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UKMLA Prep > acute and emergency > Flashcards

acute and emergency Flashcards

presentation and conditions

1
Q

Haematuria

A

-Microscopic or dipstick positive haematuria is increasingly termed non-visible haematuria

-Macroscopic haematuria is termed visible haematuria.

-Non-visible haematuria is found in around 2.5% of the population.

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2
Q

What are the causes of SPIRIOUS non-visible haematuria

A

-urinary tract infection
-menstruation
-vigorous exercise (this normally settles after around 3 days)
-sexual intercourse

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3
Q

Causes of PERSISTANT non-visible haematuria

A

-cancer (bladder, renal, prostate)
-stones
-benign prostatic hyperplasia
-prostatitis
-urethritis e.g. Chlamydia
-renal causes: IgA nephropathy, thin basement -membrane disease

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4
Q

Spurious causes - red/orange urine, where blood is not present on dipstick

A

-foods: beetroot, rhubarb
-drugs: rifampicin, doxorubicin

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5
Q

Testing for haematauria

A
  • We do not screen for haematuria as it’s very ccommon

Investigations
- urine dipstick is the test of choice for detecting haematuria

-persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart

-renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked

-urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected

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6
Q

When urgent referral is needed for non-visible haematauria

A

Aged >= 45 years AND:
-unexplained visible haematuria without urinary tract infection, or

-visible haematuria that persists or recurs after successful treatment of urinary tract infection

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test

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7
Q

Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test- what are the likely diagnosis

A
  • UTI
  • Bladder Cancer
  • Prostatitis
  • Renal Parenchymal Disease
    -Benign Prostatic Hyperplasia (BPH)
    -Kidney Stones
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8
Q

Differential diagnosis Aged >= 45 years AND:
-unexplained visible haematuria without urinary tract infection, or

-visible haematuria that persists or recurs after successful treatment of urinary tract infection

A
  • Urinary Tract Stones (Nephrolithiasis or Urolithiasis)
  • bladder cancer
    -Exercise-Induced Hematuria:
    -Renal Trauma or Injury
    -Medication-Induced Hematuria
    -Coagulopathy or Bleeding Disorders
    -Renal Parenchymal Disease
  • Renal bladder stones
    -UTI
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9
Q

Reasons for non-urgent referral when haematauria is discovered

A

Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection

patients under the age of 40 years with normal renal function, no proteinuria and who are normotensive do not need to be referred and may be managed in primary care

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10
Q

Nephrotic syndrome and the four signs of it

A
  • Kidney disorder where there is damage done to the glomeruli.
  • ## large amounts of protein leaking into the urine.1.Proteinuria:

2.Hypoalbuminemia

  1. Edema.
  2. Hyperlipidemia
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11
Q

What are risk factors for suicide?

A
  • mental health conditions
  • previous suicide attempts
  • family history
  • stressful life hx
  • access to means
  • chronic illness
  • males are more likely
  • making efforts not to be found
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12
Q

Anaphylaxis

A
  • life-threatening allergic reaction which occurs in minutes after exposure to a trigger

Symptoms
- swelling of the lips, mouth, throat and tongue
- rash on the body
- Difficulty breathing
- unconscious

typically for anaphylaxis to be diagnosed, 2/4 conditions need to be diagnosed with

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13
Q

Managment of anaphylaxis

A

ALL AGES NEED A-E MANAGEMENT

-Children weighing 15-30 kg: 0.15 mg (0.15 mL)
-Children weighing >30 kg: 0.3 mg (0.3 mL)
- Adults (0.5ml of 1:1,000 adenaline)

Antihistamines (e.g., cetirizine, diphenhydramine) and corticosteroids (e.g., hydrocortisone) may be given to help relieve symptoms and prevent recurrence.

Nebulized bronchodilators (e.g., salbutamol) may be used for severe respiratory symptoms.

Refer to allergy clinic where 2 epi-pens and training need to be given.

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14
Q

Sepsis

A

Sepsis is a life-threatening condition that occurs when the body’s response to an infection causes widespread inflammation, leading to organ dysfunction and failure.

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15
Q

Sepsis 6 (BUFALO)

A

take 3/give 3

take
- Bloods
-Urea
-Lactate

Give
- Fluids
-Oxygen
- Antibiotics

BUFALO
-Bloods
-Urea
Fluids
-Antibiotcs
-Lactate
-Oxygen

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16
Q

what are the symptoms of Sepsis

A
  • Decreased Urine output
  • low blood pressure
  • fever
  • tachycardia
  • tachypnoea
  • altered mental status
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17
Q

causes of sepsis

A
  • UTI
  • pneumonia
  • abdo infections
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18
Q

complications of Sepsis

A

-ARDS
-DIC
- Multiple organ failure
- acute kidney injury

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19
Q

Criteria for sepsis

A

Sequential Organ Failure Assessment (SOFA) score and the quick SOFA (qSOFA) score are commonly used to assess the severity of organ dysfunction and predict outcomes in sepsis.

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20
Q

Neutropenic sepsis

A

Neutropenic sepsis, also known as febrile neutropenia, is a medical emergency characterized by the presence of fever (usually defined as a single oral temperature ≥38.3°C or a sustained temperature ≥38.0°C over 1 hour) in a patient with neutropenia.

typically occurs to patients undergoing chemotherapy or other bone marrow supression tx

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21
Q

Symptoms of neutropenic sepsis

A

-chills
-malaise
- weakness
- signs of systemic infection, such as tachycardia, hypotension, or altered mental status.

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22
Q

Pathogens which typically affect patients with neutropaenic sepsis

A

-Pseudomonas aeruginosa,
Candida species, Aspergillus species, Staphylococcus Aeurus,
Enterococcus species
Escherichia coli
Streptococcus pneumoniae
Herpes Simplex Virus

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23
Q

managment of neutropaenic sepsis

A

-Sepsis 6
- consider anti-fungals and and antivirals
granulocyte colony-stimulating factors (G-CSF) to stimulate neutrophil production
-Consultation with Hematology/Oncology Specialists

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24
Q

Shock

A

Shock is a life-threatening medical emergency characterized by inadequate tissue perfusion, resulting in cellular hypoxia and organ dysfunction.

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25
Q

what are the types of shock

A

-Hypovolemic shock
-Cardiogenic Shock
-Distributive Shock
-Obstructive Shock

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26
Q

Further breakdown of distributive shock

A
  • anaphylactic shock
    -neutrogenic shock
  • septic shock
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27
Q

Managment of shock

A
  • ABCDE response
  • fluid resus
    -vasopressors
    -O2 managment
  • underlying causes
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28
Q

Neutropathic pain

A

Neuropathic pain may be defined as pain which arises following damage or disruption of the nervous system.

It is often difficult to treat and responds poorly to standard analgesi

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29
Q

Examples of neutropathic pain

A
  • diabetic neuropathy
  • post-herpetic neuralgia
    -trigeminal neuralgia
    -prolapsed intervertebral disc
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30
Q

First line treatment of neuropathic pain?

A

first-line treatment*: amitriptyline, duloxetine, gabapentin or pregabalin

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31
Q

What if the first-line treatment of pain does not manage the pain?

A

Try the other three drugs
- amitriptyline, duloxetine, gabapentin or pregabline

Drugs should be switched, not added

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32
Q

Rescue therapy Drug for neuropathic pain

A

Tramadol

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33
Q

When is Capsaicin used?

A

Localised neuropathic pain (e.g post-herpes)

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34
Q

Opioids

A

Opioids include substances like endorphins, semi-synthetic, and synthetic compounds that act on opioid receptors

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35
Q

G-coupled receptors for opioids

A

These receptors, present in the CNS, mediate the actions of opioids.

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36
Q

Mu (µ) Receptors:

A
  • Brain, brainstem, and spinal cord.
  • µ1-receptors: Involved in pain transmission; activation leads to analgesia
  • µ2- and µ3-receptors: Found in the brainstem; their activation causes
  • respiratory depression
  • reduced gastrointestinal motility,
  • vasodilation
  • pupillary constriction in overdose.
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37
Q

Kappa (κ) Receptors:

A

Spread throughout the brain, brainstem, and spinal cord.
Associated with cognitive effects, dysphoria, hallucinations, and depressed consciousness.

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38
Q

Delta (δ) Receptors:

A

Almost exclusively in the brain and brainstem.
Potentiate µ-receptors, enhancing analgesia, respiratory depression, and dependence.

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39
Q

Endogenous Opioids

A

Include endorphins, dynorphins, and enkephalins, produced mainly in the brain and brainstem.
β-Endorphin: Targets µ-receptors, influences appetite, sexual behaviour, and pain control during exercise.
Met-enkephalin: Acts on δ-receptors, modulating the flight-or-fight response.
Dynorphin: Involved in appetite, mood, and stress regulation.

