Acute Care and Trauma AKI --> DIC Flashcards
(197 cards)
1
Q
Define ARDS
A
Syndrome of acute and persistent lung inflammation with increased vascular permeability with bilateral infiltrates
2
Q
What are the characteristics of ARDS?
A
1) Acute onset
2) Bilateral inflitrates consistent with pulmonary oedema
3) Hypoxaemia
4) No clinical evidence of increase left arterial pressure
5) Severe end of acute lung injury spectrum
3
Q
What is the aetiology of ARDS?
A
Diffuse alveolar damage injures the alveolar-capillary membrane. Alveoli are then flooded with oedematous fluid, along with inflammatory cytokines and cells which cause inflammation.
4
Q
List common causes of ARDS
A
1) Sepsis (Most common)
2) Aspiration
3) Pneumonia
4) Pancreatitis
5) Severe trauma
6) Massive transfusion
7) Drugs and alcohol
5
Q
In patients with ARDS predisposed to serious infection, what cause should be first considered?
A
Sepsis
6
Q
What are the three discrete stages of ARDS?
A
Exudative –> Proliferative –> Fibrotic
7
Q
What is the incidence of ARDS in the UK?
A
1/6000 annually
8
Q
What are the presenting symptoms of ARDS?
A
1) Rapid deterioration of respiratory function
2) Dyspnoea
3) Respiratory distress
4) Coughing with frothy pulmonary oedema
9
Q
What can be found upon examination of a patient with ARDS?
A
1) Hypoxia
2) Requires PEEP to maintain >90% SpO2
3) Widespread inspiratory crepitations
4) Tachypnoea
5) Tachycardia
10
Q
List investigations that might be used in suspected ARDS
A
1) CXR
2) ABG
3) Sputum culture
4) Blood culture
5) Amylase and Lipase
6) Urine culture
11
Q
What would CXR of an ARDS patient show?
A
Bilateral alveolar infiltrates and interstitial shadowing
12
Q
What bloods should be requested if ARDS is suspected?
A
FBC U&E LFTs CRP Amylase/Lipase ABG Blood culture BNP (<100 ng/mL makes heart failure less likely)
13
Q
Why is echocardiography useful for suspected ARDS?
A
Abnormal left ventricular function would suggest cardiogenic pulmonary oedema instead of ARDS
14
Q
How does pulmonary artery catheterisation help with ARDS invetigation?
A
PAOP ?18 mmHg suggests ARDS
15
Q
Why might bronchoscopy be used in a patient with suspected ARDS?
A
1) Patients with suspected pneumonia
2) Patients without defined predisposing condition - to exclude non-infectious lung parenchyma disease
16
Q
Define alcohol withdrawal
A
Symptoms that present when an alcohol-dependent suddenly stops drinking
17
Q
Explain the aetiology of alcohol withdrawal
A
Chronic alcohol consumption suppresses glutamate, body responds by increasing sensitivity. Cold turkey to alcohol leads to overload of SNS activity
18
Q
Summarise the epidemiology of alcohol withdrawal
A
1) 8% of all admitted patients are at risk of withdrawal
2) 5% will progress to delirium tremens
19
Q
List some symptoms of alcohol withdrawal
A
1) Restlessness
2) Tremors
3) Anxiety
4) Tachycardia
5) Hypertension
6) Nausea
7) Insomnia
8) Auditory and visual hallucinations
20
Q
When do severe withdrawal symptoms present?
A
Severe symptoms like hallucinations or severe anxiety present after 24 hours and peak at day 2
21
Q
What is delirium tremens?
A
Most severe form of alcohol withdrawal
22
Q
What comprises delirium tremens?
A
1) Hallucinations
2) Confusion
3) Agitation
Note: Can be fatal
23
Q
What screening tool is used to identify alcohol-dependents
A
CAGE
24
Q
Identify complications of alcohol withdrawal
A
Seizures and possible death
25
How can alcohol withdrawal be managed?
