

A
  • Bloods -> FBCs, ESR, CRP, U&E, LFT, B12, Folate, Ferritin
  • Stool culture
  • Colonoscopy/small bowel enteroscopy
107
Q

What is ischaemic heart disease? Give some risk factors for IHD

A
  • A spectrum of disease which includes stable angina, unstable angina and MI
  • Non-modifable = age, male gender, family history
  • Modifable = smoking, hypertension, DM, hyperlipidaemia, obesity, sedentary lifestyle
108
Q

How do you tell the difference between a STEMI and a NSTEMI

A
  • STEMI -> MI with tall t waves ST elevation on ECG

- NSTEMI -> MI with ST depression and T wave inversion or normal

109
Q

What is the difference between unstable angina and NSTEMI? How can you differentiate the two clinically?

A
  • No myocyte necrosis in unstable angina

- Troponin levels will be raised in NSTEMI as released due to myocyte necrosis

110
Q

What are the most common causes of acute coronary syndrome?

A

-Plaque rupture, thrombosis and inflammation

111
Q

How does ischaemic heart disease differ from ACS?

A

-IHD includes stable angina

112
Q

What is the difference between stable and unstable angina?

A
  • Stable angina = chest pain only occurs on exertion and is relieved by rest of GTN spray
  • Unstable angina occurs at rest or with increasing frequency or severity
113
Q

What are the associated symptoms of an MI?

A

-Nausea, vomiting, dyspnoea, palpitations, sweating

114
Q

Give some differential diagnoses of an MI

A

-Angina, pericarditis, aortic dissection, PE

115
Q

How is MI induced bradycardia commonly treated? How does this work?

A
  • Atropine

- Anti-muscarinic to decrease parasympathetic activation

116
Q

What drugs are used for rate control in AF?

A

-B-blocker, verapamil, digoxin

117
Q

What is osteoarthritis?

A

-Degenerative joint disorder in which there is progressive loss of hyaline cartilage resulting in pain on movement, crepitus which is worse at the end of the day. Can be primary or secondary and stiffness occurs after rest

118
Q

How is osteoarthritis treated?

A
  • Focus history to find out how much it is affecting ADL and social circumstances
  • Decrease weight, physio to improve local muscle strength and supportive footwear
  • Analgesia with paracetamol and topical NSAIDs
  • Joint injections
119
Q

Name some common causes of peptic ulcer disease

A

-NSAIDs, steroids, stress, H.pylori, Zollinger Ellison, smoking and alcohol

120
Q

Describe the differences in presentation between gastric and peptic ulcers. Give some other presenting features of both

A
  • Both present with epigastric pain but duodenal is worse before meals or at night and is relieves by eating. Gastric is worse on eating and relieved by antacids
  • Haematemesis, malaena, anaemic symptoms
121
Q

What test is commonly used to detect H.pylori in PUD? Are there any special conditions for this test? Describe the mechanism behind it

A
  • Urease breath test (c13)
  • Make sure PPI is stopped for at least 2 weeks before
  • Give patient urea tablet labelled with carbon 13 wait 30 mins and test exhaled breath for isotope. H.pylori uses urease enzyme and will break down urea
122
Q

How is PUD treated?

A
  • Lose weight, stop smoking and avoid ethanol, avoid hot drinks and spicy foods, stop NSAIDs, OTC antactids
  • H.pylori eradication with PAC (PPI, amoxicillin and clarythromycin)
  • PPIs or H2As if needed
123
Q

What is rheumatoid arthritis? Who does it most commonly affect? Which joints does it most commonly affect?

A
  • Chronic autoimmune-linked, systemic inflammatory disease characterised by a symmetrical deforning peripheral polyarthritis
  • Females
  • MCP and PIPs
124
Q

How does rheumatoid arthritis differ from osteoarthritis?

A
  • Rheumatoid is auto immine linked
  • RA affects MCPs and PIPs vs OA affecting PIPs and DIPs
  • RA is worse on a morning and gets better with exercise, OA gets worse throughout the day
  • OA affects the hyaline cartilage, RA affects the synovium
  • RA affects multiple joints, OA often only one large joint
125
Q

How is RA treated pharmacologically?

A
  • DMARDs such as methotrexate/sulphasalazine
  • Biologicals such as Infliximab (anti-TNF)
  • Steroids for exacerbations eg prednisolone
  • NSAIDs for symptom relief
126
Q

Give some side effects of methotrexate

A
  • Lung fibrosis
  • Hepatotoxicity
  • Myelosuppression
127
Q

Give some side effects of anti-TNFs

A
  • Increased infection

- Hypercalcaemia

128
Q

Which antibodies are found in RA?

A
  • Rheumatoid factor

- Anti CCP

129
Q

Describe the xray changes on osteoarthritis

A

-LOSS -> loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts

130
Q

Describe the xray changes of RA

A

-Soft tissue swelling, loss of joint space, erosion of bone or sublaxations

131
Q

Give some risk factors for DVT/PE

A
  • Surgery
  • Long haul flights
  • Pregnancy
  • Smoking
  • Age
  • OCP/HRT
  • Cancer
  • Obesity
  • Immobility
132
Q

What are the signs of a DVT?