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40
Q

Which enzyme system is responsible for opioid metabolism?

A

cytochrome P450 (CYP450

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41
Q

Phase I metabolism of opioids

A
  • oxidation, reduction, and hydrolysis
    Cytochrome P450 enzymes CYP3A4 and CYP2D6 —> modifying opioids to form more water-soluble metabolites.
    Example: Codeine —>CYP2D6 —>morphine (more active)
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42
Q

Phase II of opioid metabolism

A

Involves conjugation reactions like glucuronidation.
Morphine is glucuronidated to morphine-3-glucuronide (inactive) and morphine-6-glucuronide (active and potent).

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43
Q

Genetic variability of opioid breakdown

A

Genetic polymorphisms in CYP450 enzymes, especially CYP2D6, can significantly affect the metabolism of certain opioids (like codeine and tramadol), leading to variability in clinical response.

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44
Q

Active metabolites of opioid breakdown

A

Some opioids have active metabolites that contribute to their analgesic effect or side effects. For example, the metabolites of morphine include both analgesic and neuroexcitatory compounds.

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45
Q

Renal excretion of opioids

A

Most opioid metabolites are excreted by the kidneys.
Renal impairment can lead to the accumulation of these metabolites, increasing the risk of toxicity, especially in opioids with active metabolites.

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46
Q

Palliative care prescribing

A

offer patients with advanced and progressive disease regular oral modified-release (MR) or oral immediate-release morphine (depending on patient preference), with oral immediate-release morphine for breakthrough pain

No co-morbidities, use 20-30mg of MR with 5mg morphine for breakthrough pain

I.e 15mg modified-release morphine tablets twice a day with 5mg of oral morphine solution as required

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47
Q

Side effects of morphine and side prescriptions

A

-constipation (laxatives)
- nausea and vomiting (antiemetic)
- respiratory depression
- drowsiness (adjust prescription if an issue)

Oral morphine is preferred to transdermal morphine prescription

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48
Q

Breakthrough dose calculation

A
  • Breakthrough dose morphine is 1/6 of daily dose
  • all patients who receive opioid should be given a laxative
  • care should be taken with patients with chronic kidney disease
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49
Q

Palliative care and renal impairment prescriptions

A

oxycodone is preferred to morphine in palliative patients with mild-moderate renal impairment

if renal impairment is more severe, alfentanil, buprenorphine and fentanyl are preferred

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50
Q

Metastatic bone pain prescription

A

may respond to strong opioids, bisphosphonates or radiotherapy.

Studies do not support use of NSAIDS

Strong opioids have the lowest number needed to treat for relieving the pain and can provide quick relief, in contrast to radiotherapy and bisphosphonates*. All patients, however, should be considered for referral to a clinical oncologist for consideration of further treatments such as radiotherapy

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51
Q

How to increase opioid doses

A

Dose should be increased by 30-50%

Add bisphosphonates, radiotherapy and denosumab to treat metastatic bone pain.

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52
Q

Transient side effects of opioids

A

Nausea
Drowsiness

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53
Q

Persistent side effects of opioids

A

Constipation

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54
Q

Conversion between opioids

A
  • Oral codeine to oral morphine- divide by 10
  • Oral tramadol to oral morphine - divide by 10
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55
Q

Morphine to oxycodone conversion

A

Divide by 1.5 or 2

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56
Q

Oral morphine to subcutaneous morphine conversion

A

Divide by 2

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57
Q

Oral morphine to subcutaneous diamorphine

A

Divide by 3

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58
Q

Oral oxycodone to subcutaneous diamorphine

A

Divide by 1.5

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59
Q

Diagnostic criteria for AKI

A

Rise in creatinine of 26µmol/L or more in 48 hours OR
>= 50% rise in creatinine over 7 days OR
Fall in urine output to < 0.5ml/kg/hour for more than 6 hours in adults (8 hours in children) OR
>= 25% fall in eGFR in children / young adults in 7 days.

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60
Q

Stage 1 AKI criteria

A

Increase in creatinine to 1.5-1.9 times baseline, or
Increase in creatinine by ≥26.5 µmol/L, or
Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours

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61
Q

Stage 2 AKI criteria

A

Increase in creatinine to 2.0 to 2.9 times baseline, or
Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours

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62
Q

Stage 3 AKI criteria

A

Increase in creatinine to ≥ 3.0 times baseline, or
Increase in creatinine to ≥353.6 µmol/L or
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2

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63
Q

When to refer to a nephrologist with AKIs

A

Renal tranplant
ITU patient with unknown cause of AKI
Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
AKI with no known cause
Inadequate response to treatment
Complications of AKI
Stage 3 AKI (see guideline for details)
CKD stage 4 or 5
Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)

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64
Q

What increases the risk of AKIs

A

Emergency surgery, ie, risk of sepsis or hypovolaemia
Intraperitoneal surgery
CKD, ie if eGFR < 60
Diabetes
Heart failure
Age >65 years
Liver disease
Use of nephrotoxic drugs
NSAIDs
aminoglycosides
ACE inhibitors/angiotensin II receptor antagonists
diuretics

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65
Q

Acute interstitial nephritis

A

Accounts to 25% of drug-induced AKis

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66
Q

Causes of AIN

A

drugs: the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci

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67
Q

Pathophysiology of AIN

A

histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

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68
Q

Features of AIN

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

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69
Q

Investigations for AIN

A

sterile pyuria
white cell casts

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70
Q

Anterpartum haemorrhage

A

Antepartum haemorrhage is defined as bleeding from the genital tract after 24 weeks pregnancy, prior to delivery of the fetus

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71
Q

Placental abruption

A

shock out of keeping with visible loss
pain constant
tender, tense uterus*
normal lie and presentation
fetal heart: absent/distressed
coagulation problems
beware pre-eclampsia, DIC, anuria

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72
Q

Placental praevia

A

shock in proportion to visible loss
no pain
uterus not tender
lie and presentation may be abnormal
fetal heart usually normal
coagulation problems rare
small bleeds before large

vaginal examination should not be performed in primary care for suspected antepartum haemorrhage - women with placenta praevia may haemorrhage

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73
Q

Threatened miscarriage

A

painless vaginal bleeding occurring before 24 weeks, but typically occurs at 6 - 9 weeks
the bleeding is often less than menstruation
cervical os is closed
complicates up to 25% of all pregnancies

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74
Q

Missed (delayed) miscarriage

A

a gestational sac which contains a dead fetus before 20 weeks without the symptoms of expulsion
mother may have light vaginal bleeding / discharge and the symptoms of pregnancy which disappear. Pain is not usually a feature
cervical os is closed
when the gestational sac is > 25 mm and no embryonic/fetal part can be seen it is sometimes described as a ‘blighted ovum’ or ‘anembryonic pregnancy’

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75
Q

Inevitable miscarriage

A
  • heavy bleeding with clots and pain
    Cervical os is open
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76
Q

Incom plete miscarriage

A

not all products of conception have been expelled
pain and vaginal bleeding
cervical os is open

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77
Q

Expectant management of miscarriage

A

Waiting for a spontaneous miscarriage’
First-line and involves waiting for 7-14 days for the miscarriage to complete spontaneously
If expectant management is unsuccessful then medical or surgical management may be offered

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78
Q

Medical or surgical management.of miscarriage risks

A

increased risk of haemorrhage
she is in the late first trimester
if she has coagulopathies or is unable to have a blood transfusion
previous adverse and/or traumatic experience associated with pregnancy (for example, stillbirth, miscarriage or antepartum haemorrhage)
evidence of infection

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79
Q

Medical management of missed miscarriage

A

oral mifepristone.

48 hours later, misoprostol

If bleeding has not started within 48 hours after misoprostol treatment, they should contact their healthcare professional

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80
Q

Incomplete miscarriage

A

a single dose of misoprostol (vaginal, oral or sublingual)

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81
Q

Management of all miscarriages

A

women should be offered antiemetics and pain relief
a pregnancy test should be performed at 3 weeks

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82
Q

Surgical management of miscarriage

A

Undergoing a surgical procedure under local or general anaesthetic’
The two main options are vacuum aspiration (suction curettage) or surgical management in theatre
Vacuum aspiration is done under local anaesthetic as an outpatient

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83
Q

Causes of recurrent miscarriages

A

antiphospholipid syndrome
endocrine disorders: poorly controlled diabetes mellitus/thyroid disorders. Polycystic ovarian syndrome
uterine abnormality: e.g. uterine septum
parental chromosomal abnormalities
smoking

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84
Q

Immediate first aid for burns

A

airway, breathing, circulation
burns caused by heat: remove the person from the source. Within 20 minutes of the injury irrigate the burn with cool (not iced) water for between 10 and 30 minutes. Cover the burn using cling film, layered, rather than wrapped around a limb
electrical burns: switch off power supply, remove the person from the source
chemical burns: brush any powder off then irrigate with water. Attempts to neutralise the chemical are not recommended

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85
Q

Wallace’s rule of nines

A

head + neck = 9%,
each arm = 9%,
each anterior part of leg = 9%,
each posterior part of leg = 9%,
anterior chest = 9%,
posterior chest = 9%,
Anterior abdomen = 9%,
posterior abdomen = 9%

The palmar surface is approximately 1%

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86
Q

Superficial epidermal burn

A

First degree

Red and painful, no dry blisters

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87
Q

Patial thickness (superficial dermal)

A

Second degree burn
Pale piping, painful, blistered and reduced cap refill time

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88
Q

Partial thickness burn (deep dermal)

A

Second degree

Typically white, but may have non-blanching erythema

Reduced sensation

Painful to deep pressure

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89
Q

Full thickness burn

A
  • third degree burn
  • white (waxy)
  • brown (leathery)
    Black in colour with no blisters or pain
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90
Q

Acynotic congenital heart disease

A

ventricular septal defects (VSD) - most common, accounts for 30%
atrial septal defect (ASD)
patent ductus arteriosus (PDA)
coarctation of the aorta
aortic valve stenosis

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91
Q

Cyanotic causes of congenital heart disease

A

tetralogy of Fallot
transposition of the great arteries (TGA)
tricuspid atresia

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92
Q

Peripheral cyanosis in neonatal period

A

very common in the first 24 hours of life and may occur when the child is crying or unwell from any cause

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93
Q

Central cyanosis in neonatal period

A

Central cyanosis can be recognised clinically when the concentration of reduced haemoglobin in the blood exceeds 5g/dl

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94
Q

Nitrogen washout test

A

nitrogen washout test (also known as the hyperoxia test) may be used to differentiate cardiac from non-cardiac causes. The infant is given 100% oxygen for ten minutes after which arterial blood gases are taken. A pO2 of less than 15 kPa indicates cyanotic congenital heart disease

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95
Q

Causes of cyanotic congenital heart disease

A

tetralogy of Fallot (TOF)
transposition of the great arteries (TGA)
tricuspid atresia

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96
Q

Management of suspected cyanotic congenital heart disease

A

supportive care
prostaglandin E1 e.g. alprostadil
used to maintain a patent ductus arteriosus in ductal-dependent congenital heart defect
this can act as a holding measure until a definite diagnosis is made and surgical correction performed

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97
Q

Acrocyanosis

A

refers to cyanosis around the mouth and the extremities such as the hands and feet

occurs immediately after birth in healthy infants. It is a common finding and may persist for 24 to 48 hours.

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98
Q

Teraology of Fallot

A

Most common cause of congenital heart disease
Presents around 1-2 months but may not be picked up until the baby is 6 months old

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99
Q

Four characteristic features of teralogy of fallot

A

ventricular septal defect (VSD)
right ventricular hypertrophy
right ventricular outflow tract obstruction, pulmonary stenosis
overriding aorta

severity of the right ventricular outflow tract obstruction determines the degree of cyanosis and clinical severity

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100
Q

Features of TOF

A

cyanosis
unrepaired TOF infants may develop episodic hypercyanotic ‘tet’ spells due to near occlusion of the right ventricular outflow tract
features of tet spells include tachypnoea and severe cyanosis that may occasionally result in loss of consciousness
they typically occur when an infant is upset, is in pain or has a fever
causes a right-to-left shunt
ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur)
a right-sided aortic arch is seen in 25% of patients
chest x-ray shows a ‘boot-shaped’ heart, ECG shows right ventricular hypertrophy

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101
Q

Management of TOF

A

surgical repair is often undertaken in two parts
cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm

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102
Q

Transposition of the great arteries (TGA)

A

Transposition of the great arteries (TGA) is a form of cyanotic congenital heart disease. It is caused by the failure of the aorticopulmonary septum to spiral during septation. Children of diabetic mothers are at an increased risk of TGA.

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103
Q

Anatomical changes in TGA

A

aorta leaves the right ventricle
pulmonary trunk leaves the left ventricle

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104
Q

Clinical features of TGA

A

cyanosis
tachypnoea
loud single S2
prominent right ventricular impulse
‘egg-on-side’ appearance on chest x-ray

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105
Q

Management of TGA

A

maintenance of the ductus arteriosus with prostaglandins
surgical correction is the definite treatment.

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106
Q

Extramural haematoma

A

collection of blood that is between the skull and the dura.

It is almost always caused by trauma and most typically by ˜low-impact’ trauma (e.g. a blow to the head or a fall).

Collection is typically in the temporal region (MIDDLE MENINGEAL ARTERY)

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107
Q

patient who initially loses, briefly regains and then loses again consciousness after a low-impact head injury.

A

Extradural haematoma
Ludic period

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108
Q

Imaging of extradural haematoma

A

biconvex (or lentiform), hyperdense collection around the surface of the brain. They are limited by the suture lines of the skull.

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109
Q

Treatment of extradural haematoma

A

treatment is craniotomy and evacuation of the haematoma.

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110
Q

Hypoglycaemia causes

A

insulinoma - increased ratio of proinsulin to insulin
self-administration of insulin/sulphonylureas
liver failure
Addison’s disease
alcohol
causes exaggerated insulin secretion
mechanism is thought to be due to the effect of alcohol on the pancreatic microcirculation → redistribution of pancreatic blood flow from the exocrine into the endocrine parts → increased insulin secretion
nesidioblastosis - beta cell hyperplasia

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111
Q

Features of hypoglycaemia

A

blood glucose levels and the severity of symptoms are not always correlated, especially in patients with diabetes.
blood glucose concentrations <3.3 mmol/L cause autonomic symptoms due to the release of glucagon and adrenaline (average frequency in brackets):
Sweating
Shaking
Hunger
Anxiety
Nausea
blood glucose concentrations below <2.8 mmol/L cause neuroglycopenic symptoms due to inadequate glucose supply to the brain:
Weakness
Vision changes
Confusion
Dizziness
Severe and uncommon features of hypoglycaemia include:
Convulsion
Coma

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112
Q

Management of hypoglycaemia in hospital settings

A

If the patient is alert, a quick-acting carbohydrate may be given (as above)
If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given.
Alternatively, intravenous 20% glucose solution may be given through a large vein

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113
Q

Managment of hypoglycaemia

A

in the community (for example, diabetes mellitus patients who inject insulin):
Initially, oral glucose 10-20g should be given in liquid, gel or tablet form
Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel.
A ‘HypoKit’ may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home

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114
Q

Signs and symptoms of hypoglycaemia

A

blood glucose levels and the severity of symptoms are not always correlated, especially in patients with diabetes.
blood glucose concentrations <3.3 mmol/L cause autonomic symptoms due to the release of glucagon and adrenaline (average frequency in brackets):
Sweating
Shaking
Hunger
Anxiety
Nausea
blood glucose concentrations below <2.8 mmol/L cause neuroglycopenic symptoms due to inadequate glucose supply to the brain:
Weakness
Vision changes
Confusion
Dizziness
Severe and uncommon features of hypoglycaemia include:
Convulsion
Coma

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115
Q

Subarachnoid haemorrhage (SAH)

A

intracranial haemorrhage that is defined as the presence of blood within the subarachnoid space, i.e. deep to the subarachnoid layer of the meninges.

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116
Q

Causes of spontaneous SAH

A

intracranial aneurysm (saccular ˜berry’ aneurysms)
accounts for around 85% of cases
conditions associated with berry aneurysms include hypertension,adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
arteriovenous malformation
pituitary apoplexy
mycotic (infective) aneurysms

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117
Q

Classical presentation of SAH

A
  • Headache (sudden onset, thunderclap)
  • severe (worst in my life)
  • occipital

typically peaking in intensity within 1 to 5 minutes
there may be a history of a less-severe ‘sentinel’ headache in the weeks prior to presentation
nausea and vomiting
meningism (photophobia, neck stiffness)
coma
seizures
ECG changes including ST elevation may be seen
this may be secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines

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118
Q

Investigation for SAH

A

Non-contrast CT (acute blood, hypodense, bright on CT)
If CT done within 6 hours of symptoms, may appear to be normal
LP after 12 hours of symptoms shows Xathochromia
CSF will also show normal or raised opening pressure

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119
Q

Managment of SAH

A

supportive
bed rest
analgesia
venous thromboembolism prophylaxis
discontinuation of antithrombotics (reversal of anticoagulation if present)
vasospasm is prevented using a course of oral nimodipine
intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon

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120
Q

Complications of SAH

A

re-bleeding
happens in around 10% of cases and most common in the first 12 hours
if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged
associated with a high mortality (up to 70%)
hydrocephalus
hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt
vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
ensure euvolaemia (normal blood volume)
consider treatment with a vasopressor if symptoms persist
hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
seizures

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121
Q

Predictive factors of SAH

A

conscious level on admission
age
amount of blood visible on CT head

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122
Q

What is subdural haematoma

A

subdural haematoma is a collection of blood deep to the dural layer of the meninges.

The blood is not within the substance of the brain and is therefore called an ˜extra-axial’ or ˜extrinsic’ lesion. They can be unilateral or bilateral.

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123
Q

Classifications of subdural haemorrhage

A

Acute: Symptoms usually develop within 48 hours of injury, characterised by rapid neurological deterioration
Subacute: Symptoms manifest within days to weeks post-injury, with a more gradual progression.
Chronic: Common in the elderly, developing over weeks to months. Patients may not recall a specific head injury.

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124
Q

Neurological features of subdural haemorrhage

A

Altered Mental Status: Ranging from mild confusion to deep coma. Fluctuations in the level of consciousness are common.
Focal Neurological Deficits: Weakness on one side of the body, aphasia, or visual field defects, depending on the haematoma’s location.
Headache: Often localised to one side, worsening over time.
Seizures: May occur, particularly in acute or expanding hematomas.

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125
Q

Physical examination findings of subdural haemorrhage

A

Papilloedema: Indicates raised intracranial pressure.
Pupil Changes: Unilateral dilated pupil, especially on the side of the haematoma, indicating compression of the third cranial nerve.
Gait Abnormalities: Including ataxia or weakness in one leg.
Hemiparesis or Hemiplegia: Reflecting the mass effect and midline shift.

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126
Q

Behavioural and cognitive change in subdural haemorrhage

A

Memory loss- especially in chronic SDH

Personality Changes: Irritability, apathy, or depression.
Cognitive Impairment: Difficulty with attention, problem-solving, and other executive functions.

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127
Q

Other associated features of SDH

A

Nausea and Vomiting: Secondary to increased intracranial pressure.
Drowsiness: Progressing to stupor and coma in severe cases.
Signs of Increased Intracranial Pressure: Such as bradycardia, hypertension, and respiratory irregularities (Cushing’s triad).

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128
Q

GCS

A

Motor, verbal and eye features
(M6, V5, E4)

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129
Q

Motor response

A
  1. Infant moves spontaneously or purposefully
  2. Infant withdraws from touch
  3. Infant withdraws from pain
  4. Abnormal flexion to pain for an infant (decorticate response)
  5. Extension to pain (decerebrate response)
  6. No motor response
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130
Q

Verbal response

A
  1. Orientated
  2. Confused
  3. Words
  4. Sounds
  5. None
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131
Q

Eye response

A
  1. Spontaneous
  2. To speech
  3. To pain
  4. None
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132
Q

Fluid therapy in adults

A

25-30 ml/kg/ day
1 mol/kg/day of K+, Na+ and CL-
Approximately 50-100g per day of glucose to limit strvation and ketosis

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133
Q

Prescription of fluids contradictions and concerns

A

0.9% saline
if large volumes are used there is an increased risk of hyperchloraemic metabolic acidosis

Hartmann’s
contains potassium and therefore should not be used in patients with hyperkalaemia

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134
Q

Fluid therapy in children (when required)

A

IV fluids required when:

the child is > 10% dehydrated, or

the child is if 5-10% dehydrated and oral or enteral rehydration is not tolerated or possible.

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135
Q

24hr fluid requirement- under 10kg

A

100ml/kg

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136
Q

24hr fluid requirement 10-20kg

A

100 mL/kg for the first 10 kg
50 mL/kg for each 1 kg body weight over 10 kg

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137
Q

24 hr fluid requirement over 20kg

A

100 mL/kg for the first 10 kg
50 mL/kg for each 1 kg body weight between 10-20 kg
20 mL/kg for each 1 kg body weight over 20 kg
(max. 2 litres in females, 2.5 litres in males)

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138
Q

IV fluids in children

A

The fluid type routinely used is 0.9% sodium chloride + 5% dextrose. Potassium is added as required.

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139
Q

Hyperosmolar hyperglycaemic state (HHS)

A

Medical emergency with 20% mortality

Hyperglycaemia results in osmotic diuresis, severe dehydration, and electrolyte deficiencies. HHS typically presents in the elderly with type 2 diabetes mellitus (T2DM).

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140
Q

Pathophysiology of HHS

A

Hyperglycaemia results in osmotic diuresis, severe dehydration, and electrolyte deficiencies. HHS typically presents in the elderly with type 2 diabetes mellitus (T2DM).

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141
Q

Precipitating factors of HHS

A
  • intercurrent illness
    -dementia
    -sedative drugs
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142
Q

Clinical features of HHS

A
  • occurs over many days, associated with dehydration and metabolic disturbances
  • volume loft (polyuria, polydipsia, signs of dehydration)

Systemic
- lethargy
- nausea and vomiting

neurological
-altered level of consciousness
-focal neurological deficits

haematological
-hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)

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143
Q

Signs and symptoms of HHS

A

hypovolaemia
marked hyperglycaemia (>30 mmol/L)
significantly raised serum osmolarity (> 320 mosmol/kg)
can be calculated by: 2 * Na+ + glucose + urea
no significant hyperketonaemia (<3 mmol/L)
no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 - acidosis can occur due to lactic acidosis or renal impairment)

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144
Q

Managment of HHS

A

fluid replacement
fluid losses in HHS are estimated to be between 100 - 220 ml/kg
IV 0.9% sodium chloride solution
typically given at 0.5 - 1 L/hour depending on clinical assessment
potassium levels should be monitored and added to fluids depending on the level
insulin
should not be given unless blood glucose stops falling while giving IV fluids
venous thromboembolism prophylaxis
patients are at risk of thrombosis due to hyperviscosity

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145
Q

Complications of HHS

A

Vascular complications:
- MI
- stroke

146
Q

What are the causes of hypercalcaemia?

A
  1. Primary hyperparathyroidism
  2. Malignancy (SCLS, bone mets, myeloma)
  3. Sarcoidosis
  4. Vit D intoxication
  5. Acromegaly
  6. Thyrotoxicosis
  7. Milk- alkali syndrome
  8. Thiazides
    9/ calcium containing antacids
    10 dehydatraion
    11 Addison’s disease
    12 pager’s disease of the bone
147
Q

Features of hypercalcaemia

A

bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension

148
Q

Hyperkalaemia

A
  • regulated by a number of factors including aldosterone, acid-base balance and insulin levels
  • metabolic acidosis is associated
149
Q

Causes of hyperkalaemia

A

acute kidney injury
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
metabolic acidosis
Addison’s disease
rhabdomyolysis
massive blood transfusion

  • salt substitutes
  • bananas, oranges, kiwi, avos, spinach and tonatoes
150
Q

Managment of hyperkalaemia

A
  • Stabilisation of the cardiac membrane
    IV calcium gluconate
    does NOT lower serum potassium levels

Short-term shift in potassium from extracellular (ECF) to intracellular fluid (ICF)
compartment
combined insulin/dextrose infusion
nebulised salbutamol

Removal of potassium from the body
calcium resonium (orally or enema)
enemas are more effective than oral as potassium is secreted by the rectum
loop diuretics
dialysis
haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia

151
Q

Staging of hyperkalaemia

A

mild: 5.5 - 5.9 mmol/L
moderate: 6.0 - 6.4 mmol/L
severe: ≥ 6.5 mmol/L

152
Q

ECG changes of hyperkalaemia

A

peaked or ‘tall-tented’ T waves (occurs first)
loss of P waves
broad QRS complexes
sinusoidal wave pattern

153
Q

Practical managment of hyperkalaemia

A

IV calcium gluconate: to stabilise the myocardium
insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
other treatments such as nebulised salbutamol may be given to temporarily lower the serum potassium

Further management
stop exacerbating drugs e.g. ACE inhibitors
treat any underlying cause
lower total body potassium
calcium resonium
loop diuretics
dialysis

154
Q

Hypernatraemia causes

A
  • dehydration
    -osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
    diabetes insipidus
    excess IV saline
155
Q

Risks of treating hypernatremia

A

owering of other osmolytes (and importantly water) occurs at a slower rate, predisposing to cerebral oedema, resulting in seizures, coma and death

Should be corrected at 0.5mmol/hour

156
Q

Causes of hypocalcaemia

A

vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis

157
Q

False positive hypocalcaemia

A

Contamination of blood samples with EDTA may also give falsely low calcium levels.

