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Sofia Notes > Acute Care and Trauma AKI --> DIC > Flashcards

Acute Care and Trauma AKI --> DIC Flashcards

1
Q

Define ARDS

A

Syndrome of acute and persistent lung inflammation with increased vascular permeability with bilateral infiltrates

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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

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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.

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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

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5
Q

In patients with ARDS predisposed to serious infection, what cause should be first considered?

A

Sepsis

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6
Q

What are the three discrete stages of ARDS?

A

Exudative –> Proliferative –> Fibrotic

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7
Q

What is the incidence of ARDS in the UK?

A

1/6000 annually

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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

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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

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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

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11
Q

What would CXR of an ARDS patient show?

A

Bilateral alveolar infiltrates and interstitial shadowing

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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)
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13
Q

Why is echocardiography useful for suspected ARDS?

A

Abnormal left ventricular function would suggest cardiogenic pulmonary oedema instead of ARDS

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14
Q

How does pulmonary artery catheterisation help with ARDS invetigation?

A

PAOP ?18 mmHg suggests ARDS

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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

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16
Q

Define alcohol withdrawal

A

Symptoms that present when an alcohol-dependent suddenly stops drinking

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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

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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

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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

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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

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21
Q

What is delirium tremens?

A

Most severe form of alcohol withdrawal

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22
Q

What comprises delirium tremens?

A

1) Hallucinations
2) Confusion
3) Agitation
Note: Can be fatal

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23
Q

What screening tool is used to identify alcohol-dependents

A

CAGE

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24
Q

Identify complications of alcohol withdrawal

A

Seizures and possible death

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25
Q

How can alcohol withdrawal be managed?

A

1) Chlordiazepoxide
2) Phenobarbital if refractory to benzodiazepines
3) Thiamine to prevent Wernicke’s/Korsakoff

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26
Q

In which patient group is propofol reserved for if treating alcohol withdrawal?

A

1) Patients resistant to benzodiazepine therapy

2) Patients requiring mechanical ventilation

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27
Q

Summarise prognosis of alcohol withdrawal

A

Delirium tremens mortality of 35% if untreated, <2% with early detection and treatment

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28
Q

Define acute kidney injury

A

An abrupt decrease in kidney function, resulting in:

1) Retention of urea and other waste products
2) Dysregulation of extracellular volume and electrolytes

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29
Q

Is acute kidney injury usually reversible?

A

Yes, the decline in GFR is usually reversible

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30
Q

What are the three classifications of causes for acute kidney injury?

A

1) Pre-renal
2) Intrinsic renal
3) Post-renal

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31
Q

How can pre-renal AKI develop

A

1) Renal ischemia due to generalised decrease in tissue perfusion
2) Selective renal ischemia

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32
Q

List some pre-renal causes of AKI

A

1) Hypovolemia (eg. dehydration, vomiting)
2) Heart failure
3) Cirrhosis
4) Hypotension
5) Nephrotic syndrome
6) Renal ischemia

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33
Q

How can oedematous states (heart failure, cirrhosis) lead to AKI?

A

Oedematous states reduce the perfusion of the kidneys

1) Heart failure causes decrease CO and splanchnic venous pooling
2) Cirrhosis causes systemic vasodilation

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34
Q

What medications are contraindicated by renal artery stenosis?

A

1) ACEi
2) ARBs
3) Direct renal inhibitors

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35
Q

Why are ACEi, ARBs, and direct renal inhibitors contraindicated in renal artery stenosis?

A

They cause efferent arteriolar vasodilation which in the context of renal artery stenosis reduces GFR

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36
Q

Which is the most common form of acute kidney injury?

A

Acute tubular necrosis due to prolonged or severe ischemia

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37
Q

List some intrinsic renal causes of AKI

A

1) Glomerular - Glomerulonephritis
2) Tubular - Acute tubular necrosis
3) Interstitial - Acute interstitial nephritis (NSAIDS, autoimmune)
4) Vasculities (eg. Wegner’s granulomatosis)
5) Eclampsia

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38
Q

List some post-renal causes of AKI

A

1) Caliculi
2) Urethral stricutre
3) Prostatic hypertrophy
4) Bladder tumour

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39
Q

What are the risk factors for acute kidney injury?

A

1) Male sex
2) Old age
3) Hypertension
4) ACEi or ARB use
5) Hypovolemia
6) Diabetes mellitus

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40
Q

Summarise the epidemiology of AKI

A

1) 15% of adults admitted will develop an AKI

2) Most common in the elderly

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41
Q

List some symptoms of acute kidney injury

A

1) Oliguria/anuria
2) Vomiting
3) Dizziness
4) Orthopnoea

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42
Q

List the signs of acute kidney injury on examination

A

1) Pulmonary oedema
2) Peripheral oedema
3) Hypotension (pre-renal azotemia)
4) Hypertension (intravascular volume expansion)
5) Tachycardia

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43
Q

What investigations should be used to explore possible acute kidney injury?

A

1) Urinalysis
2) Bloods
3) Fluid challenge
4) Renal ultrasound
5) ECG
6) CXR
7) Immunology screening

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44
Q

Explain urinalysis results in acute kidney injury

A

Patients with glomerular disease typically present with:

1) Proteinuria
2) Microscopic haematuria

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45
Q

What bloods would be requested if acute kidney injury is suspected?

A

1) FBC
2) U&Es
3) Clotting
4) CRP
5) Blood film
6) Immunological markers
7) Virology (HIV & hepatitis)

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46
Q

What immunological markers would be tested for in acute kidney injury?

A

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

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47
Q

Which disease is associated with anti-nuclear antibodies?

A

SLE

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48
Q

Describe abnormal immunological markers in active lupus+B4B48:C57

A

1) anti-dsDNA - High in active lupus

2) Complement levels - Low in active lupus

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49
Q

Whichimmunological marker is associated with Goodpasture’s Syndrome?

A

Anti-GBM antibodies

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50
Q

Why is ultrasound useful for suspected acute kidney injury?

A

1) Check for post-renal obstruction

2) Identify hydronephrosis

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51
Q

What might X-Rays show in a patient with acute kidney injury?

A

1) CXR - Pulmonary oedema

2) AXR - Renal stones

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52
Q

List the four main components to AKI management

A

1) Protect from hyperkalaemia
2) Optimise fluid balance
3) Stop nephrotoxic drugs
4) Consider dialysis

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53
Q

What is the general management plan for AKI?

A

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

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54
Q

How is pre-renal AKI treated?

A

1) Volume expansion with crystalloid

2) Vasopressor

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55
Q

How is intrinsic renal failure treated?

A

1) Treat underlying cause of failure

2) Cease nephrotoxics (eg. ACEi, ARB)

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56
Q

How is obstructive renal failure treated?

A

1) Bladder catheterisation

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57
Q

When should renal replacement therapy be considered for a patient with AKI?

A

1) Hyperkalemia refractory to medicine
2) Pulmonary oedema refractory to medicine
3) Severe metabolic acidemia
4) Uraemic complications

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58
Q

List the possible complications of acute kidney injury

A

1) Pulmonary oedema
2) Acidemia
3) Uraemia
4) Hyperkalemia
5) Bleeding

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59
Q

What are patients who develop an acute kidney injury at risk of?

A

Chronic kidney disease

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60
Q

In a patient with acute kidney injury, what traits indicate poor prognosis?

A

1) Age
2) Multiple organ failure
3) Oliguria
4) Hypotension
5) CKD

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61
Q

Define anaphylaxis

A

Acute life-threatening multisystem syndrome cause by sudden release of mast cell and basophil derived mediators into the circulation

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62
Q

What is the aetiology of anaphylaxis?

A

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)

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63
Q

Describe pathophysiology of anaphylaxis

A

Release of inflammatory mediators (eg. histamine) leads to:

1) Bronchospasm
2) Vasodilation
3) Increased capillary permeability

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64
Q

List some common allergens which can cause anaphylaxis

A

Drugs
Peanuts
Shellfish
Latex

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65
Q

How can repeated blood infusion in an IgA deficient patient cause anaphylaxis?

A

Repeat infusions leads to the formation of anti-IgA antibodies

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66
Q

List some presenting symptoms of anaphylaxis

A 
Wheezing
SOB
Choking
Swelling of lips and face
Pruritus
Rash
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67
Q

What signs of anaphylaxis may be found on examination?

A 
Tachypnoea
Wheeze
Cyanosis
Swollen upper airways and eyes
Urticarial rash
Hypotension
Tachycardia
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68
Q

What is the 1st line investigation for anaphylaxis?

A

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

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69
Q

Why is serum tryptase tested for in anaphylaxis?

A

Serum tryptase is normally undetectable, but in patients with recent anaphylaxis it is >100 ng/mL

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70
Q

Following anaphylactic attack, what investigations should be considered?

A

1) IgE testing - Confirms the presence of atopy

2) Allergen skin test

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71
Q

What is the management plan for anaphylaxis?

A

1) ABCDE
2) High flow oxygen
3) IM adrenaline
4) Antihistamine
5) Hydrocortisone
6) If respiratory deterioration persists, my require bronchodilator therapy

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72
Q

What are the possible complications of anaphylaxis?

A

1) SHOCK (Hypopefusion associated with hypotension)

2) Organ damage secondary to shock

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73
Q

What is the prognosis for an anaphylactic patient?

A

Good if provided prompt treatment

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74
Q

Define aspirin overdose

A

Excessive ingestion of aspirin causing toxicity

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75
Q

What is the amount of aspirin which causes moderate-severe toxicity in adults?

A

10-20 mg

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76
Q

How does aspirin toxicity develop?

A

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.

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77
Q

What might occur in a severe aspirin overdose?

A

CNS depression

Respiratory failure

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78
Q

Are all patients with aspirin overdose symptomatic?

A

No. Patient might be asymptomatic initially

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79
Q

How can aspirin overdose symptoms be divided?

A

Early and late symptoms

80
Q

List early and late symptoms of aspirin overdose

A

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
Q

What signs of aspirin overdose may be found on examination?

A

Fever
Tachycardia
Hyperventialtion
Epigastric tenderness

82
Q

What investigations may be used in the event of aspirin overdose?

A

Blood tests

ECG

83
Q

What blood tests would be ordered for possible aspirin overdose?

A 
Salicylate
FBC
U&amp;E
LFT
Clotting screen
Glucose
Other drug levels
ABG
84
Q

How can a salicylate test determine severity of aspirin overdose?

A

500-750 mg/L is moderate overdose

>750 mg/L is a severe overdose

85
Q

What would LFTs show in aspirin overdose?

A

Increased AST/ALT

86
Q

What would clotting screen show in aspirin overdose?

A

Increased PT time

87
Q

What might an ABG show in aspirin overdose?

A

Mixed metabolic acidosis and respiratory alkalosis

88
Q

What might be seen on the ECG of a patient with aspirin overdose?

A

Signs of hypokalemia:

1) Small T-waves
2) U-waves

89
Q

Define asthma

A

Chronic inflammatory airway disease characterised by:

1) Reversible airway obstruction
2) Airway hyper-responsiveness
3) Bronchial inflammation

90
Q

Explain the aetiology of asthma

A

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
Q

List some genetic risk factors for asthma

A

Family history

Atopy

92
Q

List some environmental risk factors for asthma

A 
Dust mites
Pollen
Pets
Smoke
Viral respiratory infections
Aspergillus spores
Occupational allergens
93
Q

List some symptoms of asthma

A

Episodic reversible shortness of breath
Wheeze
Coughing worse at night

94
Q

What signs of asthma might be observed on examination

A 
Tachypnoea
Use of accessory muscles
Prolonged expiratory wheeze
Polyphonic wheeze
Hyperinflated chest
95
Q

What investigations might be used to investigate acute asthma

A 
Peak flow
Pulse oximetry
CXR (Exclude other pathologies)
ABG
FBC (Raised WCC if infective exacerbation)
CRP
U&amp;Es
Blood culture
Sputum culture
96
Q

What investigations might be used to investigate chronic asthma

A

Peak flow rate monitoring
Pulmonary function test
Bloods: Eosinophilia, IgE, Aspergillus antibody
Skin prick test

97
Q

What should the PCO2 levels in a patient having an asthma attack be

A

Low because they should be blowing off CO2

98
Q

How should acute asthma be managed?

A 
ABCDE
High-flow oxygen
Nebulised salbutamol, ipratroprium
Steroids (IV magnesium sulfate if no improvement)
Treat underlying cause
Ventilate if severe
99
Q

How should chronic asthma be managed?

A

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
Q

Identify complications of asthma

A 
Growth retardation
Chest wall deformity
Recurrent infections
Pneumothorax
Respiratory failure
Death
101
Q

What is the prognosis for asthmatics?

A

Most children improve as they age

Adult-onset asthma usually chronic

102
Q

Define burns injury

A

When tissue damage occurs by thermal, electrical or chemical injury

103
Q

List possible causes of burns injury

A

Heat
Electricity
Chemicals
Irradiation

104
Q

Which patients are most at risk of burns injury?