1) Chlordiazepoxide
2) Phenobarbital if refractory to benzodiazepines
3) Thiamine to prevent Wernicke's/Korsakoff
26
In which patient group is propofol reserved for if treating alcohol withdrawal?
1) Patients resistant to benzodiazepine therapy
| 2) Patients requiring mechanical ventilation
27
Summarise prognosis of alcohol withdrawal
Delirium tremens mortality of 35% if untreated, <2% with early detection and treatment
28
Define acute kidney injury
An abrupt decrease in kidney function, resulting in:
1) Retention of urea and other waste products
2) Dysregulation of extracellular volume and electrolytes
29
Is acute kidney injury usually reversible?
Yes, the decline in GFR is usually reversible
30
What are the three classifications of causes for acute kidney injury?
1) Pre-renal
2) Intrinsic renal
3) Post-renal
31
How can pre-renal AKI develop
1) Renal ischemia due to generalised decrease in tissue perfusion
2) Selective renal ischemia
32
List some pre-renal causes of AKI
1) Hypovolemia (eg. dehydration, vomiting)
2) Heart failure
3) Cirrhosis
4) Hypotension
5) Nephrotic syndrome
6) Renal ischemia
33
How can oedematous states (heart failure, cirrhosis) lead to AKI?
Oedematous states reduce the perfusion of the kidneys
1) Heart failure causes decrease CO and splanchnic venous pooling
2) Cirrhosis causes systemic vasodilation
34
What medications are contraindicated by renal artery stenosis?
1) ACEi
2) ARBs
3) Direct renal inhibitors
35
Why are ACEi, ARBs, and direct renal inhibitors contraindicated in renal artery stenosis?
They cause efferent arteriolar vasodilation which in the context of renal artery stenosis reduces GFR
36
Which is the most common form of acute kidney injury?
Acute tubular necrosis due to prolonged or severe ischemia
37
List some intrinsic renal causes of AKI
1) Glomerular - Glomerulonephritis
2) Tubular - Acute tubular necrosis
3) Interstitial - Acute interstitial nephritis (NSAIDS, autoimmune)
4) Vasculities (eg. Wegner's granulomatosis)
5) Eclampsia
38
List some post-renal causes of AKI
1) Caliculi
2) Urethral stricutre
3) Prostatic hypertrophy
4) Bladder tumour
39
What are the risk factors for acute kidney injury?
1) Male sex
2) Old age
3) Hypertension
4) ACEi or ARB use
5) Hypovolemia
6) Diabetes mellitus
40
Summarise the epidemiology of AKI
1) 15% of adults admitted will develop an AKI
| 2) Most common in the elderly
41
List some symptoms of acute kidney injury
1) Oliguria/anuria
2) Vomiting
3) Dizziness
4) Orthopnoea
42
List the signs of acute kidney injury on examination
1) Pulmonary oedema
2) Peripheral oedema
3) Hypotension (pre-renal azotemia)
4) Hypertension (intravascular volume expansion)
5) Tachycardia
43
What investigations should be used to explore possible acute kidney injury?
1) Urinalysis
2) Bloods
3) Fluid challenge
4) Renal ultrasound
5) ECG
6) CXR
7) Immunology screening
44
Explain urinalysis results in acute kidney injury
Patients with glomerular disease typically present with:
1) Proteinuria
2) Microscopic haematuria
45
What bloods would be requested if acute kidney injury is suspected?
1) FBC
2) U&Es
3) Clotting
4) CRP
5) Blood film
6) Immunological markers
7) Virology (HIV & hepatitis)
46
What immunological markers would be tested for in acute kidney injury?
1) ANA - SLE
2) anti-dsDNA - High in active lupus
3) Complement - Low in active lupus
4) Anti-GBM antibodies - Goodpasture's syndrome
5) Antistreptolysin-O antibodies - High after streptococcal infection
47
Which disease is associated with anti-nuclear antibodies?