158
Q

Managment of hypocalcaemia

A

severe hypocalcaemia (e.g. carpopedal spasm, tetany, seizures or prolonged QT interval) requires IV calcium replacement
the preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended
further management depends on the underlying cause

159
Q

Causes of Hypomagnesaemia

A

drugs
diuretics
proton pump inhibitors
total parenteral nutrition
diarrhoea
may occur with acute or chronic diarrhoea
alcohol
hypokalaemia
hypercalcaemia
e.g. secondary to hyperparathyroidism
calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle
metabolic disorders
Gitleman’s and Bartter’s

160
Q

Features of hypomagnesaemia

A

paraesthesia
tetany
seizures
arrhythmias
decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
exacerbates digoxin toxicity

161
Q

Treatment of hypoganesaemia (<0.4mmol/L or tetany, arrhythmias or seizures)

A

intravenous magnesium replacement is commonly given.
an example regime would be 40 mmol of magnesium sulphate over 24 hours

162
Q

> 0.4 mol/L hypomagnesaeima managment

A

oral magnesium salts (10-20 mmol orally per day in divided doses)
diarrhoea can occur with oral magnesium salts

163
Q

Pseudohyponatremia causes

A

Hyperlipiddaemia
Taking blood from a drip arm

164
Q

Urinary sodium > 20 mmol/l

A

Sodium depletion, renal loss (patient often hypovolaemic)
diuretics: thiazides, loop diuretics
Addison’s disease
diuretic stage of renal failure

Patient often euvolaemic
SIADH (urine osmolality > 500 mmol/kg)
hypothyroidism

165
Q

Urinary sodium < 20 mmol/l

A

Sodium depletion, extra-renal loss
diarrhoea, vomiting, sweating
burns, adenoma of rectum

Water excess (patient often hypervolaemic and oedematous)
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia

166
Q

Hyponatraemia treatment

A
167
Q

Atrial fibrillation

A

Symptomatic palpitations and inefficient cardiac function probably the most important aspect of managing patients with AF is reducing the increased risk of stroke which is present in these patients.

168
Q

Types of atrial fibrillation

A
  • paroxysmal AF- episodes of AF terminate spontaneously. Such episodes last less than 7 days
  • Persistent AF- non self-terminating AF
  • permanent AF- continuous atrial fibrillation can’t be cardioverted or deemed inappropriate
169
Q

Symptoms of AF

A

palpitations
dyspnoea
chest pain

170
Q

Signs of AF

A

Irregular irregular puls

171
Q

Investigations of AF

A
  • ECG
172
Q

Management of AF

A
  • rate and rhythm control
  • reducing stroke risk
173
Q

Rate vs rhythm control

A

rate control **bold text control Rate ** : accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function

rhythm control: try to get the patient back into, and maintain, normal sinus rhythm. This is termed cardioversion. Drugs (pharmacological cardioversion) and synchronised DC electrical shocks (electrical cardioversion) may be used for this purpose

174
Q

What drugs are used for rate control?

A

Any of the following 2

a betablocker
diltiazem
digoxin

175
Q

CHA2DS2VS score elements

A

C- congenital
H- hypertension (or treated)
A2- age
D- diabetes
S2- prior stroke, TIA or thromboembolism
V- vascular disease (including ischameic heart disease, peripheral artery disease
S- sex (female)

176
Q

CHA2DS2-VASc

A

C- 1
H-1
A >75 (2 points)
A 65-74 (1 points)
D (1 points)
S2- (2 points)
V (1 points)
S (1 points)

177
Q

What to do with the CHADVASC score?

A

0 - no treatment needed
1- males consider anticoagulant, females don’t need
2- offer anticoagulants

178
Q

HASBLED score vs ORBIT score

A

Orbit score is encouraged to be used by NICE rather than HASBLED score

179
Q

ORBIT score

A

0-2, low risk which is 2.4 bleeds per 100 pt per year

3, medium, 4.7

4-7, high, 8.1

180
Q

HASBLED score

A

Haemoglobin ‘
Age >74
Bleeding (GI bleed, intracranial bleed, haemorrhagic stroke)
Renal impairment (GFR <60 ml/min)
Treatment with antiplatelet agent

181
Q

Points in HAS-BLED

A

H-2
A-1
S
B- 2
L
E- 1
D- 1

182
Q

Doacs to reduce AF stroke risk

A

apixaban
dabigatran
edoxaban

Warfarin is recommended as second line if DOAC contradicted

Do not prescribe aspirin

183
Q

When cardioversion in AF

A

electrical cardioversion as an emergency if the patient is haemodynamically unstable
electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred.

184
Q

How ECG and electrocardioversion carried out in AF

A

Electrical cardioversion is synchronised to the R wave to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when ventricular fibrillation can be induced.

185
Q

AF onset <48 hours

A

If AF less than 48 hours, patient should be heparanised

Patients with risk of ischaemic stroke should be put on lifelong oral anticoagulation

Otherwise cardiovert the patient

186
Q

Cardioversion in AF patients onset <48 hours

A

electrical - ‘DC cardioversion’
pharmacology - amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease

187
Q

Onset > 48 hours of AF

A

AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion.

An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately.

188
Q

What if there is high risk of AF failure in onset >48 hours

A

If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion

189
Q

Following electrocardioversion in AF patients

A
  • anticoagulants the patient for at least 4 weeks
190
Q

Features of AF

A

AF may present with palpitations, dyspnoea, dizziness/syncope
many cases are asymptomatic and are found as an incidental finding
the pulse is irregularly irregular

191
Q

Diagnosis of AF

A

ECG: absent P waves
a 24 hour ECG or event recorder is useful where paroxysmal atrial fibrillation is suspected
echocardiography is not required in all cases

192
Q

What are the two key elements of managing AF

A
  1. reducing the risk of stroke
  2. controlling the heart rate
193
Q

Agents used for effective pharmacological cardioversion

A

-amiodarone
-flecainide (if no structural heart disease)
-others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone

194
Q

Less effective agents for pharmacological cardioversion

A

beta-blockers (including sotalol)
calcium channel blockers
digoxin
disopyramide
procainamide

195
Q

Management of stroke

A

F ollowing a stroke or TIA it is obviously important to exclude a haemorrhage before starting any anticoagulation or antiplatelet therapy
for longer-term stroke prevention, NICE Clinical Knowledge Summaries recommend warfarin or a direct thrombin or factor Xa inhibitor
the timing of when to start depends on whether it is a TIA or stroke
following a TIA, anticoagulation for AF should start immediately once imaging has excluded haemorrhage
in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. Antiplatelet therapy should be given in the intervening period. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed

196
Q

Atrial flutter

A
  • sawtooth appearance
  • rate often 300/ min
  • ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min
  • flutter waves will be visible following carotid sinus massage or adenosine
197
Q

Management of Atrial flutter

A

is similar to that of atrial fibrillation although medication may be less effective
atrial flutter is more sensitive to cardioversion however so lower energy levels may be used
radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

198
Q

Broad complex tactic

A

AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms

199
Q

Peri-arrest: bradycardia

A
  1. identifying the presence of signs indicating haemodynamic compromise - ‘adverse signs’
  2. identifying the potential risk of asystole
200
Q

Adverse signs of bradycardia

A

shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure

201
Q

What is the first line treatment of bradycardia (adverse signs have been observed)

A

Atropine (500mg IV)

202
Q

What to do if unsatisfactory response to first line intervention of bradycardia

A

atropine, up to a maximum of 3mg
transcutaneous pacing
isoprenaline/adrenaline infusion titrated to response

If no response, get help with transvenous pacing

203
Q

Risk factors for asystole

A

complete heart block with broad complex QRS
recent asystole
Mobitz type II AV block
ventricular pause > 3 seconds

204
Q

Peri-arrest tachycardia adverse signs

A

shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
syncope
myocardial ischaemia
heart failure

205
Q

Management of tachcardia:

A

adverse signs are present then synchronised DC shocks should be given.

Up to three shocks can be given, then seek expert help after this

206
Q

Broad- complex tachycardia

A

assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)
loading dose of amiodarone followed by 24 hour infusion

207
Q

Irregular Broad- complex tachycardia

A

seek expert help. Possibilities include:
atrial fibrillation with bundle branch block - the most likely cause in a stable patient
atrial fibrillation with ventricular pre-excitation
torsade de pointes

208
Q

Regular narrow-complex tachycardia

A

vagal manoeuvres followed by IV adenosine
if the above is unsuccessful consider a diagnosis of atrial flutter and control rate (e.g. beta-blocker

209
Q

Irregular narrow complex tachycardia

A

probable atrial fibrillation
if onset < 48 hr consider electrical or chemical cardioversion
rate control: beta-blockers are usually first-line unless there is a contraindication

210
Q

Torsades de pointes

A
  • twisting of the points
    -forms of polymorphic ventricular tachycardia associated with long QT syndrome
  • can cause VF
  • can lead to sudden death
211
Q

Causes of Long QT-syndrome

A

congenital
Jervell-Lange-Nielsen syndrome
Romano-Ward syndrome
antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants
antipsychotics
chloroquine
terfenadine
erythromycin
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
myocarditis
hypothermia
subarachnoid haemorrhage

212
Q

What is the management of Torsades de pointes?