A
  • Red, swollen tender leg
  • Mild Fever
  • Pitting oedema
133
Q

Give some differentials of a DVT

A
  • Cellulitis
  • Ruptured bakers cyst
  • Necrotising fasciitis
  • Compartment syndrome
  • Tumour
134
Q

What blood test should be done if you suspect a DVT/PE? How does this help the diagnosis?

A
  • D Dimer
  • Not specific, if positive can also be raised in other situations such as infection and malignancy, if negative and low clinical probablity it rules out PE and DVT
135
Q

What is the treatment for DVT?

A

-LMWH and warfain

136
Q

Where do PEs usually arise from?

A

-DVT

137
Q

How does PE commonly present?

A

-Dyspnoea, pleuritic pain, haemoptysis, syncope, tachycardia, cyanosis, RHF

138
Q

Give some differential diagnoses of PE

A

-MI, pneumothorax, angina,

139
Q

When is thrombolysis considered in PE?

A

-If it is very large

140
Q

Give the signs and symptoms of hyperthyroidism

A
  • Heat intolerance/sweats
  • Palpitations
  • Diarrhoea
  • Irritability
  • Anxiety
  • Weight loss with increased appetite
  • Tremor
  • Oligomenorrhoea
  • goitre
141
Q

What is the most common cause of hyperthrypidism? Explain what happens

A
  • Graves disease

- Autoimmune, anti-TSH receptor antibody causes stimulation of receptor leading to excessive production of T4/T3

142
Q

Describe and explain the TFT results in thyrotoxicosis

A
  • Low TSH due to negative feedback on hypothalamus and pituitary by circulating T3/T4
  • High T3/T4 production independant of HP axis
143
Q

Apart from graves, give 2 causes of thyrotoxicosis

A
  • Too much thyroxine

- Toxic multinodular goitre

144
Q

How is thyrotoxicosis treated?

A
  • Treat initial symptoms with b-blocker
  • Carbimazole
  • Thyroidectomy
145
Q

What are two possible adverse outcomes of thyroidectomy?

A
  • Recurrent laryngeal nerve palsy causing horse voice

- Hypoparathyroidism

146
Q

Give some signs and symptoms of hypothyroidism

A
  • Cold intolerance
  • Lethargy
  • Decreased appetite and increased weight
  • Constipation
  • Menorrhagia
  • Depression
  • Bradycardia
  • Dry hair and skin
  • Puffy face
  • Goitre
147
Q

What are the most common causes of hypothyroidism?

A
  • Atrophic Thyroiditis -> lymphocytic infiltration of the thyroid
  • Hashimotos -> Anti-TPO antibody
  • Iodine deficiency
148
Q

Describe and explain the TFT results in hypothyroidism

A
  • High TSH -> negative feedback from low circulating levels of T3/T4
  • Low T3/T4 -> problem with thyroid in producing the hormones
149
Q

How is hypothyroidism treated?

A

-Thyroxine

150
Q

What is vasovagal syncope? What causes it? Describe the onset, duration and recoveru

A
  • Reflex bradycardia with or without peripheral vasodilation causing cerebral hypoperfusion = syncope
  • Provoked by emotion, fear, pain or standing for too long
  • Onset is over seconds rather than instantaneous and is often preceded by nausea, pallor, sweating and vision disturbance and it cannot occur laying down
  • Duration is approx 2 mins and clonic jerks can occur
  • Recovery is rapid
151
Q

Give some differentials for vasovagal syncope

A
  • Arrythmias
  • Postural hypotension
  • Situation syncope = on coughing, micturition
  • Epilepsy
  • Carotid-sinus syncope
  • Hypoglycaemia
152
Q

What are some key questions which need to ask in syncope history?

A
  • Any witnesses?
  • Onset -> prodrome, auras, duration,
  • Duration -> limb jerking, incontinence, tongue biting, stiffness, associated symptoms, length
  • After -> amnesia, muscle ache, lethargy, confused
  • Previous? frequency? precipitants? family history
153
Q

Give 2 cardiac causes of clubbing

A
  • Cyanotic congenital heart disease

- Infective endocarditis

154
Q

give some pulmonary causes of clubbing

A
  • Lung cancer
  • CF
  • Interstitial lung disease
  • Sarcoidosis
155
Q

Give some GI causes of clubbing

A
  • IBD

- Liver disease

156
Q

What are janeway lesions and oslar nodes

A
  • signs of infective endocarditis
  • Janeway lesions are reddened flat nodules on the palms and soles which are painless and caused by necrosis of the dermis
  • Osler nodes are painful raised lesions caused by immune complex deposition
157
Q

What causes the 3rd heart sound? What pathology causes it?

A
  • Rapid filling of the ventricles

- Mitral regurg, VSD, post MI

158
Q

What causes the 4th heart sound? In what pathologies is it heard?

A
  • Atria contracting against a stiff ventricle

- Heart failure, hypertrophy of ventricle, aortic stenosis, Hypertrophic cardiomyopathy

159
Q

What are cannon A waves?

A

-A wave on JVP curve occur in arrythmias result in the contraction of the atria and ventrices simultaneously which forces blood against a closed tricuspid valve causing a large pressure increase in the jugular vein

PPE (15 decks)

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