SLE
48
Describe abnormal immunological markers in active lupus+B4B48:C57
1) anti-dsDNA - High in active lupus
| 2) Complement levels - Low in active lupus
49
Whichimmunological marker is associated with Goodpasture's Syndrome?
Anti-GBM antibodies
50
Why is ultrasound useful for suspected acute kidney injury?
1) Check for post-renal obstruction
| 2) Identify hydronephrosis
51
What might X-Rays show in a patient with acute kidney injury?
1) CXR - Pulmonary oedema
| 2) AXR - Renal stones
52
List the four main components to AKI management
1) Protect from hyperkalaemia
2) Optimise fluid balance
3) Stop nephrotoxic drugs
4) Consider dialysis
53
What is the general management plan for AKI?
1) Treat underlying cause
2) Correct electrolyte abnormalities
3) Optimise volume status (replace or remove fluid)
4) Sodium and volume restriction
5) Poassium and phosphorous restriction
6) Avoid nephrotoxic drugs
54
How is pre-renal AKI treated?
1) Volume expansion with crystalloid
| 2) Vasopressor
55
How is intrinsic renal failure treated?
1) Treat underlying cause of failure
| 2) Cease nephrotoxics (eg. ACEi, ARB)
56
How is obstructive renal failure treated?
1) Bladder catheterisation
57
When should renal replacement therapy be considered for a patient with AKI?
1) Hyperkalemia refractory to medicine
2) Pulmonary oedema refractory to medicine
3) Severe metabolic acidemia
4) Uraemic complications
58
List the possible complications of acute kidney injury
1) Pulmonary oedema
2) Acidemia
3) Uraemia
4) Hyperkalemia
5) Bleeding
59
What are patients who develop an acute kidney injury at risk of?
Chronic kidney disease
60
In a patient with acute kidney injury, what traits indicate poor prognosis?
1) Age
2) Multiple organ failure
3) Oliguria
4) Hypotension
5) CKD
61
Define anaphylaxis
Acute life-threatening multisystem syndrome cause by sudden release of mast cell and basophil derived mediators into the circulation
62
What is the aetiology of anaphylaxis?
1) Immunogenic anaphylaxis - IgE-mediated or complement-mediated
2) Non-immunogenic - Mast cell or basophil degranulation without antibody involvement (eg. Reactions caused by vancomycin, codeine, ACEi)
63
Describe pathophysiology of anaphylaxis
Release of inflammatory mediators (eg. histamine) leads to:
1) Bronchospasm
2) Vasodilation
3) Increased capillary permeability
64
List some common allergens which can cause anaphylaxis
Drugs
Peanuts
Shellfish
Latex
65
How can repeated blood infusion in an IgA deficient patient cause anaphylaxis?
Repeat infusions leads to the formation of anti-IgA antibodies
66
List some presenting symptoms of anaphylaxis
```
Wheezing
SOB
Choking
Swelling of lips and face
Pruritus
Rash
```
67
What signs of anaphylaxis may be found on examination?
```
Tachypnoea
Wheeze
Cyanosis
Swollen upper airways and eyes
Urticarial rash
Hypotension
Tachycardia
```
68
What is the 1st line investigation for anaphylaxis?
Serum tryptase ASAP after treatment, second sample 1-2 hours later.
Note: Anaphylaxis is a clinical diagnosis so is not necessary if diagnosis is definite
69
Why is serum tryptase tested for in anaphylaxis?
Serum tryptase is normally undetectable, but in patients with recent anaphylaxis it is >100 ng/mL
70
Following anaphylactic attack, what investigations should be considered?
1) IgE testing - Confirms the presence of atopy
| 2) Allergen skin test
71
What is the management plan for anaphylaxis?
1) ABCDE
2) High flow oxygen
3) IM adrenaline
4) Antihistamine
5) Hydrocortisone
6) If respiratory deterioration persists, my require bronchodilator therapy
72
What are the possible complications of anaphylaxis?
1) SHOCK (Hypopefusion associated with hypotension)
| 2) Organ damage secondary to shock
73
What is the prognosis for an anaphylactic patient?