A

IV magnesium sulphate

213
Q

Ventricular tachycardia

A

Ventricular tachycardia (VT) is broad-complex tachycardia originating from a ventricular ectopic focus.

It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.

214
Q

What are the two main types of VT?

A
  • monomorphic VT
  • Polymorphic VT
215
Q

Causes of Monomorphic VT

A

most commonly caused by myocardial infarction

216
Q

Polymorphic VT causes

A

subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval. The causes of a long QT interva

217
Q

Congenital causes of prolonged QT interval

A

Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness)

218
Q

Drugs which cause long QT

A

amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, fluoxetine
chloroquine
terfenadine
erythromycin

219
Q

“Other” causes of prolonged QT intercal

A

electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage

220
Q

Management of VT

A
  • if any adverse signs (systolic BP < 90 mmHg, chest pain, heart failure), then IMMEDIATE CARDIOVERSION

-If absence of symptoms, then consider antiarrhythmics

  • if this fails, then SYNCHRONISED DC shock
221
Q

Drug tx of VT

A

amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide

222
Q

Vermapil and VT

A

CONTRADICTED

223
Q

What to do if drug therapy fails in VT

A

electrophysiological study (EPS)
implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function

224
Q

Causes of metabolic acidosis

A

vomiting / aspiration (e.g. peptic ulcer leading to pyloric stenos, nasogastric suction)
diuretics
liquorice, carbenoxolone
hypokalaemia
primary hyperaldosteronism
Cushing’s syndrome
Bartter’s syndrome
congenital adrenal hyperplasia

LOSS OF H+ OR GAIN OR BICARD

225
Q

Causes of respiratory acidosis

A

COPD
decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema
sedative drugs: benzodiazepines, opiate overdose

226
Q

Causes of reps alkalosis

A

anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy

227
Q

Normal anion gap metabolic acidosis causes

A

gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease

228
Q

Rasied anion gap metabolic acidosis causes

A

lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol

229
Q

Anion gap calculation

A

(sodium + potassium) - (bicarbonate + chloride)

A normal anion gap is 8-14 mmol/L

230
Q

Causes of normal anion gap or hyperchloraemic metabolic acidosis

A

gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease

231
Q

ROME

A

Respiratory = Opposite
low pH + high PaCO2 i.e. acidosis, or
high pH + low PaCO2 i.e. alkalosis

Metabolic = Equal
low pH + low bicarbonate i.e. acidosis, or
high pH + high bicarbonate i.e. akalosis

232
Q

Metabolic component of ABG

A

Metabolic component: What is the bicarbonate level/base excess?

bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l) suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis)
bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l) suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)

233
Q

Metabolic acidosis secondary to high lactate subcategories

A

lactic acidosis type A: sepsis, shock, hypoxia, burns
lactic acidosis type B: metformin

234
Q

Mechanism of metabolic alkalosis

A

activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels
in hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality

235
Q

Salicylate overdose ABG

A

Mixed respiratory alkalosis and metabolic acidosis

236
Q

Hypomagnesaemia causes

A

drugs
diuretics
proton pump inhibitors
total parenteral nutrition
diarrhoea
may occur with acute or chronic diarrhoea
alcohol
hypokalaemia
hypercalcaemia
e.g. secondary to hyperparathyroidism
calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle
metabolic disorders
Gitleman’s and Bartter’s

237
Q

Features of hypomagnesaemia

A
  • similar to hypocalaemia

paraesthesia
tetany
seizures
arrhythmias
decreased PTH secretion → hypocalcaemia
ECG features similar to those of hypokalaemia
exacerbates digoxin toxicity

238
Q

Treatment of hypomagnesaemia (<0.4mmol/L)

A

<0.4 mmol/L or tetany, arrhythmias, or seizures
intravenous magnesium replacement is commonly given.
an example regime would be 40 mmol of magnesium sulphate over 24 hours

239
Q

Treatment of >0.4 mol/L

A

oral magnesium salts (10-20 mmol orally per day in divided doses)
diarrhoea can occur with oral magnesium salts

240
Q

Epistaxis

A

Nose bleeds
Split into anterior and posterior bleeds

Kiesselbach’s plexus (anterior and visible bleed)

Posterior node bleeds more common in elderly and higher risk of apritation and airway compromise

241
Q

Causes of epistaxis

A

most cases of epistaxis tend to be benign and self-limiting. Exacerbation factors include:
nose picking
nose blowing
trauma to the nose
insertion of foreign bodies
bleeding disorders
immune thrombocytopenia
Waldenstrom’s macroglobulinaemia
juvenile angiofibroma
benign tumour that is highly vascularised
seen in adolescent males
cocaine use
the nasal septum may look abraded or atrophied, inquire about drug use. This is because inhaled cocaine
cocaine is a powerful vasoconstrictor and repeated use may result in obliteration of the septum.
hereditary haemorrhagic telangiectasia
granulomatosis with polyangiitis

242
Q

First aid management of epistaxis

A

Asking the patient to sit with their torso forward and their mouth open
avoid lying down unless they feel faint
his decreases blood flow to the nasopharynx and allows the patient to spit out any blood in their mouth
it also reduces the risk of aspirating blood
Pinch the cartilaginous (soft) area of the nose firmly
this should be done for at least 20 minutes
also ask the patient to breathe through their mouth.

243
Q

Epistaxis when first aid measurements are successful

A

consider using a topical antiseptic such as Naseptin (chlorhexidine and neomycin) to reduce crusting and the risk of vestibulitis
cautions to this include patients that have peanut, soy or neomycin allergies
Mupirocin is a viable alternative
admission and follow up care may be considered in patients under if
a comorbidity (e.g. coronary artery disease, or severe hypertension) is present, an underlying cause is suspected
they are aged under 2 years (as underlying causes such as haemophilia or leukaemia are more likely in this age group)
self-care advice involves reducing the risk of re-bleeding
patients should be informed that blowing or picking the nose, heavy lifting, exercise, lying flat, drinking alcohol or hot drinks should be avoided

244
Q

If bleeding does not stop after 10-15 minuted of continuous pressure

A

cautery should be used initially if the source of the bleed is visible and cautery is tolerated
it is not so well-tolerated in younger children!
ask the patient to blow their nose in order to remove any clots. Be wary that bleeding may resume.
use a topical local anaesthetic spray (e.g. Co-phenylcaine) and wait 3-4 minutes for it to take effect
identify the bleeding point and apply the silver nitrate stick for 3-10 seconds until it becomes grey-white. Avoid touching areas which do not require treatment, and only cauterise one side of the septum as there is a risk of perforation.
dab the area clean with a cotton bud and apply Naseptin or Muciprocin
packing may be used if cautery is not viable or the bleeding point cannot be visualised
anaesthetise with topical local anaesthetic spray (e.g. Co-phenylcaine) and wait for 3-4 minutes
pack the patient’s nose while they are sitting with their head forward, following the manufacturer’s instructions
pressure on the cartilage around the nostril can cause cosmetic changes and this should be reviewed after inserting the pack.
examine the patient’s mouth and throat for any continuing bleeding, and consider packing the other nostril as this increases pressure on the septum and offending vessel.
patients should be admitted to hospital for observation and review, and to ENT if available

245
Q

When should patients be referred to ED with epistaxis

A

haemodynamically unstable or compromised should be admitted to the emergency department

246
Q

What occurs at ED when patients presents with epistaxis?

A

control bleeding with first aid measures in the interim
patients with a bleed from an unknown or posterior source (i.e. the bleeding site cannot be located on speculum, bleeding from both nostrils or profuse) should be admitted to hospital.

247
Q

Epistaxis emergency treatment?

A

sphenopalatine ligation in theatre

248
Q

Carbon monoxide poisoning

A
  • CO positioning causes left shift of the oxygen dissociation curve
    Causes tissue hypoxia
    Every year there are approximately 50 deaths due to CO poisoning
249
Q

Pathophysiology of CO poisoning

A

carbon monoxide binds readily to haemoglobin, forming carboxyhaemoglobin → reduced oxygen-carrying capacity
in carbon monoxide poisoning the oxygen saturation of haemoglobin decreases leading to an early plateau in the oxygen dissociation curve

250
Q

Features of CO poisoning?

A

headache: 90% of cases
nausea and vomiting: 50%
vertigo: 50%
confusion: 30%
subjective weakness: 20%
severe toxicity: ‘pink’ skin and mucosae, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death

251
Q

Investigations of CO poisoning?

A

pulse oximetry may be falsely high due to similarities between oxyhaemoglobin and carboxyhaemoglobin
therefore a venous or arterial blood gas should be taken
typical carboxyhaemoglobin levels
< 3% non-smokers
< 10% smokers
10 - 30% symptomatic: headache, vomiting
> 30% severe toxicity
an ECG is a useful supplementary investgation to look for cardiac ischaemia

252
Q

Management of CO poisoning?

A
  • assess in ED
    -100% high flow 02 non-rebreather mask
    -Hyperbaric oxygen
253
Q

Features of lead poisoning

A

abdominal pain
peripheral neuropathy (mainly motor)
neuropsychiatric features
fatigue
constipation
blue lines on gum margin (only 20% of adult patients, very rare in children)

Acute intermittent porphyria
Defective ferrochelatase and ALA dehydrates function

254
Q

Investigations of Lead poisoning

A

the blood lead level is usually used for diagnosis. Levels greater than 10 mcg/dl are considered significant
full blood count: microcytic anaemia. Blood film shows red cell abnormalities including basophilic stippling and clover-leaf morphology
raised serum and urine levels of delta aminolaevulinic acid may be seen making it sometimes difficult to differentiate from acute intermittent porphyria
urinary coproporphyrin is also increased (urinary porphobilinogen and uroporphyrin levels are normal to slightly increased)
in children, lead can accumulate in the metaphysis of the bones although x-rays are not part of the standard work-up

255
Q

Management of lead poisoning

A

various chelating agents are currently used:
dimercaptosuccinic acid (DMSA)
D-penicillamine
EDTA
dimercaprol

256
Q

Organophosphate insecticide poisoning

A

inhibition of acetylcholinesterase leading to upregulation of nicotinic and muscarinic cholinergic neurotransmission. In warfare, sarin gas is a highly toxic synthetic organophosphorus compound that has similar effects.

257
Q

Features of organophosphate insecticide poisoning
SLUD

A

accumulation of acetylcholine (mnemonic = SLUD)

Salivation
Lacrimation
Urination
Defecation/diarrhoea
cardiovascular: hypotension, bradycardia
also: small pupils, muscle fasciculation

258
Q

Management of Organophosphate insecticide poisoning

A

atropine
the role of pralidoxime is still unclear - meta-analyses to date have failed to show any clear benefit

259
Q

Paracetamol overdose

A

activated charcoal if ingested < 1 hour ago
N-acetylcysteine (NAC)
liver transplantation

260
Q

Salicylate management

A

urinary alkalinization with IV bicarbonate
haemodialysis

261
Q

Opioid overdose

A

Naloxone

262
Q

Benzodiazepines overdose

A

Flumazenil
The majority of overdoses are managed with supportive care only due to the risk of seizures with flumazenil. It is generally only used with severe or iatrogenic overdoses.

263
Q

Tricyclic antidepressant management

A

IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity
arrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias
dialysis is ineffective in removing tricyclics

264
Q

Lithium management

A

mild-moderate toxicity may respond to volume resuscitation with normal saline
haemodialysis may be needed in severe toxicity
sodium bicarbonate is sometimes used but there is limited evidence to support this. By increasing the alkalinity of the urine it promotes lithium excretion

265
Q

Warfarin management

A

Vitamin K, prothrombin complex

266
Q

Heparin management

A

Vitamin K
Prothrombin complex

267
Q

Beta blocker overdose

A

if bradycardic then atropine
in resistant cases glucagon may be used

268
Q

Ethylene glycol overdose

A

fomepizole
Can use ethanol as well

269
Q

Methanol poisoning

A

fomepizole or ethanol
haemodialysis

270
Q

Organophosphate insecticide management

A

atropine
the role of pralidoxime is still unclear - meta-analyses to date have failed to show any clear benefit

271
Q

Digoxin overdose management

A

Digoxin-specific antibody fragments

272
Q

Iron overdose management

A

Desferrioxamine, a chelating agent

273
Q

Lead overdose

A

Dimercaprol, calcium edentate

274
Q

Cyanide overdose management

A

Hydroxocobalamin; also combination of amyl nitrite, sodium nitrite, and sodium thiosulfate

275
Q

Synthetic cannaboid toxicity features

A

CNS: agitation, tremor, anxiety, confusion, somnolence, syncope, hallucinations, changes in perception, acute psychosis, nystagmus, convulsions and coma.

Cardiac: tachycardia, hypertension, chest pain, palpitations, ECG changes.

Renal: acute kidney injury.

Muscular: hypertonia, myoclonus, muscle jerking and myalgia.

Other: cold extremities, dry mouth, dyspnoea, mydriasis, vomiting and hypokalaemia

276
Q

Cocaine toxicity

A

Blocks the uptake of dopamine, noradrenaline and serotonin

277
Q

Adverse cariovascular effects of cocaine

A

coronary artery spasm → myocardial ischaemia/infarction
both tachycardia and bradycardia may occur
hypertension
QRS widening and QT prolongation
aortic dissection

278
Q

Cocaine neurological features

A

seizures
mydriasis
hypertonia
hyperreflexia

279
Q

Cocaine psychiatric effects

A

agitation
psychosis
hallucinations

280
Q

Other effects of cocaine

A

ischaemic colitis is recognised in patients following cocaine ingestion. This should be considered if patients complain of abdominal pain or rectal bleeding
hyperthermia
metabolic acidosis
rhabdomyolysis

281
Q

Management of cocaine toxicity

A
  • benzodiazepines

-if with chest pain add GTN

hypertension: benzodiazepines + sodium nitroprusside

282
Q

MDMA poisioning

A

Ecstacy

283
Q

Clinical features of Ecstasy poisoning

A

neurological: agitation, anxiety, confusion, ataxia
cardiovascular: tachycardia, hypertension
hyponatraemia
this may result from either syndrome of inappropriate ADH secretion or excessive water consumption whilst taking MDMA
hyperthermia
rhabdomyolysis

284
Q

Management of ecstasy poisoning

A

supportive
dantrolene may be used for hyperthermia if simple measures fail

285
Q

Exacerbation of chronic bronchitis

A

Amoxicillin
Tetracycline
Clarithromycin

286
Q

Uncomplicated community-acquired pneumonia

A

Amoxicillin (Doxycycline or clarithromycin in penicillin allergic, add flucloxacillin if staphylococci suspected e.g. In influenza)

287
Q

Pneumonia possibly caused by atypical pathogens

A

Clarithromycin

288
Q

Hospital acquired pneumonia

A

Within 5 days of admission: co-amoxiclav or cefuroxime

More than 5 days after admission: piperacillin with tazobactam OR a broad-spectrum cephalosporin (e.g. ceftazidime) OR a quinolone (e.g. ciprofloxacin)

289
Q

Lower urinary tract infection

A

Nitrofurantoin or trimethoprim

Alternative amoxicillin or cephalosporin

290
Q

Acute pyelonephritis

A

Broad-spectrum cephalosporin or quinolone

291
Q

Acute prostatitis

A

Quinolone or trimethoprim

292
Q

Impetigo

A

Topical hydrogen peroxide, oral flucloxacillin or erythromycin if widespread

293
Q

Cellulitis

A

Flucloxacillin (clarithromycin, erythromycin or doxycycline if penicillin-allergic)

294
Q

Cellulitis near eyes or nose

A

Co-amoxiclav (clarithromycin, + metronidazole if penicillin-allergic)

295
Q

Erysipelas

A

Flucloxacillin* (clarithromycin, erythromycin or doxycycline if penicillin-allergic)

296
Q

Animal or human bite

A

Co-amoxiclav (doxycycline + metronidazole if penicillin-allergic)

297
Q

Mastitis during breast-feeding

A

Flucloxacillin

298
Q

Throat infection

A

Phenoxymethylpenicillin (erythromycin alone if penicillin-allergic)

299
Q

Sinusitis

A

Phenoxymethylpenicillin

300
Q

Otitis media

A

Amoxicillin (erythromycin if penicillin-allergic)

301
Q

Otitis external

A

Flucloxacillin (erythromycin if penicillin-allergic)

302
Q

Periapical or periodontal abscess

A

Amoxicillin

303
Q

Gingivitis: acute necrotising ulcerative

A

Metronidazole

304
Q

Gonorrhoea

A

Intramuscular ceftriaxone

305
Q

Chlamydia

A

Doxycycline or azithromycin

306
Q

Pelvic inflammatory disease

A

Oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline and oral metronidazole

307
Q

Syphilis

A

Benzathine benzylpenicillin
Doxycycline
Erythromycin

308
Q

Bacterial vaginosis

A

Oral or topical metronidazole
Topical clindamycin

309
Q

Clostridioides difficile

A

First episode: oral vancomycin
Second or subsequent: oral fidaxomicin

310
Q

Campylobacter enteritis

A

Clarithromycin

311
Q

Salmonella (non-typhoid

A

Ciprofloxacin

312
Q

Shigellosis

A

Ciprofloxacin

313
Q

Acute upper GI bleed

A
  • common, usually caused by oesophageal varicose or peptic ulcer disease
314
Q

Clinical features of GI bleeds

A
  • haematemesis

the most common presenting feature
often bright red but may sometimes be described as ‘coffee gound’
melena
the passage of altered blood per rectum
typically black and ‘tarry’
a raised urea may be seen due to the ‘protein meal’ of the blood
features associated with a particular diagnosis e,g,
oesophageal varices: stigmata of chronic liver disease
peptic ulcer disease: abdominal pain

315
Q

Oesophageal varicose

A

Usually a large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.