A

Young children

Elderly

105
Q

What is the incidence of burns injury in the UK?

A

> 12,000 admitted per year

106
Q

What should be considered when seeing a patient with burns injury

A

Time, temperature, length of contact with agent
Smoke inhalation
Carbon monoxide poisoning

107
Q

What signs might be observed upon examination of a burns injury patient?

A

Stridor
Dyspnoea
Hoarseness
Carbonaceous sputum

108
Q

Classify the types of burns that might be encountered

A 
Partial thickness (superficial/deep)
Full thickness
109
Q

Describe a superficial partial thickness burn

A

Red and oedematous skin
Painful
Heals within around 7 days

110
Q

Describe a deep partial thickness burn

A

Blistered and mottled
Painful
Heals over 3 weeks
Usually no scarring

111
Q

Describe a full thickness burn

A 
Destruction of epidermis and dermis
Painless
Loss of sensation
Charred leathery eschars
Healing either by scarring or contractures (requires grafts)
112
Q

How is the size of a burn assessed?

A

Percentage of body area

113
Q

What investigations should be used when dealing with burns injury?

A 
FBC
U&amp;E
Group and save
O2 Sats
ABG
Carboxyhemoglobin (if inhalational)
114
Q

What investigations should be used when dealing with electrical burns?

A

Serum CK
ECG
Urine myoglobin (check for muscle damage)

115
Q

Define cardiac arrest

A

Acute cessation of cardiac function

116
Q

What are the classic reversible causes of cardiac arrest?

A

4 Hs & 4Ts

Hypoxia
Hypothermia
Hypovolemia
Hypo/Hyperkalemia
Tamponade
Tension pneumothorax
Thromboembolism
Toxins
117
Q

Describe onset of cardiac arrest

A

Sudden

118
Q

List some symptoms that may precede cardiac arrest

A

Fatigue
Dizziness
Blackout
Fainting

119
Q

What signs may be found on examination of a patient in cardiac arrest?

A

Unconscious
Not breathing
Absent carotid pulse

120
Q

What investigations should be made for cardiac arrest?

A

Cardiac monitor

Blood tests

121
Q

Why is a cardiac monitor useful for investigating cardiac arrest?

A

It classifies the type of cardiac rhythm which is required to decide on the management plan

122
Q

Which blood parameters should be tested for in cardiac arrest?

A 
FBC
U&amp;Es
Clotting screen
Glucose
ABG
Cross-match
Toxicology screen
123
Q

What are the two stages of cardiac arrest management?

A

Basic life support

Advanced life support

124
Q

In cardiac arrest, which cardiac rhythms are shockable or non-shockable?

A

Shockable:
Pulseless VT
VF

Non-shockable:
PEA
Asystole

125
Q

If after BLS, rhythm is assessed to be pulseless VT or VF, what is the management?

A

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
Q

If after BLS, rhythm is assessed to be PEA or asystole, what is the management?

A

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
Q

How should the reversible causes of cardiac arrest be treated?

A

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
Q

What are some possible complications of cardiac arrest?

A

Death

Irreverisble hypoxic damage

129
Q

What is the prognosis of a patient with cardiac arrest?

A

1) Increased duration of inadequate cardiac output worsens prognosis
2) Resuscitation outside hospital less successful

130
Q

Define cardiac failure

A

Inability of cardiac output to meet body’s demands despite normal venous pressure

131
Q

What is the difference between low output and high output cardiac failure?

A

Low output: Reduced cardiac output

High output: Increased demand by tissues

132
Q

Which is more common, low or high output cardiac failure?

A

Low output

133
Q

List the types of low output cardiac failure

A

Left heart failure
Right heart failure
Congestive heart failure

134
Q

List causes of left heart failure

A 
Ischemic heart disease
Hypertension
Cardiomyopathy
Aortic valve disease
Mitral regurgitation
135
Q

List causes of right heart failure

A 
Secondary to left heart failure
Infarction
Cardiomyopathy
Pulmonary hypertension/embolus
Chronic lung disease
Tricuspid regurgitation
Constrictive pericarditis
136
Q

List causes of congestive heart failure

A

Arrythmia
Cardiomyopathy
Myocarditis
Drug toxicity

137
Q

List causes of high output cardiac failure

A 
Anemia
Beriberi
Pregnancy
Paget's disease
Hyperthyroidism
AV malformation
138
Q

What is the incidence of cardiac failure?

A

10% of >65 year olds

139
Q

What signs can be found on examination of left heart failure?

A 
Tachycardia
Tachypnoea
Displaced apex beat
Bilateral basal crackles
Third heart sound
Pansystolic murmur (functional mitral regurgitation)
140
Q

What signs can be found on examination of right heart failure?

A 
Raised JVP
Ankle/sacral pitting oedema
Hepatomegaly
Ascites
Signs of functional tricuspid regurgitation
141
Q

What are the stages of dyspnoea?

A

1) No dyspnoea
2) Dyspnoea on ordinary activities
3) Dyspnoea on less than ordinary activities
4) Dyspnoea at rest

142
Q

What are the symptoms of right heart failure?

A 
Swollen ankles
Fatigue
Increased weight (b/c of oedema)
Decreased exercise tolerance
Nausea
143
Q

What investigations would be performed to explore possible heart failure?

A 
Bloods
CXR
ECG
Echocardiogram
Swan-Ganz catheter
144
Q

What bloods would be tested for in heart failure

A 
FBC
CRP
LFTs
TFTs
U&amp;Es
Lipids
Glucose
145
Q

In addition to the basic blood investigations for cardiac failure, what would be added for acute left ventricular failure?

A

ABG
Troponin
BNP

146
Q

What would low plasma BNP suggest in the context of heart failure?

A

Rules out cardiac failure with 90% sensitivity

147
Q

List the 5 signs of heart failure on CXR

A 
ABCDE
Alveolar shadowing
Kerley B lines
Cardiomegaly
Diversion of upper pulmonary vessels
Effusion in pleura
148
Q

Why is a swan-ganz catheter a useful investigation for cardiac failure

A

Allows measurements of right atrial, right ventricular, pulmonary artery, pulmonary wedge, and left ventricular end-diastolic pressures

149
Q

What is the management of acute left ventricular failure?

A

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
Q

What is the primary management of chronic left ventricular failure?

A

ACEi
Beta-blocker
Lifestyle changes

151
Q

What medications are used in the treatment of chronic left ventricular failure and give an example of each

A 
ACEi (ramipril)
Beta-blocker (carvedilol)
Loop diuretic (furosemide)
Aldosterone antagonist (spirinolactone)
ARB (candesartan)
Hydralazine and a nitrate
Digoxin
152
Q

What should be monitored if a patient takes aldosterone antagonists or ARBs

A

K+ levels as these drugs can cause hyperkalemia

153
Q

When might hydralazine and a nitrate be added for chronic LVF treatment?

A

In patients with persistent symptoms despite ACEi and beta-blockers, often Afro-Carribeans

154
Q

What surgical intervention can be used for chronic LVF?

A

LVEF <35%: no LBBB
- Implantable cardiac defibrillator

LVEF <30%: LBBB
Cardiac resynchronisation therapy with biventricular pacemaker

155
Q

How does cardiac resynchronisation therapy work?

A

Simultaneous activation of both ventricles with a biventricular pacemaker decrease dyssynchronous contraction, enhancing ventricular contraction and reducing functional mitral regurgitation

156
Q

List the complications of cardiac failure

A

Respiratory failure
Cardiogenic shock
Death

157
Q

What is the prognosis for a patient with cardiac failure?

A

50% die within 2 years

158
Q

Define COPD

A

Chronic, progressive lung disorder characterised by airflow obstruction with chronic bronchitis and/or emphysema

159
Q

Define chronic bronchitis

A

Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years

160
Q

Define emphysema

A

Permanent destructive enlargement of air spaces distal to the terminal bronchioles

161
Q

Which structures are damaged in COPD?

A

Bronchi

Alveoli

162
Q

List causes of COPD

A

Environmental toxins - cigarette smoke

A1-antitrypisin deficiency

163
Q

When should you consider A1-antitrypsin deficiency?

A

Young patients who develop COPD despite never smoking

164
Q

What is the prevalence of COPD?

A

Very common (8%)

165
Q

When does COPD usually present?

A

Middle age or later

166
Q

What symptoms does COPD present with?

A

Chronic cough and sputum production
Breathlessness
Wheeze
Decreased exercise tolerance

167
Q

What signs might be found on physical examination of COPD patients?

A

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
Q

What investigations would be performed to explore COPD?

A 
Spirometry and pulmonary function tests
CXR
Bloods
ABG
ECG &amp; Echocardiogram (cor pulmonale)
Sputum sample &amp; blood cultures (acute exacerbations)
A1-antitrypsin levels (young patients)
169
Q

Define cor pulmonale

A

Abnormal enlargement of right side of heart as a result of disease of lungs or pulmonary blood vessels

170
Q

What lung function test results would suggest COPD

A

Decreased PEF rate
Decreased FEV1:FVC ratio
Increased lung volumes

171
Q

How does FEV1:FVC ratio correspond to COPD severity?

A

Mild: 60-80%
Moderate: 40-60%
Severe: <40%

172
Q

Outline the management of COPD

A

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
Q

Define diabetic ketoacidosis

A

Diabetic ketoacidosis is a biochemical triad of hyperglycemia, ketonemia, and acidemia which presents with rapid symptom onset

174
Q

List the symptoms of DKA

A

Polydipsia
Polyuria
Weakness
Weight Loss

175
Q

List the signs of DKA

A 
Tachycardia
Dry mucous membranes
Poor skin turgor
Hypotension
Shock (Severe cases)
176
Q

Describe the aetiology of DKA

A

Reduction in net circulating insulin along with elevation of counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone)

177
Q

What are the two most common predisposing factors for DKA?

A

Inadaequate insulin therapy

Infection

178
Q

What investigations should be made for DKA and what results might be seen?

A 
Plasma glucose - Elevated
ABG - 7.015 mmol/L
Capillary/Serum ketones 
Urinalysis (+ve glucose and ketones)
U&amp;Es (Urea elevated, electrolytes vary)
179
Q

What is the diagnostic criteria for DKA?

A

Acidemia (venous blood pH<7.3 or HCO3-<15.0 mmol/L
Hyperglycemia (Blood glucose >11.0 mmol/L)
Ketonemia (?3.0 mmol/L)

180
Q

Why is serum sodium often low in DKA?

A

Osmotic reflux of water from intracelllular to extracellular space in the presence of hyperglycemia

181
Q

What does hypernatremia in the presence of hyperglycemia in DKA indicate?

A

Profound volume depletion

182
Q

What is the treatment for DKA?

A

IV fluids
Insulin therapy
Electrolyte replacement

Note: Depends on degree of volume depletion

183
Q

List some possible complications for DKA

A 
Cerebral oedmea
Aspiration pneumonia
Hypokalemia
Hypomagnesemia
Hypophosphatemia
Thromboembolism
184
Q

Define DIC

A

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

185
Q

What are the two main characteristics of DIC

A

1) Continuous generation of intravascular fibrin

2) Depletion of procoagulants and platelets

186
Q

List some causes of DIC

A

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)

187
Q

What are the two types of DIC and what are their causes

A

1) Acute DIC (Rapid onset conditions) - Major trauma, sepsis

2) Chronic DIC (Non-acute conditions) - Malignancies, raynaud’s disease

188
Q

Describe the pathophysiology of acute DIC

A

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

189
Q

How does the pathophysiology of chronic DIC differ from acute DIC

A

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

190
Q

What is the epidemiology of DIC?

A

Seen in severely ill patients

191
Q

What are the presenting symptoms of DIC?

A

1) Symptoms of cause
2) Dyspnoea
3) Confusion
4) Evidence of bleeding

192
Q

What are the general signs of DIC (acute or chronic) on examination?

A

1) Signs of cause
2) Fever
3) Shock (hypotension, tachycardia)

193
Q

What are the signs of acute DIC on examination?

A

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

194
Q

What are the specific signs of chronic DIC on examination?

A

1) Signs of deep vein and arterial thrombosis/embolism

2) Superficial venous thrombosis

195
Q

What investigations would be suitable to explore DIC?

A

1) Platelet count
2) Clotting screen (PT, aPTT, Fibrinogen)
3) Fibrin degradation products/D-dimer
4) Blood film

196
Q

What anomalies would be seen on the blood tests of a patient with DIC?

A

1) Platelets - Decrease
2) Clotting (PT, aPTT) - Increased
3) Fibrinogen - Decreased
4) Fibrin degradation products/D-dimer - Increased

197
Q

What anomaly would be seen on the blood film of a patient with DIC?

A

Schistocytes

Sofia Notes (2 decks)

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