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Module 5 > Study Day Condition Pathophysiology > Flashcards

Study Day Condition Pathophysiology Flashcards

1
Q

Hyperglycaemia

Definition - what causes it?

A
  1. Decreased insulin
  2. Decreased glucose in cells
  3. Increased BGL
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2
Q

Hyperglycaemia

What is insulin and how does it affect diabetic patients?

A

Insulin is a hormone secreted by B-cells within the pancreas. Insulin is required to move the glucose into the cells. When insulin is low, the glucose remains within the blood stream.

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3
Q

Hyperglycaemia

What 4 counter-regulatory hormones does the body increase in response to high BGL?

To attempt top produce an energy source

A
  1. Glucagon
  2. Cortisol
  3. Epinephrine
  4. Growth Hormone (GH)
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4
Q

Hyperglycaemia

Increased BGL (from glucose and additional hormones) cause an overflow into urine. This stage is called Osmotic Diuresis. What 4 symptoms are associated with this stage of hyperglycaemia?

A
  1. Polydipsia
  2. Polyphagia
  3. Polyuria
  4. Dehydration
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5
Q

Hyperglycaemia

When the body creates an energy source by converting lipids/fatty acids - what chemical do we see build up within blood/urine?

A

Ketones

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6
Q

Hyperglycaemia

What sign of DKA is caused by ketones?

A

Fruity Breath

Caused by Acetone

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7
Q

Hyperglycaemia

Can Ketones or Glucose cross the blood brain barrier into cells?

A

Ketones

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8
Q

Hyperglycaemia

Are Ketones Acidic or Basic?

A

Acidic

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9
Q

Hyperglycaemia

What does an increase in ketones cause our diabetic patients?

A

Metabolic Acidosis

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10
Q

Hyperglycaemia

Why does Kussmals breathing occur in diabetic patients?

A

It’s the bodies response to metabolic acidosis. The ketones cause the overall body pH to be acidic. Kussmals breathing is deep and laboured and is effective at offloading CO2 to restore metabolic homeostasis.

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11
Q

Hyperglycaemia

AV CPG - what are the 3 identifying markers of DKA?

A
  • Pre-existing hx of diabetes
  • BGL >11 AND
  • Clinical features of DKA
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12
Q

Hyperglycaemia

AV CPG - what are the 3 identifying markers of HSS?

A
  • Pts are typically older
  • BGL >30
  • Usually NIL DKA signs
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13
Q

Hyperglycaemia

What are the clinical features of HHS/DKA?

(x7)

A
  • Dehydration
  • Tachypnoea
  • Polydipsia
  • Polyohagia
  • Polyuria
  • Kussmals Breathing
  • Hx diabetes
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14
Q

Hyperglycaemia

Why treat HSS/DKA with fluid?

A

Patients with DKA/HSS have a large fluid defecit due to the 3xPs. The patients will likely be dehydrated and we are giving fluid under that guideline.

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15
Q

Anaphylaxis

What antibody does the body produce in an anaphylactic response?

A

IgE antibodies

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16
Q

Anaphylaxis

How does an anaphylactic response occur?

A
  1. *(1st time) *The body comes in contact with an antigen (allergen) - T-cells detect it and alert B-cells, telling them to produce immuglobin (IgE) antibodies (strong immune response)
  2. IgE antibodies bind to immune cells (mast cells + basophils) and will automatically be released in the following immune response(s).
    4.* (2nd time)* The body comes in contact with an antigen - mast cells + basophils degranulate (release all their histomine stores)
  3. Degranulation causes vasodilation, vascular permeability, constriction of the smooth muscles + increase in mucous production.
  4. Airway compromise + hypoxia + circulatory collapse = death
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17
Q

Anaphylaxis

Why do we see swelling/oedema in anaphylaxis?

In the setting of Anaphylaxis

A

Vasodilation and vascular hyperpermiability.
Capillaries dilate, filling with fluid at the site of injury/response causing hyperpermiability between the capillaries and the interstitial fluid. Most anaphylactic reaction is caused by ingestion/inhalation so that ‘site
is commonly the mouth, lips, upper and lower airways.

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18
Q

Anaphylaxis

Why do we see respiratory distress in anaphylaxis?