Good if provided prompt treatment
74
Define aspirin overdose
Excessive ingestion of aspirin causing toxicity
75
What is the amount of aspirin which causes moderate-severe toxicity in adults?
10-20 mg
76
How does aspirin toxicity develop?
Aspirin (acetylsalicylate) increases respiration stimulating CNS, causing respiratory alkalosis. Compensatory bicarbonate and K+ excretion causes dehydration and hypokalemia. Loss of bicarbonate together with uncoupled mitochondrial oxidative phosphorylation by salicylic acid and build up of lactic acid can lead to metabolic acidosis.
77
What might occur in a severe aspirin overdose?
CNS depression
| Respiratory failure
78
Are all patients with aspirin overdose symptomatic?
No. Patient might be asymptomatic initially
79
How can aspirin overdose symptoms be divided?
Early and late symptoms
80
List early and late symptoms of aspirin overdose
Early:
1) Flushed appearance
2) Fever
3) Sweating
4) Hyperventilation
5) Dizziness
6) Tinnitus
7) Deafness
Late:
1) Lethargy
2) Confusion
3) Convulsions
4) Drowziness
5) Respiratory Depression
6) Coma
81
What signs of aspirin overdose may be found on examination?
Fever
Tachycardia
Hyperventialtion
Epigastric tenderness
82
What investigations may be used in the event of aspirin overdose?
Blood tests
| ECG
83
What blood tests would be ordered for possible aspirin overdose?
```
Salicylate
FBC
U&E
LFT
Clotting screen
Glucose
Other drug levels
ABG
```
84
How can a salicylate test determine severity of aspirin overdose?
500-750 mg/L is moderate overdose
| >750 mg/L is a severe overdose
85
What would LFTs show in aspirin overdose?
Increased AST/ALT
86
What would clotting screen show in aspirin overdose?
Increased PT time
87
What might an ABG show in aspirin overdose?
Mixed metabolic acidosis and respiratory alkalosis
88
What might be seen on the ECG of a patient with aspirin overdose?
Signs of hypokalemia:
1) Small T-waves
2) U-waves
89
Define asthma
Chronic inflammatory airway disease characterised by:
1) Reversible airway obstruction
2) Airway hyper-responsiveness
3) Bronchial inflammation
90
Explain the aetiology of asthma
Early Phase: Inhaled allergens induce inflammatory mediater release, causing smooth muscle contraction, mucous secretion and airway obstruction
Late Phase: Recruitment of inflammatory cells leads to persistent inflammation and bronchial hyper-responsiveness
91
List some genetic risk factors for asthma
Family history
| Atopy
92
List some environmental risk factors for asthma
```
Dust mites
Pollen
Pets
Smoke
Viral respiratory infections
Aspergillus spores
Occupational allergens
```
93
List some symptoms of asthma
Episodic reversible shortness of breath
Wheeze
Coughing worse at night
94
What signs of asthma might be observed on examination
```
Tachypnoea
Use of accessory muscles
Prolonged expiratory wheeze
Polyphonic wheeze
Hyperinflated chest
```
95
What investigations might be used to investigate acute asthma
```
Peak flow
Pulse oximetry
CXR (Exclude other pathologies)
ABG
FBC (Raised WCC if infective exacerbation)
CRP
U&Es
Blood culture
Sputum culture
```
96
What investigations might be used to investigate chronic asthma
Peak flow rate monitoring
Pulmonary function test
Bloods: Eosinophilia, IgE, Aspergillus antibody
Skin prick test
97
What should the PCO2 levels in a patient having an asthma attack be
Low because they should be blowing off CO2
98
How should acute asthma be managed?
```
ABCDE
High-flow oxygen
Nebulised salbutamol, ipratroprium
Steroids (IV magnesium sulfate if no improvement)
Treat underlying cause
Ventilate if severe
```
99
How should chronic asthma be managed?
Step 1: Inhaled SABA; if need >1/day then move to step 2
Step 2: Step 1 + Regular inhaled low-dose steroids
Step 3: Step 2 + Inhaled LABA; if inadequate control with LABA increase steroid dose, if unresponsive to LABA stop and increase steroid dose
Step 4: Increase inhaled steroids, add 4th drug
Step 5: Add regular oral steroids, maintain high dose steroids, refer to specialist
100
Identify complications of asthma
```
Growth retardation
Chest wall deformity
Recurrent infections
Pneumothorax
Respiratory failure
Death
```
101
What is the prognosis for asthmatics?
Most children improve as they age
| Adult-onset asthma usually chronic
102
Define burns injury
When tissue damage occurs by thermal, electrical or chemical injury
103
List possible causes of burns injury
Heat
Electricity
Chemicals
Irradiation
104
Which patients are most at risk of burns injury?
Young children
| Elderly
105
What is the incidence of burns injury in the UK?
>12,000 admitted per year
106
What should be considered when seeing a patient with burns injury
Time, temperature, length of contact with agent
Smoke inhalation
Carbon monoxide poisoning
107
What signs might be observed upon examination of a burns injury patient?
Stridor
Dyspnoea
Hoarseness
Carbonaceous sputum
108
Classify the types of burns that might be encountered
```
Partial thickness (superficial/deep)
Full thickness
```
109
Describe a superficial partial thickness burn
Red and oedematous skin
Painful
Heals within around 7 days
110
Describe a deep partial thickness burn
Blistered and mottled
Painful
Heals over 3 weeks
Usually no scarring
111
Describe a full thickness burn
```
Destruction of epidermis and dermis
Painless
Loss of sensation
Charred leathery eschars
Healing either by scarring or contractures (requires grafts)
```
112
How is the size of a burn assessed?
Percentage of body area
113
What investigations should be used when dealing with burns injury?
```
FBC
U&E
Group and save
O2 Sats
ABG
Carboxyhemoglobin (if inhalational)
```
114
What investigations should be used when dealing with electrical burns?
Serum CK
ECG
Urine myoglobin (check for muscle damage)
115
Define cardiac arrest
Acute cessation of cardiac function
116
What are the classic reversible causes of cardiac arrest?
4 Hs & 4Ts
```
Hypoxia
Hypothermia
Hypovolemia
Hypo/Hyperkalemia
Tamponade
Tension pneumothorax
Thromboembolism
Toxins
```
117
Describe onset of cardiac arrest
Sudden
118
List some symptoms that may precede cardiac arrest
Fatigue
Dizziness
Blackout
Fainting
119
What signs may be found on examination of a patient in cardiac arrest?
Unconscious
Not breathing
Absent carotid pulse
120
What investigations should be made for cardiac arrest?
Cardiac monitor
| Blood tests
121
Why is a cardiac monitor useful for investigating cardiac arrest?
It classifies the type of cardiac rhythm which is required to decide on the management plan
122
Which blood parameters should be tested for in cardiac arrest?
```
FBC
U&Es
Clotting screen
Glucose
ABG
Cross-match
Toxicology screen
```
123
What are the two stages of cardiac arrest management?
Basic life support
| Advanced life support
124
In cardiac arrest, which cardiac rhythms are shockable or non-shockable?
Shockable:
Pulseless VT
VF
Non-shockable:
PEA
Asystole
125
If after BLS, rhythm is assessed to be pulseless VT or VF, what is the management?
1) Defibrillate once
2) Resume CPR for 2 mins, then re-assess rhythm. If still 'shockable rhythm', defibrillate again
3) 1mg IV adrenaline after second defibrillation and again every 3-5 mins
4) If 'shockable rhythm' persists after third shock, 300mg IV bolus amiodarone
126
If after BLS, rhythm is assessed to be PEA or asystole, what is the management?
1) CPR for 2 mins, then reassess rhythm, if still 'non-shockable rhythm', continue CPR
2) 1mg IV adrenaline every 3-5 mins
3) 3mg IV atropine, once only, if asystole or PEA with rate <60 bpm
127
How should the reversible causes of cardiac arrest be treated?
