Patho Flashcards

1
Q

Why does a croup patient present with stridor?

A

The virus causes inflammation in the larynx & trachea. The loud sound of stridor is made by the air passing through the narrowed airway on inspiration.

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2
Q

As per the CPG what are the S&S associated with mild croup?

A

Behaviour: Normal
Stridor: None or only when active
RR: Normal
Accessory muscle use: None
Sp02: >96%

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3
Q

As per the CPG what are the S&S associated with moderate croup?

A

Behaviour: Intermittent mild agitation
Stridor: Intermittent at rest
RR: Increased
Accessory muscle use: Moderate chest wall retraction
Sp02: >96%

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4
Q

As per the CPG what are the S&S associated with severe croup?

A

Behaviour: Increasing agitation, drowsiness
Stridor: Persistent at rest or decreasing (late sign)
RR: Marked increase or decreased (late sign)
Accessory muscle use: Marked chest wall retraction
Sp02: <96%

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5
Q

What pharmacological effect of adrenaline is desired when treating a paed with Croup?

A

Vasocontriction which reduce bronchial and tracheal epithelial vascular permeability

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6
Q

What is the management of severe croup?

A

Adrenaline 5mg nebs 5 minutely until improvement, dexamethasone 600mcg/kg orally once & transport.

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7
Q

What are the age ranges most common to present with Croup?

A

3 months to 3 years.

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8
Q

Define croup?

A

A viral illness characterised by inflammation of the larynx & trachea.

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9
Q

What pharmacological effect does dexamethasone have on these patients?

A

Corticosteroids are beneficial due to their anti-inflammatory action which decreases both laryngeal and mucosal oedema.

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10
Q

What are some differential diagnosis for Croup?

A

Epiglottitis, Anaphylaxis & Foreign body airway obstruction.

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11
Q

Differentiate between croup and epiglottitis with regards to infection type, location & other S&S?

A

Type: Croup = Viral. Epiglottitis = Bacterial
Location: Croup = Larynx & trachea. Epiglottitis = Epiglottis
S&S: Croup = Barking cough
Epiglottitis= Drooling, preference to sit, dysphagia (difficulty swallowing)

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12
Q

How does hyperglycaemia cause dehydration & how is this managed prehospitally?

A

Hyperglycaemia alters the concentration gradient between intracellular & extracellular fluid which causes the fluid to shift from cells to interstitial space.
Hyperglycaemia also causes osmotic diuresis (polyuria & glycosuria) which causes absolute fluid loss & therefore dehydration.
Normal saline 20ml/kg (if <adequate perfusion) is administered to replace lost fluid until glucose levels can be normalised at hospital.

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13
Q

What causes elevated Ketone levels in blood?

A

The lack of glucose brought into the cell by insulin triggers the metabolism of fatty acids for energy which produces ketones as a by-product.

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14
Q

What are 2 considerations that would cause a hyperglycaemic patient to recieve a reduces IV saline dose?

A

Elderly & impaired renal or cardiac function.

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15
Q

Define HHS & list 3 characteristics?

A

Hyperosmolar Hyperglycaemic State (HHS) occurs in people with type 2 diabetes who experience very high blood glucose levels (often over 40mmol/l). It can develop over a course of weeks through a combination of illness (e.g.infection) and dehydration.
Characteristics include: typically older people, BSL >30mmol/L & usually don’t present with clinical features of DKA (kussmaul respirations & elevated ketones)

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16
Q

Define DKA & list 3 characteristics?

A

Diabetic ketoacidosis, also known as DKA, is when there is a severe lack of insulin in the body which causes metabolism of fatty acids, releasing ketones as a byproduct. The elevation of ketones causes an acidotic state.
Characteristics: Kussmauls breathing, dehydration, polydipsia, tachypnoea, confusion.

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17
Q

At hospital pt has high ketones & develops Kussmaul respirations- why is this?

A

Metabolic acidosis occurs secondary to the break down of triglycerides & release of fatty acids. The respiratory system compensates by increasing Vt & RR (MV) to release more C02 which is an acid in an attempt to return the pH to a normal range.

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18
Q

The patient you attended has her own insulin available. If she was more alert would you advise her to self administer additional insulin prior to transport.

A

No, patients should not be encouraged to administer additional oses of insulin prior to transport.

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19
Q

Which medication can make patients unresponsive to adrenaline and what action would you take?

A

Metoprolol. Administer Glucagon 1mg (IV/IM). Repeat once after 5 mins if required. Glucagon admin should not delay further adrenaline administration.

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20
Q

What are some potential mimics of hypovolaemia?