A

The inflammatory response causes broncho-constriction (contraction of smooth muscle tissue) as well as airway oedema caused by the vasodilation + vascular hyper-permeability.

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19
Q

Anaphylaxis

Why do we see skin changes in anaphylaxis?

Rash, hives, flushed skin

A

Vasodilation and vascular hyperpermiability.
Capillaries dilate, filling with fluid at the site of injury/response causing hyperpermiability between the capillaries and the interstitial fluid. Most anaphylactic reaction is caused by ingestion/inhalation so that ‘site’
is commonly the mouth, lips or skin from handling the antigen.

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20
Q

Anaphylaxis

Why do we see hypotension in anaphylaxis?

A

Vasodilation and vascular capillary hyperpermiability.
The vasodilation causes a decrease in systemic vascular resistance (SVR) and an increase in blood flow, resulting in a reduction of blood pressure

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21
Q

Anaphylaxis

Why do we see GIT symptoms in anaphylaxis?

Nausea, vomiting, diarrhea

A

The inflammatory cascade causes the contriction of smooth muscles - which is what the stomach/GIT is made up of.
This causes irritibility within the walls of the stomach - causing nausea/vomiting/diarrhea.

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22
Q

Anaphylaxis

What type of shock is anaphylaxis?

A

Distributive

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23
Q

Anaphylaxis

What is distributive shock?

A

Distributive shock characteristically demonstrates widespread peripheral vasodilation caused by loss of vascular smooth muscle reactivity - in this setting, caused by the IgE immune response.

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24
Q

Anaphylaxis

What is the role of ADRENALINE in anaphylaxis?

A

Adrenaline has the opposite physiological effects to the inflammatory agents.
Peripheral vasoconstriction + bronchodilation

Vasoconstriction - Increase CO, decrease permeability, decrease swelling
Bronchodilation - Widening of airways

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25
Q

Anaphylaxis

What is Adrenaline? What are its actions?

A

Naturally occuring alpha and beta-adrenergic stimulant.
1. Increase HR - SA node (B1)
2. Increase conduction velocity - AV node (B1)
3. Increase myocardial contractility (B1)
4. Increase irritability of the ventricles (B1)
5. Bronchodilation (B2)
6. Peripheral vasoconstriction (Alpha)**

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26
Q

Anaphylaxis

What is the onset time/peak/duration for IM adrenaline?

A

O: 30-90s
P: 4-10m
D: 5-10m

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27
Q

Anaphylaxis

What antibody does the body produce in an anaphylactic response?

A

IgE antibodies

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28
Q

Anaphylaxis

How does an anaphylactic response occur?

A
  1. *(1st time) *The body comes in contact with an antigen (allergen) - T-cells detect it and alert B-cells, telling them to produce IgE antibodies (strong immune response)
  2. IgE antibodies bind to immune cells (mast cells + basophils) and will automatically be released in the following immune response(s).
    4.* (2nd time)* The body comes in contact with an antigen - mast cells + basophils degranulate (release all their histomine stores)
  3. Degranulation causes vasodilation and contraction of the smooth muscles
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29
Q

Anaphylaxis

Why do we see swelling/oedema in anaphylaxis?

In the setting of Anaphylaxis

A

Vasodilation and vascular hyperpermiability.
Capillaries dilate, filling with fluid at the site of injury/response causing hyperpermiability between the capillaries and the interstitial fluid. Most anaphylactic reaction is caused by ingestion/inhalation so that ‘site
is commonly the mouth, lips, upper and lower airways.

How well did you know this?
1
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30
Q

Anaphylaxis

Why do we see respiratory distress in anaphylaxis?

A

The inflammatory response causes broncho-constriction (contraction of smooth muscle tissue) as well as airway oedema caused by the vasodilation + vascular hyper-permeability.

How well did you know this?
1
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2
3
4
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31
Q

Anaphylaxis

Why do we see skin changes in anaphylaxis?

Rash, hives, flushed skin

A

Vasodilation and vascular hyperpermiability.
Capillaries dilate, filling with fluid at the site of injury/response causing hyperpermiability between the capillaries and the interstitial fluid. Most anaphylactic reaction is caused by ingestion/inhalation so that ‘site’
is commonly the mouth, lips or skin from handling the antigen.

How well did you know this?
1
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32
Q

Anaphylaxis

Why do we see hypotension in anaphylaxis?