Hypoxia - Oxygen
Hypothermia - Warm slowly
Hypovolemia - IV colloids, crystalloids and blood products
Hypo/Hyperkalemia - Correct electrolytes
Tamponade - Pericardiocentesis
Tension pneumothorax - Aspiration/Chest drain
Thromboembolism - Treat as PE or MI
Toxins - Use necessary antidote
128
What are some possible complications of cardiac arrest?
Death
| Irreverisble hypoxic damage
129
What is the prognosis of a patient with cardiac arrest?
1) Increased duration of inadequate cardiac output worsens prognosis
2) Resuscitation outside hospital less successful
130
Define cardiac failure
Inability of cardiac output to meet body's demands despite normal venous pressure
131
What is the difference between low output and high output cardiac failure?
Low output: Reduced cardiac output
| High output: Increased demand by tissues
132
Which is more common, low or high output cardiac failure?
Low output
133
List the types of low output cardiac failure
Left heart failure
Right heart failure
Congestive heart failure
134
List causes of left heart failure
```
Ischemic heart disease
Hypertension
Cardiomyopathy
Aortic valve disease
Mitral regurgitation
```
135
List causes of right heart failure
```
Secondary to left heart failure
Infarction
Cardiomyopathy
Pulmonary hypertension/embolus
Chronic lung disease
Tricuspid regurgitation
Constrictive pericarditis
```
136
List causes of congestive heart failure
Arrythmia
Cardiomyopathy
Myocarditis
Drug toxicity
137
List causes of high output cardiac failure
```
Anemia
Beriberi
Pregnancy
Paget's disease
Hyperthyroidism
AV malformation
```
138
What is the incidence of cardiac failure?
10% of >65 year olds
139
What signs can be found on examination of left heart failure?
```
Tachycardia
Tachypnoea
Displaced apex beat
Bilateral basal crackles
Third heart sound
Pansystolic murmur (functional mitral regurgitation)
```
140
What signs can be found on examination of right heart failure?
```
Raised JVP
Ankle/sacral pitting oedema
Hepatomegaly
Ascites
Signs of functional tricuspid regurgitation
```
141
What are the stages of dyspnoea?
1) No dyspnoea
2) Dyspnoea on ordinary activities
3) Dyspnoea on less than ordinary activities
4) Dyspnoea at rest
142
What are the symptoms of right heart failure?
```
Swollen ankles
Fatigue
Increased weight (b/c of oedema)
Decreased exercise tolerance
Nausea
```
143
What investigations would be performed to explore possible heart failure?
```
Bloods
CXR
ECG
Echocardiogram
Swan-Ganz catheter
```
144
What bloods would be tested for in heart failure
```
FBC
CRP
LFTs
TFTs
U&Es
Lipids
Glucose
```
145
In addition to the basic blood investigations for cardiac failure, what would be added for acute left ventricular failure?
ABG
Troponin
BNP
146
What would low plasma BNP suggest in the context of heart failure?
Rules out cardiac failure with 90% sensitivity
147
List the 5 signs of heart failure on CXR
```
ABCDE
Alveolar shadowing
Kerley B lines
Cardiomegaly
Diversion of upper pulmonary vessels
Effusion in pleura
```
148
Why is a swan-ganz catheter a useful investigation for cardiac failure
Allows measurements of right atrial, right ventricular, pulmonary artery, pulmonary wedge, and left ventricular end-diastolic pressures
149
What is the management of acute left ventricular failure?
1) Treating cardiogenic shock (severe cardiac failure with low BP)
a) Use ionotropes (eg. dobutamine)
2) Treating pulmonary oedema
a) Sit patient up
b) 60-100% oxygen and consider CPAP
c) Diamorphine (venodilator + anxiolytic)
d) GTN infusion (venodilator to reduce preload)
e) IV furosemide (venodilator and subsequent diuretic)
f) Monitor BP, RR, O2 sats, Urine output, ECG
h) TREAT THE CAUSE
150
What is the primary management of chronic left ventricular failure?