A

Significant pain (splinting), TPT, Environmental exposure (heat/cold)

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21
Q

A pt with a suspected pelvic # presents with BP 65/35mmHg- what is your management?

A

Normal saline 250ml IV- repeat 250ml bolus as required to 2L max.
Titrate to aim >SBP70mmHg. Consider AAV & blood products. Consult for further management.

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22
Q

Explain the principle permissive hypotension.

A

Permissive hypotension refers to managing trauma patients by restricting the amount of fluid resuscitation administered while maintaining blood pressure in the lower than normal range if there is still active bleeding. If too much fluid is given it will increase intravascular volume & therefore BP which will contribute to worsening bleeding.

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23
Q

List 2 general principles of good prehospital fracture management.

A

1) Control external haemhorrage
2) Apply good splinting practices
3) Resolve neurological or vascular compromise where possible
4) Use judicious analgesia

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24
Q

Explain why large doses of normal saline in haemhorragic hypovolaemia can be detrimental.

A

NS doesn’t contain haemoglobin or clotting factors.
Administration can lead to haemodilution and the triad of death
1) Acidosis
2) Coagulopathy
3) Hypothermia

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25
Q

What is the appropriate splinting management of a patient with both a suspected pelvic # and middle third femur fracture?

A

Pelvic splinting and the CT-6 traction splint can be applied however pelvic splint should be prioritised.

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26
Q

What does PILSDUCT stand for?

A

Pain, irregularity, loss of function, swelling, deformity, unnatural movement, crepitus & tenderness.

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27
Q

What does SCPMCT used for & what does it stand for?

A

Sensation, pulse, cap refill, movement, colour, temperature.

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28
Q

What is an absence seizure?

A

A sudden lapse in awareness and responsiveness that look like brief staring spells or daydreaming

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29
Q

What is a tonic clonic seizure?

A

The body stiffens (tonic) and then the limbs begin to jerk rhythmically (the clonic phase)

30
Q

What is a myoclonic seizure?

A

Sudden single jerks of a muscle or a group of muscles that may last no more than a second or two

31
Q

What is a tonic seizure?

A

Can occur when a person is asleep or awake and involves a brief stiffening of the body, arms of legs.

32
Q

What is an atonic seizure?

A

brief seizures that cause a sudden loss of muscle tone and the person often falls to the ground or will have a sudden head nod if sitting

33
Q

What is a clonic seizure?

A

Although uncommon, they cause jerking in various parts of the body

34
Q

When do you reduce the dose of IM midazolam in the setting of seizures & why?

A

Chronic renal failure, elderly & frail
Midazolam is excreted by the kidneys, in patients with severe renal impairment midazolam can cause more pronounced and prolonged sedation (resp & CVS depression) due to decreased excretion

35
Q

When would you suspect subtle SE in patients post seizure?

A

If the TC seizure activity ceases but the patient presents with ongoing coma and no improvement in conscious state (with or without subtle convulsive movements).

36
Q

Pt 37/40 gestation with 6min TC seizure activity- would midazolam be appropriate?

A

Yes. Although it crosses the placenta and may cause adverse effects to the baby, it is still required as GCSE is life-threatening to both baby and mother.

37
Q

Define COPD

A

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. It is characterised by breathing difficulty, cough, mucous production and wheezing.
COPD can be classified as one or all of the three following conditions :
1) Emphysema
2) Chronic bronchitis
3) Refractory Asthma/chronic asthma

38
Q

As per 02 therapy CPG, what is the optimal Sp02 for COPD patients?

A

Chronic hypoxaemia: Sp02 88-92%

39
Q

Why do we aim Sp02 88-92% in pt with chronic hypoxaemia eg COPD patients?

A

This range provides adequate tissue oxygenation while avoiding the complication of hyperoxic hypercapnea. By providing too much oxygen in COPD patients you remove the anoxic (02 deprived) stimulus (hypoxic drive) thus the patient will decrease MV, initially.

40
Q

Patients with neurogenic shock may present bradycardic. Explain what leads to this bradycardia?

A

Neurogenic shock usually refers to the loss of sympathetic nervous system control over the cardiovascular system. Without sympathetic innervation, the parasympathetic innervation of the heart (vagus nerve) is left without antagonism resulting in bradycardia, vasodilation & diminished contractility.

41
Q

Describe why patients presenting with isolated SCI receives a lower dose of NS IVT?

A

An isolated spinal cord injury creates a relative hypovolaemia which means the patient doesn’t have insufficient circulating volume, but rather they cannot vasoconstrict vessels to manage their BP resulting in inadequate perfusion

42
Q

List the modified NEXUS criteria for spinal clearance

A

1) Age >65
2) History of bone/muscle weakening disease
3) Altered conscious state
4) Intoxication
5) Significant distracting injury
6) Midline pain/tenderness on palpation of vertebrae
7)Patient is unable to actively rotate neck 45 deg without pain

43
Q

Explain your assessment in clearing a patients spine.