A

Vasodilation and vascular capillary hyperpermiability.
The vasodilation causes a decrease in systemic vascular resistance (SVR) and an in blood flow, resulting in a reduction of blood pressure

How well did you know this?
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33
Q

Anaphylaxis

Why do we see GIT symptoms in anaphylaxis?

Nausea, vomiting, diarrhea

A

The inflammatory cascade causes the contriction of smooth muscles - which is what the stomach/GIT is made up of.
This causes irritibility within the walls of the stomach - causing nausea/vomiting/diarrhea.

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34
Q

Anaphylaxis

What type of shock is anaphylaxis?

A

Distributive

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35
Q

Anaphylaxis

What is distributive shock?

A

Distributive shock characteristically demonstrates widespread peripheral vasodilation caused by loss of vascular smooth muscle reactivity - in this setting, caused by the IgE immune response.

How well did you know this?
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3
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36
Q

Anaphylaxis

What is the role of ADRENALINE in anaphylaxis?

A

Adrenaline has the opposite physiological effects to the inflammatory agents.
Peripheral vasoconstriction + bronchodilation

Vasoconstriction - Increase CO, decrease permeability, decrease swelling
Bronchodilation - Widening of airways

How well did you know this?
1
Not at all
2
3
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37
Q

Anaphylaxis

What is Adrenaline? What are its actions?

A

Naturally occuring alpha and beta-adrenergic stimulant.
1. Increase HR - SA node (B1)
2. Increase conduction velocity - AV node (B1)
3. Increase myocardial contractility (B1)
4. Increase irritability of the ventricles (B1)
5. Bronchodilation (B2)
6. Peripheral vasoconstriction (Alpha)**

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38
Q

Anaphylaxis

What is the onset time/peak/duration for IM adrenaline?

A

O: 30-90s
P: 4-10m
D: 5-10m

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39
Q

Opioid OD

Half life of Methadone?

A

24hours may need continuous naloxone

40
Q

Opioid OD

In what settings should we avoid administeration of Naloxone?

A
  1. Folling opioid associated cardiac arrest - maintain assisted ventilations
  2. Following a head injury - maintain assisted ventilations if required
41
Q

Opiod OD

Why do patients have a likelihood to deteriorate once again after naloxone admin?

A

The duration of Naloxone is shorter than Heroin

Heroin 3-5 hours
Naloxone: 30-45 minutes

42
Q

Opioid OD

How do we mitigate patient agitation post naloxone admin?

A

Adequate ventilation and oxygenation prior to admin of naloxone. Agitation is commonly caused by hypoxia in the setting of opioid OD

43
Q

Opioid OD

Which nervous system is effected by opioids?

A

Opioid drugs act in both the central and peripheral nervous systems. Within the central nervous system, opioids have effects in many areas, including the spinal cord

44
Q

Opioid OD

Why do opioids causes respiratory depression?

A

Opioids induce respiratory depression via activation of μ-opioid receptors at specific sites in the central nervous system including the pre-Bötzinger complex, a respiratory rhythm generating area in the pons (section of the brain resposible for regulation of breathing)

45
Q

Acute Behavioural Disturbance

SAT score

A

+3
Combative, violent out of control // Continual loud outbursts // Ketamine

+2
Very anxious and agitated // Loud outbursts // Droperidol

+1
Anxious restless // Normal talkative // Olanzapine

0
Awake and calm &cooperative // Speaks normally

-1
Asleep but rouses if name is called // Slurring or prominent slowing

-2
Responds to physical stimulation // Few recognizable words

-3
No response to stimulation

46
Q

Acute Behavioural Disturbance

Why do we call MICA for assistance post-ketamine sedation

A
  1. IV midazolam in order to facilitate continuous sedation
  2. Potential of patient to need continuous airway management and RSI
47
Q

Acute Behavioural Disturbance

Why do we avoid midazolam in the setting of agitation secondary to head injury?

A

Head injuried patients agitation is often secondary to pain, which can be managed with opioid analgesia. Cerebral perfusion is a cornerstone in management of a traumatic head injury. Midazolam (CNS depressant) may decrease cerebral perfusion and can have negative outcomes

48
Q

Acute Behavioural Disturbance

Why are both lewybody dementia and parkinsons both a precaution for Droperidol?

A

It may worsen symptoms of both conditions. In particular worsening agitation in parkinsons patients.

49
Q

Acute Behavioural Disturbance

Which form of sedation is prefered for agitation secondary to serotonin syndrome?

A

Benzodiazepines (midazolam) due to the CNS depression effects

50
Q

Acute Behavioural Disturbance

Potential contibutors to acute behavioural distubances in young patients?

A

Neurodiversity (e.g. autism, ADHD)

Severe developmental trauma (e.g. family violence)

51
Q

Acute Behavioural Disturbance

What are potential causes of acute behavioural disturbances:

A

— Physical injury and / or pain (e.g. head injury)
— Acute medical conditions (e.g. hypoglycemia, postictal state)
— Unmet needs (e.g. bladder distension, constipation, hunger, thirst, alcohol/nicotine withdrawal)
— Substance abuse / poisoning (e.g. methamphetamine, alcohol)
— Acute and uncontrolled mental health condition (e.g. panic attack, acute mania)

52
Q

Acute Behavioural Disturbance

What age are we required to consult RCH for sedation of a paediatric?

A

<16 years

53
Q

Behaviours of Concern?

A

Confused
Irritable
Boisterous
Physical threats
Verbal threats
Attacking objects

54
Q

Grounding Exercise 5 senses

A

5 things you can see
4 things you can feel
3 things you can hear
2 things you can smell
1 things you can taste

55
Q

Neurogenic Shock: Patho

A
  1. Injury to T5 or above
  2. Decreased sympathetic tone
  3. Vagal stimulation
  4. Parasympathic NS dominance
  5. Severe vasodilation
  6. Leaky capillaries
  7. Decreased SVR and BP
  8. Relative hypovolaemia
  9. Decrease CO = V/Q mismatch
  10. Decrease in CPP = death
56
Q

Neurogenic shock: Definition

A

Primary + Secondary SCI.
Primary - Direct damage to the spinal cord membrane that leads to disruption of sympathetic tone.
Secondary - Is a result from vascular changes, electrolyte shifts and oedema that lead to necrosis at the site of injury.

The combination leads to a loss of sympathetic tone and therefore unopposed parasympathic response (driven by the vagus nerve). This presents as instability in BP, HR and temperature regulation.

57
Q

Signs & Symptoms of SCI

A
  • Loss of neurological activity at or below injury
  • Neurogenic Shock
  • Priaprism
  • Temperature irregularities below the injury site (hypothermia)

For priaprism- blood pools below injury site due to lack of sympathetic tone - blood literally can’t be re-distributed so it pools in extremities (and penis).
For temp - due to loss of sympathetic mediation of temperature control and sweat regulation - can’t redistribute blood to generate heat through muscler activity

58
Q

Envenomation

What are signs of snake envenomation?

A
  • Eyelid drooping, double vision, slurred speech, drooling, generalised muscle weakness (typical of tiger snake)
  • Pain (generalised muscle pain, pain at site, abdominal pain, headache)
  • Nausea, vomiting, sweating
  • Respiratory distress (late sign)
  • Loss of consciousness, paralysis
  • Bleeding (site, nose, gums, dark red urine)
59
Q

What is the most severe presentation from a blue ring octopus envenomation?

A

Respiratory arrest due to paralysis and subsequent hypoxia

60
Q

What envenomation is likely to caused anaphylaxis?

A

A tick bite

61
Q

What do you do if the tick is still attached to the patient?

A

Leave it/Cover it. DO NOT REMOVE. Requires careful removal to ensure the head detaches from patient skin.

62
Q

Why do we use pressure immobilistion bandages?

A

The pressure immobilisation technique slows the flow of lymph by which venoms gain access to the circulation.
If we were to stop the venom completely ,(tourniquet) it would cause isolated tissue necrosis at the bite - slowing it down within the lymph system will overall slow down the systemic effects.

63
Q

How do snake bites effect the nervous system?

A

The venom/toxins blocks the transmission oif the pre/post-synaptic nerve impulses at the neuromuscular junction, resulting in paralysis of voluntary muscle and respiratory muscles

64
Q

How do snake bites effect haemostasis?

A

Snake venom contains toxins that interfere with the blood’s clotting cascade. The process ultimately consumes all circulating fibrinogen (among other clotting factors) at which this point the patient is no longer to form blood clots. This process only take minutes and to restore it requires antivenom or enough time for the venom to naturally break down and go through homeostasis (>6h)

65
Q

Envenomation

What is rhabdomyolysis? What are it’s effects on the body?

A

Rhabdo occurs when damaged muscle tissue releases proteins (myoglobin) and electrolytes into the blood stream.

Myoglobin can cause kidney damage by causing renal tubular obstruction, nephrotoxicity (ischaemia), vasoconstriction - leading to acute kidney injury (AKI).

66
Q

Patho of: Hypovolaemic Shock

A
  1. Injury
  2. Slow continuous haemorrhage
  3. Decrease venous return, decrease CO
  4. Detected by baroreceptors - compensatory mechanism activated
  5. Bodys limit reached - begins to decompensate
  6. Hypo/brady
  7. Decrease O2 in cells, increase in waste leads to tissue damage, coma and death
67
Q

Defintion: Shock

A

Widespread decrease in tissue perfusion resulting in inadequate delivery of O2/removal of waste products - resulting in impaired cellular function.

68
Q

How many litres of blood can you lose from an unstable pelvic fracture?

A

4-6L

69
Q

Why are pelvic fractures high risk?

A

The pelvis is surrounded by organs, nerves and blood vessels all of which have a high chance of being punctured/ruptured with force and can not be managed in the prehospital setting.

70
Q

Why do we tolerate hypotension w/o fluid replacement in haem hypovolaemia? (SBP>70)

A
  1. Blood product are the preffered fluid for resus
  2. If the haemorrhage isn’t controlled, fluid is just going to re-circulate out of the patient. This process would be diluting the reduced volume of blood.
71
Q

What is non-haemorrhagic hypovolaemia and relative hypovolaemia?

A

Non-haemorrhagic- Loss of volume from circulation while blood cells are preserved (dehydration).
Relative - Loss of volume from fluid shifting from circulation to interstitial space (anaphylaxis, sepsis, burns).

72
Q

What are the stages of shock?

A

1.** Compensatory -** homeostatic mechanisms activated: Increase sympathetic tone = increase SVR, HR, thirst, fluid retention
2. Decompensatory - if the cause of shock isn’t compensatory mechanisms becomes overwhelmed, decrease in perfusion/conscious/BP
3. Irreversible - mechanisms failed (coma, death)

73
Q

Patho: Jackson’s Burn Model

A
  1. The **zone of coagulation **is the closest to the heat source + the primary injury - irriversible tissue injury
  2. Surrounding, the zone of ischaemia - damaged but potentially viable tissure.
  3. Surrounding, the zone of hyperemia - reversible increase in blood flow/inflammartion
74
Q

Signs and symptoms of airway burns? BOSHER

A

B - Burns to neck, face, upper torso
O - Odema (airway, lips)
S - Sooty sputum
H - Hypoxia (decreased GCS, cyanois, irritability)
E - Enclosed spaces
R - Respiratory distress

75
Q

How do we asses burns?

A
  1. Appearance (dry/pale/pink - blanching/non-blanching)
  2. Colour (red, pink, white, charred)
  3. Sensation (normal, increased, reduced, none)
  4. Pathology (epidermis, dermis, full thickness
  5. Blisters
76
Q

Relative VS total fluid loss - how does it cause shock? Burns

A

Relative - The heat/burn will trigger the release of histamine* internally* (inflammatory mediators) which causes vasodilation, increased permeability and oedema.

**Total **- The burned epidermis layer leakes fluid externally from blood vessels. This fluid is either gathered in the form of a blister or excreted - contributing to th overall fluid loss + leading to shock.

77
Q

Croup: patho

A

Croup is a viral infectionof the larynx, trachea, bronchi and bronchioles which causes inflammation + obstructs air flow. Increaed respiratory effort cause fatigue, hypercapnia and decreased conscious state.

78
Q

What are the “classic symptoms” of croup?

A
  • Generalled aged between 6m-6y
  • Worse at night
  • Baring cough
  • Stridor + hoarse voice
79
Q

Why is croup worse at night?

A

The body’s natural levels of steroids drop at night making the airway oedema worse than daytime.

80
Q

Why nebulised adrenaline in croup?

A

Adrenaline reduces bronchial and tracheal epithelial vascular permeability thereby decreasing airway oedema, increasing the airway radius and improving airflow

81
Q

Why not salbutamol in croup?

A

There is no smooth muscle in the airway - salbutamol is a smooth muscle relaxant which is targetting the bronchioles in respiratory conditions. It would have no effect on airway oedema.

82
Q

What is epiglottitis?

A

Bacterial infection that spread through the upper respiratory tract - primarily effecting the epiglottis.
Identified by the four D’s:
1. Drooling
2. Dysphagia (difficulty swallowing)
3. Dysphonia (poor voice quality)
4. Distress

83
Q

What is a flail segment?

A

A flail chest is a condition in which multiple rib fractures occur, causing a segment of the chest wall to become detached and move paradoxically during inspiration and expiration.

84
Q

Tension Pneumothorax

A

A tension pneumothorax is a life-threatening condition in which air enters the pleural cavity and cannot escape, causing the lung to collapse and putting pressure on the heart and other vital organs.

85
Q

Simple Pneumothorax

A
86
Q

Hemothorax?

A

Hemothorax is a condition in which blood collects in the pleural cavity, usually due to trauma or injury to the chest.

87
Q

Pericardial Tamponade

A

A pericardial tamponade is a life-threatening condition in which fluid accumulates in the pericardial sac, putting pressure on the heart and impairing its ability to pump blood effectively

88
Q

Simple Pneumothorax

A

A simple pneumothorax occurs when air enters the pleural space, causing the lung to collapse. This can be caused by trauma, underlying lung disease, or spontaneous rupture of a small air sac (known as a bleb) on the lung surface. The air in the pleural space exerts pressure on the lung, which prevents it from fully expanding during inspiration, leading to symptoms such as shortness of breath, chest pain, and a dry cough

89
Q

Simple vs tension pneumothorax

A

both simple pneumothorax and tension pneumothorax involve air in the pleural space, tension pneumothorax is a medical emergency that requires immediate attention, while simple pneumothorax is less urgent but still requires medical evaluation and treatment.

90
Q

Neurogenic shock vs Autonomic Dysreflexia

A

autonomic dysreflexia and neurogenic shock are both conditions that can occur after a spinal cord injury, but they have different pathophysiologies. Autonomic dysreflexia is an exaggerated sympathetic response to a noxious stimulus, while neurogenic shock is a loss of sympathetic tone resulting in vasodilation and decreased blood pressure.

neurogenic shock is a type of shock that occurs due to a loss of sympathetic tone and unopposed action of the parasympathetic nervous system. This leads to widespread vasodilation, a decrease in vascular resistance, and a decrease in venous return, which ultimately results in a decrease in cardiac output and tissue perfusion

91
Q

What is a seziure?

A

A seizure represents the uncontrolled, abnormal electrical activity of the brain that may cause changes in the level of consciousness, behavior, memory.

92
Q

Partial vs generalises seizures?

A

In a partial seizure, the most common seizure type in adults, one area of the cortex activates first and may manifest through simple symptoms such as a motor or sensory phenomena.

Generalized seizures result from diffuse cortical activation at seizure onset or generalization of partial seizure activity.

93
Q

Seizures on a cellular level

A
  • Seizures start with the excitation of susceptible neurons, which leads to discharges of progressively larger groups of connected neurons.
  • Neurotransmitters are involved.
  • Glutamate is the most common excitatory neurotransmitter, and gamma-aminobutyric acid (GABA) is an important inhibitory neurotransmitter.
  • An imbalance of excess excitation and decreased inhibition initiates the abnormal electrical activity.
94
Q

Seizures on a cellular level

A
  • Seizures start with the excitation of susceptible neurons, which leads to discharges of progressively larger groups of connected neurons.
  • Neurotransmitters are involved.
  • Glutamate is the most common excitatory neurotransmitter, and gamma-aminobutyric acid (GABA) is an important inhibitory neurotransmitter.
  • An imbalance of excess excitation and decreased inhibition initiates the abnormal electrical activity.
95
Q

Generalized seizure systemic changes

A
  • lactic acidosis
  • increased catecholamine levels
  • hyperthermia
  • respiratory compromise
  • decrease BGL
  • decrease GCS

Module 5 (4 decks)

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