ACEi
Beta-blocker
Lifestyle changes
151
What medications are used in the treatment of chronic left ventricular failure and give an example of each
```
ACEi (ramipril)
Beta-blocker (carvedilol)
Loop diuretic (furosemide)
Aldosterone antagonist (spirinolactone)
ARB (candesartan)
Hydralazine and a nitrate
Digoxin
```
152
What should be monitored if a patient takes aldosterone antagonists or ARBs
K+ levels as these drugs can cause hyperkalemia
153
When might hydralazine and a nitrate be added for chronic LVF treatment?
In patients with persistent symptoms despite ACEi and beta-blockers, often Afro-Carribeans
154
What surgical intervention can be used for chronic LVF?
LVEF <35%: no LBBB
- Implantable cardiac defibrillator
LVEF <30%: LBBB
Cardiac resynchronisation therapy with biventricular pacemaker
155
How does cardiac resynchronisation therapy work?
Simultaneous activation of both ventricles with a biventricular pacemaker decrease dyssynchronous contraction, enhancing ventricular contraction and reducing functional mitral regurgitation
156
List the complications of cardiac failure
Respiratory failure
Cardiogenic shock
Death
157
What is the prognosis for a patient with cardiac failure?
50% die within 2 years
158
Define COPD
Chronic, progressive lung disorder characterised by airflow obstruction with chronic bronchitis and/or emphysema
159
Define chronic bronchitis
Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years
160
Define emphysema
Permanent destructive enlargement of air spaces distal to the terminal bronchioles
161
Which structures are damaged in COPD?
Bronchi
| Alveoli
162
List causes of COPD
Environmental toxins - cigarette smoke
| A1-antitrypisin deficiency
163
When should you consider A1-antitrypsin deficiency?
Young patients who develop COPD despite never smoking
164
What is the prevalence of COPD?
Very common (8%)
165
When does COPD usually present?
Middle age or later
166
What symptoms does COPD present with?
Chronic cough and sputum production
Breathlessness
Wheeze
Decreased exercise tolerance
167
What signs might be found on physical examination of COPD patients?
Inspection: Respiratory distress, use of accessory muscles, barrel-shaped chest, cyanosis
Percussion: Hyper-resonance, loss of liver and cardiac dullness
Auscultation: Quiet breath sounds, prolonged expiration, wheeze
Signs of CO2 retention: Asterixis (CO2 flap), bounding pulse, warm peripheries. In late stages, signs of right heart failure
168
What investigations would be performed to explore COPD?
```
Spirometry and pulmonary function tests
CXR
Bloods
ABG
ECG & Echocardiogram (cor pulmonale)
Sputum sample & blood cultures (acute exacerbations)
A1-antitrypsin levels (young patients)
```
169
Define cor pulmonale
Abnormal enlargement of right side of heart as a result of disease of lungs or pulmonary blood vessels
170
What lung function test results would suggest COPD
Decreased PEF rate
Decreased FEV1:FVC ratio
Increased lung volumes
171
How does FEV1:FVC ratio correspond to COPD severity?
Mild: 60-80%
Moderate: 40-60%
Severe: <40%
172
Outline the management of COPD
1) Stop smoking
2) Bronchodilators: SABA and anticholinergics. LABA if >2 exacerbations per year
3) Steroids: Inhaled becomethasone for FEV1<50% predicted, or >2 exacerbations per year
4) Pulmonary rehabilitation
5) Oxygen therapy
6) Vaccinations (pneumococcal vaccine)
173
Define diabetic ketoacidosis
Diabetic ketoacidosis is a biochemical triad of hyperglycemia, ketonemia, and acidemia which presents with rapid symptom onset
174
List the symptoms of DKA
Polydipsia
Polyuria
Weakness
Weight Loss
175
List the signs of DKA
```
Tachycardia
Dry mucous membranes
Poor skin turgor
Hypotension
Shock (Severe cases)
```
176
Describe the aetiology of DKA
Reduction in net circulating insulin along with elevation of counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone)
177
What are the two most common predisposing factors for DKA?
Inadaequate insulin therapy
| Infection
178
What investigations should be made for DKA and what results might be seen?
```
Plasma glucose - Elevated
ABG - 7.015 mmol/L
Capillary/Serum ketones
Urinalysis (+ve glucose and ketones)
U&Es (Urea elevated, electrolytes vary)
```
179
What is the diagnostic criteria for DKA?
Acidemia (venous blood pH<7.3 or HCO3-<15.0 mmol/L
Hyperglycemia (Blood glucose >11.0 mmol/L)
Ketonemia (?3.0 mmol/L)
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Why is serum sodium often low in DKA?
Osmotic reflux of water from intracelllular to extracellular space in the presence of hyperglycemia
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What does hypernatremia in the presence of hyperglycemia in DKA indicate?
Profound volume depletion
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What is the treatment for DKA?
IV fluids
Insulin therapy
Electrolyte replacement
Note: Depends on degree of volume depletion
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List some possible complications for DKA
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Cerebral oedmea
Aspiration pneumonia
Hypokalemia
Hypomagnesemia
Hypophosphatemia
Thromboembolism
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Define DIC
An acquired disorder of the caogulation characterised by activation of coagulation pathways, leading to formation of intravascular thrombi and depletion of platelets and coagulation factors
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What are the two main characteristics of DIC
1) Continuous generation of intravascular fibrin
| 2) Depletion of procoagulants and platelets
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List some causes of DIC
1) Sepsis
2) Major trauma
3) Malignancies (AML, lung, breast, GI)
4) Severe organ failure (pancreatitis, liver failure)
5) Immunological reactions (transplant rejection, blood transfusion reaction)
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What are the two types of DIC and what are their causes
1) Acute DIC (Rapid onset conditions) - Major trauma, sepsis
| 2) Chronic DIC (Non-acute conditions) - Malignancies, raynaud's disease
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Describe the pathophysiology of acute DIC
1) Endothelial damage and increased granulocyte/macrophage procoagulants lead to activation of coagulation cascade
2) Subsequent explosive thrombin generation depletes clotting factors and platelets while simultaneously activating the fibrinolytic system
3) Increased bleeding into subcutaneous tissues, skin, mucous membranes occur
4) Microvascular occlusion by fibrin causes microangiopathic haemolytic anaemia and ischaemic organ damage
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How does the pathophysiology of chronic DIC differ from acute DIC
1) Same process as DIC but at a slower rate, allowing compensatory responses
2) Compensatory responses diminish bleeding risk but cause hypercoagulable states, allowing thrombosis to occur
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What is the epidemiology of DIC?
Seen in severely ill patients
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What are the presenting symptoms of DIC?
1) Symptoms of cause
2) Dyspnoea
3) Confusion
4) Evidence of bleeding
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What are the general signs of DIC (acute or chronic) on examination?
1) Signs of cause
2) Fever
3) Shock (hypotension, tachycardia)
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What are the signs of acute DIC on examination?
1) Petechiae
2) Ecchymosis
3) Epistaxis
4) Mucosal bleeding
5) Respiratory distress
6) Signs of end organ damage
7) Hemorrhage
8) Oliguria due to renal failure
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What are the specific signs of chronic DIC on examination?
1) Signs of deep vein and arterial thrombosis/embolism
| 2) Superficial venous thrombosis
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What investigations would be suitable to explore DIC?
1) Platelet count
2) Clotting screen (PT, aPTT, Fibrinogen)
3) Fibrin degradation products/D-dimer
4) Blood film
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What anomalies would be seen on the blood tests of a patient with DIC?
1) Platelets - Decrease
2) Clotting (PT, aPTT) - Increased
3) Fibrinogen - Decreased
4) Fibrin degradation products/D-dimer - Increased
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What anomaly would be seen on the blood film of a patient with DIC?
Schistocytes