A

Neurological exam:
Motor function- arms (push pull grasp)
Legs (push, pull, leg raise)
Sensory function- arms (palms & back of hands)
Legs (lateral aspect of foot)
Suprasternal notch

44
Q

List causes of undifferentiated nausea & vomiting?

A

1) Secondary to opioid analgesia
2) Secondary to cytotoxic drugs or radiotherapy
3) Severe gastroenteritis

45
Q

List 4 of the nine abdominal regions and one organ that belongs in each?

A

1) Right hypochondriac region (RUQ)- Liver, right kidney, gallbladder
2) Left hypochondriac region (LUQ)- Stomach, pancreas, spleen and left kidney
3) Epigastric region (central upper)- Stomach, pancreas, liver

4) Right lumbar (RMQ)- Intestines
5) Left lumbar (LMQ)- Intestines
6) Umbilical region (central abdo)- Intestines

7) Right iliac (inguinal region- RLQ)- Appendix, right fallopian tube/ovary
8) Left iliac (inguinal region- LLQ)- Intestine & left fallopian tube/ovary
9) Hypogastric (pubic region- central)- Intestine, uterus, prostate & bladder

46
Q

What is the main focus in nausea & vomiting treatment for paediatrics

A

Oral rehydration

47
Q

Apart from motion sickness, list 4 common causes of N+V in paeds.

A

1) Gastrointestinal infections
2) Appendicitis
3) Food poisoning
4) Allergy
5) Meningitis
6) Regurgitation/reflux in infants
7) Metabolic disorders (diabetes)

48
Q

What is the minimum age & dose of ondansetron?

A

1yo & 2mg

49
Q

What are 2 circumstances that Ondanstron is required prophylactically & why?

A

1) Awake patients with potential spinal injuries & immobilised: to prevent vomiting and spine movement or airway compromise
2) Eye trauma: to prevent vomiting which increases intraocular pressure and may cause expulsion of ocular contents

50
Q

Describe the pathophysiology of nausea & vomiting.

A
51
Q

What are 4 signs of significant dehydration in a paediatric?

A

1) Postural perfusion changes (ST, hypotension, dizziness)
2) Decreased sweating or urination
3) Poor skin turgor, dry mouth, dry tongue
4) Fatigue & altered consciousness
5) Evidence of poor fluid intake compared to fluid loss
6) Dark yellow or brown urine
7) Fewer wet nappies
8) Thirst
9) Lethargy, irritable, drowsy or confused
10) Sunken eyes
11) Tears may be absent when crying
12) Cold peripheries

52
Q

List 2 common causes of an upper GI haemhorrage?

A

1) Oesophageal varices
2) Gastric ulcer
3) Gastritis
4) Oesophagitis
5) Cancer

53
Q

What are the 3 neuranatomic categories of abdominal pain & discuss one?

A

1) Visceral pain: described as crampy, dull or achy and can either be steady or intermittent (colicky) and is poorly localised. Obstruction, ischaemia or inflammation can cause stretching of the unmyelinated fibres that innervate the wallsor capsules of organs resulting in visceral pain
2) Parietal (somatic) pain: is caused by irritation of myelinated fibres that innervate the parietal peritoneum, usually the portion covering the anterior abdominal wall. This is sharp, well localised pain frequently over the region where the pathology is arising from
3) Referred pain: this is pain which is felt at a distance from the actual site of the pathology (eg shoulder tip pain from diaphragmatic irritation)

54
Q

What are the non-pharmacological pain relief options?

A

Splinting, cold/heat therapy

55
Q

List the Pre-hospital vital signs major trauma criteria for a Newborn & small infant

A

HR: <100 or >180
RR: >60
SBP: <50
Sp02: <90%
GCS: <15

56
Q

List the Pre-hospital vital signs major trauma criteria for a large infant

A

HR: <100 or >180
RR: >50
SBP: <60
Sp02: <90%
GCS: <15

57
Q

List the Pre-hospital vital signs major trauma criteria for a small child

A

HR: <90 or >160
RR: >40
SBP: <70
Sp02: <90%
GCS: <15

58
Q

List the Pre-hospital vital signs major trauma criteria for a medium child

A

HR: <80 or >140
RR: >30
SBP: <80
Sp02: 90%
GCS: <15

59
Q

List the Pre-hospital vital signs major trauma criteria for adults

A

HR: <60 or >120
RR: >30
SBP: <90
Sp02: <92%
GCS: <13 if 15yo+ or <15 if 12-15

60
Q

What type of sling is indicated for the following injuries?
A) Forearm injuries (radius/ulnar/wrist)
B) Clavicle and shoulder injuries

A

A) Standard arm sling
B) Collar and cuff sling

61
Q

List and describe 2 different types of long bone fractures?