316
Q

Oesophagitis

A

Small volume of fresh blood, often streaking vomit. Malena rare. Often ceases spontaneously. Usually history of antecedent GORD type symptoms.

317
Q

Oesophageal Cancer

A

Usually small volume of blood, except as a preterminal event with erosion of major vessels. Often associated symptoms of dysphagia and constitutional symptoms such as weight loss. May be recurrent until malignancy managed.

318
Q

Mallory Weiss tear

A

Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting. Malena rare. Usually ceases spontaneously.

319
Q

Gastric ulcer

A

Small low volume bleeds are more common so would tend to present as iron deficiency anaemia. Erosion into a significant vessel may produce considerable haemorrhage and haematemesis.

320
Q

Gastric cancer

A

Frank haematamesis or altered blood mixed into vomit
Usual prodromal features of dyspepsia and constitutional bleeding

Amount of bleeding variable but erosion of major vessel may produce considerable haemorrhage.

321
Q

Dieulafoy lesion

A

Often no prodromal features prior to haematemesis and melena, but this arteriovenous malformation may produce quite a considerable haemorrhage and may be difficult to detect endoscopically

322
Q

Diffuse erosive gastritis

A

Usually haematemesis and epigastric discomfort. Usually there is an underlying cause such as recent NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise

323
Q

Duodenal ulcer

A

These are usually posteriorly sited and may erode the gastroduodenal artery. However, ulcers at any site in the duodenum may present with haematemesis, melena and epigastric discomfort.

The pain of a duodenal ulcer is slightly different to that of gastric ulcers and often occurs several hours after eating. Periampullary tumours may bleed but these are rare.

324
Q

Aorto-enteric fistula

A

In patients with previous abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but important cause of major haemorrhage associated with high mortality.

325
Q

Managment of GI bleeds

A

NICE guidelines 2012

the Glasgow-Blatchford score at first assessment
helps clinicians decide whether patient patients can be managed as outpatients or not
the Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality
includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage

326
Q

Blactchford score 0

A

Patients may be considered for an early discharge

327
Q

Resus for patients with bleeds

A

ABC, wide-bore intravenous access * 2
platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre
fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal
prothrombin complex concentrate to patients who are taking warfarin and actively bleeding

328
Q

Endoscopy in upper GI bleeds

A

should be offered immediately after resuscitation in patients with a severe bleed
all patients should have endoscopy within 24 hours

329
Q

Managment of non-variceal bleeds

A

NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected non-variceal upper gastrointestinal bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy
if further bleeding then options include repeat endoscopy, interventional radiology and surgery

330
Q

Managment of variceal bleeds

A

terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures

331
Q

Acute treatment of variceal haemorrhage

A

-ABC response then endoscopy
- may need blood transfusion

correct clotting: FFP, vitamin K, platelet transfusions may be required

Vasoactive treatment: telipressin
- Octreotide can be used although evidence shows telepressin is better

Prophylactic IV antibiotics

332
Q

Transjugular Intrahepatic porotsystemic shunt

A

Used if original methods of managment fail

connects the hepatic vein to the portal vein
exacerbation of hepatic encephalopathy is a common complication

333
Q

Variceal haemorrhage prophylaxis

A
  • propanalol
  • Endoscopic variceal band ligation (EVL)
    -TIPSS used if above doesn’t work
334
Q

3rd nerve compression secondary to tentorial herniation

A
  • unilateral dilated pupil
  • sluggish or fixed to light response
335
Q

Poor CNS perfusion or Bilateral 3rd Nerve palsy

A

Pupils bilaterally dilated
Light response sluggish or fixed

336
Q

Optic nerve injury

A

Unilateral dilated or equally dilated
Cross reactive (Marcus Gunn light response)

337
Q

Opiates
Pontine lesion
Metabolic encephalopathy

A

Bilaterally constricted pupil
Light response may be difficult to assess

338
Q

Sympathetic pathway disruption

A

Fig

339
Q

Mechanism of alcohol withdrawal

A

chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

340
Q

Features of alcohol withdrawal

A

-6-12 hours: tremor, sweating, tachycardia, anxiety

-peak incidence of seizures at 36 hours

-peak incidence of delirium tremens is at 48-72 hours: coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia

341
Q

Managment

A

complex delirium tremens, seizures, blackouts) should be admitted to hospital for monitoring until withdrawals stabilised

first-line: long-acting benzodiazepines e.g. chlordiazepoxide or diazepam. Lorazepam may be preferable in patients with hepatic failure.

Typically given as part of a reducing dose protocol
carbamazepine also effective in treatment of alcohol withdrawal
phenytoin is said not to be as effective in the treatment of alcohol withdrawal seizures

342
Q

Basics of testicular torsion

A

-twist of the spermatic cord resulting in testicular ischaemia and necrosis.

-most common in males aged between 10 and 30 (peak incidence 13-15 years)

343
Q

Features of testicular torsion

A

-pain is usually severe and of sudden onset

-the pain may be referred to the lower abdomen
nausea and vomiting may be present

-on examination, there is usually a swollen, tender testis retracted upwards.
-The skin may be reddened
cremasteric reflex is lost
elevation of the testis does not ease the pain (Prehn’s sign)

344
Q

Managment of testicular torsion

A

treatment is with urgent surgical exploration
if a torted testis is identified then both testis should be fixed as the condition of bell clapper testis is often bilateral.

345
Q

Non-haemolytic febrile reaction

A

Thought to be caused by antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cell during storage

346
Q

Features of Non-haemolytic febrile reactions

A

Fever, chills

Red cell transfusion (1-2%)
Platelet transfusion (10-30%)

347
Q

Managment of non-haemolytic febrile reactions

A

Slow or stop the transfusion

Paracetamol

Monitor

348
Q

blood minor allergic reactions

A

Thought to be caused by foreign plasma proteins

349
Q

Features of blood minor allergic reactions

A

Thought to be caused by foreign plasma proteins Pruritus, urticaria

350
Q

Managment of minor allergic reaction blood

A

Temporarily stop the transfusion

Antihistamine

Monitor

351
Q

Blood producrs anaphylaxis

A

Can be caused by patients with IgA deficiency who have anti-IgA antibodies

352
Q

features of blood product anaphylaxis

A

Hypotension, dyspnoea, wheezing, angioedema.

353
Q

Managment of blood anaphylaxis

A

Stop the transfusion

IM adrenaline

ABC support
oxygen
fluids

354
Q

Acute haemolytic reaction

A

ABO-incompatible blood e.g. secondary to human error

355
Q

acute haemolytic reaction features

A

Fever, abdominal pain, hypotension

356
Q

Managment of acute haemolytic reaction

A

Stop transfusion

Confirm diagnosis
check the identity of patient/name on blood product
send blood for direct Coombs test, repeat typing and cross-matching

Supportive care
fluid resuscitation

357
Q

Transfusion-associated circulatory overload (TACO)

A

xcessive rate of transfusion, pre-existing heart failure

358
Q

Transfusion-associated circulatory overload (TACO) features

A

Pulmonary oedema, hypertension

359
Q

Transfusion-associated circulatory overload (TACO) managment

A

Slow or stop transfusion

Consider intravenous loop diuretic (e.g. furosemide) and oxygen

360
Q

Transfusion-related acute lung injury (TRALI)

A

Non-cardiogenic pulmonary oedema thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood

361
Q

Transfusion-related acute lung injury (TRALI) features

A

Hypoxia, pulmonary infiltrates on chest x-ray, fever, hypotension

362
Q

Transfusion-related acute lung injury (TRALI) managment

A

Stop the transfusion

Oxygen and supportive care

UKMLA Prep (30 decks)

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