A

1) Closed (simple)- broken bone but hasn’t pierced skin
2) Open (compound)- broken bone exits through skin or a wound leads to the fracture site. Infection/haemhorrage more likely
3) Greenstick- small slender crack in bone
4) Hairline- most common stress # as result from repeated stress
5) Complicated- structures around # are injures (eg vein, artery, nerves)
6) Comminuted- bone shattered into small pieces
7) Avulsion- Tendons attached to bone rip out small pieces of bone
8) Compression- two bones are forced against each other (vertebrae)

62
Q

Is it age appropriate to ask a 9yo to rate their pain 0-10

A

Yes as the numerical pain scale is appropriate for all paeds aged >6yo

63
Q

How do seizures and convulsions differ?

A

Seizure: a sudden uncontrolled event or episode of excessive electromechanical activity in the brain. It may alter behaviour, consciousness, movement, perception and/or sensation
Convulsion: An episode of excessive and abnormal motor activity (Seizures can occur without convulsion & convulsion can occur due to other reasons eg hypoxia)

64
Q

List different causes of seizures?

A

Diabetes, alcohol, poisoning, heat/cold, head trauma, neurological (tumour/CVA), Hypoxia, infarction, haemorrhage, epilepsy, med noncompliance

65
Q

Discuss the use of Midazolam for the fitting patient. Discuss the risks associated such as hypoventilation.

A
  • Midazolam may be administered at 0.1mg/kg (up to 10mg) to a total of two doses at ten minute intervals if required.
  • If the patient is aged greater than 60 years or has a blood pressure of less than 100mmHg then they should be administered a half dose (0.05mg/kg up to 5mg).
    -Patients that suffer from a Tonic Clonic seizure often have diaphragmatic spasm which does not allow for adequate ventilation. -The use of Midazolam will hopefully control this, along with controlling the sizure and allow for the patients normal ventilation to resume.
    Be aware that Midazolam may cause respiratory depression in some patients. These patients will require mechanical ventilation. The use of Midazolam may result in a depressed conscious state. This may mean that the patient requires airway management.
66
Q

What are the signs & symptoms a pt has inhaled a foreign object?

A

-Child starts coughing. -Distressed.
-Difficulty breathing . -Stridor.
-Face may change to red or cyanosed.
-Increased respiratory rate.
- No air entry heard in one lung (often right lung due to position of the right main bronchus).

67
Q

What is the difference between Simple pneumothorax & TPT?

A

Simple:
Subcutaneous emphysema, unequal breath sounds in spontaneous ventilating patient, Sp02 <92% on RA
TPT: Any of the following +/- S&S of SP
Respiratory distress in awake patient
Sp02 <92% despite 02
Decreased conscious state
Poor perfusion (ST & hypotensive)
High PIPS (stiff bag)
Decreased etC02
Increased JVT
Tracheal shift
Low sp02 on 02

68
Q

Why is there a decrease in etC02 in TPT patients?

A

ETCO2 is also affected by perfusion to the lungs. With a tension pneumothorax, decreased cardiac output causes less CO2 to be delivered to the lungs for exhalation.

69
Q

What is compartment syndrome & what are the S&S?

A

A condition caused by pressure build-up from internal bleeding or swelling of tissues.
The pressure decreases blood flow, depriving muscles and nerves of required nourishment. Can lead to crush syndrome.
Symptoms may include severe pain, sensation of pins and needles, weakness, palpable tension/swelling, pale skin of compartment, sometimes altered pulses/cap refill. pain on passive stretching of muscles of compartment.

70
Q

What is crush injury?

A

Crush injury is the localised tissue injury that occurs when a
compressive force is applied

71
Q

What is crush syndrome & what is it characterised by?

A

Crush syndrome is a systemic condition that results from
injuries sustained by compressive forces sufficient in duration
and pressure to cause widespread ischemia and necrosis to
soft tissue. Ischaemia of the muscle leads to increased
permeability of cell membranes and the release of potassium,
enzymes, and myoglobin into the systemic circulation. Crush
syndrome is characterised by rhabdomyolysis, lactic acidosis,
hyperkalaemia, renal failure, shock, dysrhythmias and death.
The development of crush syndrome is TIME and PRESSURE
dependent. Crush syndrome can develop over a short time
period where the compressive force and muscle mass is large
and, conversely, over long periods where compressive forces
are relatively small
S&S: