Medical CPGs Flashcards

1
Q

Diabetes definition

A

Disease of the endocrine system characterised by a deficiency of insulin or an inability of the body cells to respond to insulin – hyperglycaemic state

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2
Q

Type 1 diabetes IDDM definition

A

Characterised by an inadequate production of insulin by the beta cells within the pancreas (due to an autoimmune destruction of the beta cells) resulting in hyperglycaemia due to the insufficient insulin production.

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3
Q

Type 2 NIDDM definition

A

Characterised by a decrease in the production of insulin as well as a diminished tissue sensitivity to insulin (insulin resistance). Either too few insulin receptors or faulty insulin receptors.

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4
Q

Homeostasis of BGL

A

-through negative feedback cycles, balanced between regulation of insulin and counterregulatory hormones such as glucagon.

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5
Q

Action of insulin on maintaining BSL homeostasis

A
  • Insulin the primary regulator (released by beta cells in pancreas) in response to low BSL
  • insulin acts on liver to facilitate uptake of glucose and its conversion to glycogen
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6
Q

Action of Glucagon on maintaining BSL homeostasis

A

-released by alpha cells in pancreas - counter regulatory hormone which increases blood glucose levels by accelerating conversion of glycogen in liver to glucose

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7
Q

Causes of hypoglycaemia

A
  • excessive insulin action without adequate carbs
  • insulin OD - poor understanding/eyesight
  • diet
  • excessive exercise
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8
Q

Why do hypoglycaemic pts present with tachycardia, pale, sweating, agitated?

A
  • the brain metabolises sugars for energy and is unable to utilise fats/proteins available therefore the brain is starved for fuel and altered conscious/unconsciousness occurs
  • reduced blood glucose causes a counter regulatory catecholamine release and sympathetic response
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9
Q

Signs and symptoms of hypoglycaemia

A
altered conscious
tachycardia
seizure
drunk behaviour
sweat
confusion
hypothermia
fatigue
weakness
muscle tremor
headache
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10
Q

Diabetic ketoacidosis definition

A

serious complication of type 1 diabetes resulting from an absolute insulin deficiency leading to a hyperglycaemic state and metabolic acidosis

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11
Q

Causes of diabetic ketoacidosis

A
  • first time presentation
  • decrease or omission of insulin, poor compliance/education
  • infection
  • increased glucose, decreased exercise without decreased food
  • stressful events i.e infection, stroke, AMI, trauma
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12
Q

Patho of diabetic ketoacidosis

A

stressor

  • insulin deficiency
  • severe hyperglycaemia
  • cells become starved of glucose
  • breakdown of proteins and lipids
  • production of glucose and ketones
  • osmotic diuresis (due to glucose breakdown) and an acidotic state (due to ketone production)
  • dehydration
  • shock, coma, death
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13
Q

Honk/HHNK definition

A

An acute complication of type 2 diabetes resulting from a relative insulin deficiency leading to a hyperglycaemic, hyperosmolar state

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14
Q

Seizure definition

A

a sudden, uncontrolled event or episode of excessive electromechanical activity within the brain. It may alter behaviour, consciousness, movement, perception, sensation.

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15
Q

Definition of convulsion

A

episode of excessive and abnormal motor activity hence seizures can occur without convulsions and convulsions can be caused by other conditions

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16
Q

Definition of epilepsy

A

a disease process without discernible aetiology where an individual is subject to sudden, recurrent episodes of sensory disturbance, loss of consciousness or convulsions assoc with abnormal electrical activity in the brain

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17
Q

Classifications of generalised seizures

A

nearly simultaneous activation of entire cerebral cortex

  1. tonic clonic - LOC, tonic phase (rigid) followed by clonic phase (rhythmic jerking)
  2. absence - LOC with no loss of postural tone. Staring.
  3. myoclonic: brief shock like muscular contractions that may be generalised or limited to one of the extremities
  4. tonic: prolonged strained contraction of the body with deviation of head and eyes
  5. clonic: repetitive clonic jerks
  6. atonic: sudden loss of muscle tone which may be assoc with brief LOC
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18
Q

Classifications of partial seizures

A

electrical discharges within a localised region of the cerebral cortex

  1. simple: localised activity with no LOC - may involve any part of body; motor or sensory
  2. complex: localised seizures which have an effect on conscious state and motion
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19
Q

Causes of seizures

A
hypoxia
hyperthermia
hypoglycaemia
head injury 
epilepsy
drugs
pregnancy
infection
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20
Q

Post ictal complications

A
  • altered conscious
  • protection - aggressive pt
  • airway mx
  • hypoxia
  • trauma
  • hyper/hypothermic
  • lethargic
  • incontinent
  • recurrent seizures
  • long term brain injury
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21
Q

Pharma of Midaz on seizures

A

Acts on GABA receptor (post synaptic)

-increases affinity of GABA binding to GABA A receptors which enhances chloride channel opening - neuronal inhibition

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22
Q

Definition of anaphylaxis

A

A severe, life threatening systemic allergic hypersensitivity reaction to a previously encountered antigen. Characterised by: bronchospasm/oedema, peripheral vasoconstriction, increased peripheral permeability, contraction of extra vascular smooth muscle

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23
Q

Definition of allergic reaction

A

hypersensitivity reaction to a previously encountered antigen resulting in a non-systemic, non-life threatening localised reaction

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24
Q

Patho of anaphylaxis

A

Antigen exposure - activation of immune system - susceptible individuals produce IgE antibodies which bind to IgE receptors on cell membranes of Basophils and Mast Cells – next exposure to antigen - degranulation of mast cells and basophils - release of chemical mediators - systemic responses (bronchospasm, oedema, increased capillary permeability, peripheral vasodilation, contraction of extravascular smooth muscle) - relative fluid loss - clinical manifestations (angioedema, hypotension, abdo pain, bronchospasm, diarrhoea, CPC skin, urticaria) - shock, coma, death

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25
Q

Pharma of Adrenaline in Anaphylaxis

A

Increases monophosphate production in cell which stabilises mast cells, decreasing inflammatory mediator release.
Alpha: increased peripheral vasoconstriction - increased VR - increased CO and BP
-reduced peripheral vasodilation which increases VR
-reduced angio-oedema
-reduced urticaria (hives)
Beta 2: bronchodilation -interrupts positive feedback mechanism

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26
Q

Sepsis definition

A

characterised by whole body inflammatory state (systemic inflammatory response syndrome) and presence of known or suspected infection

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27
Q

Criteria for sepsis

A

temp less than 36 over 38
HR over 90
BP less than 90
RR over 20

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28
Q

Definition of SIRS

A

systemic inflammatory response to an underlying disorder/infection

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29
Q

Septic shock definition

A

A form of shock that results from a serious systemic bacterial infection - vasodilation - hypotension

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30
Q

Patho of Sepsis

A
  • systemic bacterial infection
  • release of inflammatory mediators
  • peripheral vasodilation
  • increased capillary permeability
  • interstitial oedema
  • reduced venous return
  • reduced CO
  • hypotension and inadequate tissue perfusion
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31
Q

Disseminated Intravascular Coagulation (DIC)

A

A pathological process characterised by the widespread activation of the clotting cascade that results in the formation of blood clots in the microvasculature throughout the body. this leads to compromised blood flow to tissues and can lead to multiple organ damage.

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32
Q

Meningococcal Septicaemia definition

A

-SIRS to a bacterial (rapid) or viral (slow) infection of meninges and CSF
Caused by neisseria meningitidis

33
Q

SIgns and symptoms of meningococcal

A
Typical purpuric rash 
Septicaemia signs: fever, rigors, joint and muscle pain
cold hands and feet, 
tachycardia, hypotension
tachypnoea 
Meningeal signs: headache, photophobia, neck stiffness 
nausea and vomiting, 
ACS
34
Q

Patho of meningococcal

A

Bacteria enters bloodstream where it multiples rapidly and damages blood vessel walls - bleeding into skin and formation of micro-emboli - increased vascular permeability, myocardial dysfunction

35
Q

Signs and symptoms of opioid overdose

A
Resp depression 
Altered conscious 
Pinpoint pupils 
Track marks 
Substance involved 
Exclude other causes (head injury)
36
Q

Patho of opioid overdose

A

There are 3 opioid receptors that cause the signs and symptoms seen in OD:
Mu - analgesia, sedation, resp depression, euphoria, physical dependence
Kappa - analgesia, pin point pupils, dysphoria
Delta - analgesia, cough suppression

37
Q

Types of TCAs

A

Amitriptyline
Nortriptyline
Dothiepin

38
Q

Mild to mod signs and symptoms of TCA overdose

A

THRASH DD - over 10mg/kg

  • Tachycardia
  • Hypertension
  • Resp depression
  • Ataxia
  • Slurring
  • Hyperreflexia
  • Dry membranes
  • Drowsy/confused
39
Q

Severe signs and symptomg of TCA overdose

A

SCREEEEECH over 30mg/kg

  • Seizure
  • Coma
  • Resp depression
  • ECG changes: prolonged QT, VT, SVT, PVC, long PR, QRS wide
  • Conduction delays
  • Hypotension
40
Q

Patho of TCA overdose

A

Anticholinergic effects at muscarinic receptors - tachycardia
Alpha-1 adrenergic receptor antagonism - decreased PVR - hypotension
Fast sodium channel blockage - delayed AV conduction - widening PR interval, QRS and QT intervals - increased risk of arrythmias, seizures, impaired myocardial contractility - reduced CO - hypotension
Inhibition of pre-synaptic reuptake of noradrenaline, serotonin and dopamine

41
Q

Causes of Agitation

A
Alcohol/ drug intoxication 
Epilepsy (post ictal) 
Insulin
Overdose/oxygen 
Underdose/withdrawal 
Trauma
Infection/sepsis
Pain/psych
Stroke/TIA
42
Q

Patho of organophosphate poisoning

A

Chemical enters body - accumulation of Ach at receptor sites - overstimulation of PNS - excessive muscarinic effects including salivation, sweating, bradycardia, bronchoconstriction, nausea, inadequate perfusion

43
Q

Signs and symptoms of Organophosphate poisoning

A

SLUDGE - salivation, lacrimation, urination, defecation, GI disturbance, emesis
DUMBELS - defecation, urination, muscle weakness, bronchospasm, bradycardia, emesis, lacrimation, salivation, sweating

44
Q

Autonomic dysreflexia definition

A

A potentially life threatening condition in patients with a spinal cord injury at the level of T6 or above, in response to a visceral or painful stimuli below the level of the lesion - uncontrolled severe HT

45
Q

Causes of autonomic dysreflexia

A
  • noxious stimuli below lesion
  • bladder distension, peptic ulcers, appendicitis, gallstones, fractures, tight-fitting clothing, sunburns, blisters, sexual intercourse, pregnancy and labour
46
Q

Signs and symptoms of autonomic dysreflexia

A
  • BP over 160
  • Headache
  • Blurred vision
  • Above (vasodilation): flushed skin, sweating
  • Below (vasoconstriction): pallor, goose flesh
47
Q

Patho of autonomic dysreflexia

A

Trauma at T6 or above - spinal shock resolves - painful stimuli below the lesion - SNS response - vasoconstriction - HT - baroreceptors in aortic arch detect the increase in BP causing brain to attempt to intervene - cause PNS response (vasodilation, bradycardia) - response cannot pass the lesion - dilation above the lesion - vasoconstriction persists below the lesion - uncontrolled HT - stroke, arrhythmia, seizures, death

48
Q

Stroke/TIA definition

A

Acute impairment of cerebral blood flow in one or more of the blood vessels supplying the brain interrupting/diminishing o2 supply - ischaemia - necrosis of brain tissue; caused by blockage (thrombus) or blood vessel rupture (haemorrhagic)
TIA - temporary interruption of blood flow that self resolves

49
Q

Stroke mimics

A
Hypo/hyperglycaemia
Intoxication 
Brain tumour
Electrolyte imbalance 
Syncope
Seizures
Subdural haematoma 
Sepsis
Middle ear disorder
Migraine
50
Q

Signs and symptoms of stroke

A
  • limb weakness
  • facial paralysis
  • sensory loss
  • slurred speech (dysarthria)
  • jumbled speech (dysphasia)
  • visual loss
  • poor balance (ataxia)
  • difficulty swallowing (dysphagia)
51
Q

Patho of ischaemic stroke

A

Vessel occlusion/haemorrhage - sudden cessation of cerebral blood flow to a portion of the brain - if uncorrected - ischaemia - neuronal dysfunction (symptoms depend on area of brain affected) - necrosis of brain tissue.

52
Q

Management of undifferentiated nausea and vomiting

A
  • Ondansetron 4mg ODT -repeat 4mg after 5-`0 mins if symptoms persist (max 8mg total)
  • if known C/I or allergy to Ondans and over 21yrs: Stemitil 12.5mg IM
53
Q

Management of Vestibular nausea

A

includes: motion sickness, planned evac, vertigo
If pt over 21: Stemitil 12.5mg IM
if less than 21yrs: Ondansetron as per undifferentiated N+v

54
Q

Management of prophylaxis of nausea and vomiting

A

Includes: awake spinal immbolised pt, eye trauma
Ondansetron as per undifferentiated
If known C/I, allergy and over 21yrs: Stemitil 12.5mg IM

55
Q

Hypoglycaemia management

A

BGL less than 4, responds: Glucose 15g oral
BGL less than 4 no response: Dextrose 10% 15g (150ml) IV with 10ml Saline flush
-if unable to insert IV: Glucagon 1 IU IM
If GCS less than 15 after 3 mins, repeat 10g (100ml) Dextrose

56
Q

Management of GCSE

A
  • airway, ventilation
  • if airway patent, admin high flow o2
  • Midaz 10mg IM repeat once at 10 mins
  • small, frail or elderly should have 5mg IM repeated 5mins once
  • continue to monitor airway, ventilation, conscious state, BP
57
Q

What do we do for pts who are persistently unresponsive to Adrenaline in anaphylaxis setting?

A

Glucagon 1-2 IU IM or IV under consultation

58
Q

Management of anaphylaxis

A
  • monitor heart rhythm
  • Adrenaline 500mcg IM - repeat at 5 min intervals until satisfactory results or side effects
  • small, elderly, frail have 300mcg instead
  • provide o2 therapy
  • mx resp distress as per asthma, nebulised adrenaline for airway obstruction
  • consider fluid
  • do not allow pt to stand or walk
59
Q

Management of inadequate perfusion

A

if sepsis suspected and chest clear and MICA is not available:

  • confirm MICA request
  • Normal Saline 20ml/kg IV over 30 mins
60
Q

Meningococcal management

A

IV access: Ceftriaxone 1g IV -dilute with water for injection to make 10ml, admin over 2 mins
IM access: Ceftriaxone 1g IM - dilute with 3.5ml 1% Lignocaine to make 4ml, admin to upper lateral thigh

61
Q

Management of heroin overdose

A
  • assist and maintain ventilation and airway
  • Naloxone 1.6mg -2mg IM
  • transport
62
Q

Management of other opioid overdose

A
  • assist and maintain airway and ventilation
  • Naloxone 100mcg IV - repeat 100mcg every 2 mins (max 2mg) until pt is adequately self-ventilating
  • If unable to insert IV: Naloxone 400mcg IM (single dose)
  • consider SGA
  • transport without delay
63
Q

Management of mild to moderate agitation

A
  • Midaz 5-10mg IM - administer lower doses (2.5-5mg) for elderly, frail, weight under 60kg, SBP under 100, sedating drug/alcohol involvement
  • repeat at 10min intervals if necessary, titrated to pt response (max 20mg
64
Q

Management of Extreme agitation

A
  • Ketamine IM: under 60kg-200mg, 60-90kg-300mg, over 90kg-400mg
  • if Ketamine not available: Midaz up to 2mg IM - repeat at 10 min intervals if necessary (max 40mg)
65
Q

Management of autonomic dysreflexia

A
  • GTN 300mcg (no previous admin) or 600mcg
  • repeat initial dose every 10 mins until either symptoms resolve, onset of side effects, BP less than 160
  • transport to nearest hospital
66
Q

Management of Stroke/TIA

A
  • Assess: facial droop, speech, hand grip, BGL
  • maintain airway and ventilation
  • mx symptomatically
  • provide analgesia
  • treat seizures
  • transport: pt stable with no co-morbidities, onset time less than 4.5hrs and tx time less than 1 hr, tx to nearest thrombolysis unit. If not, tx to a closer centre with stroke unit/CT
67
Q

Management of Palliative Care pts

A

-pall care service unavailable: rx n+v, rx distressing pain, mild agitation with Morphine (max 20mg) subcutaneously
-treat mild agitation not caused by pain with Midaz 2.5mg S/C
Pall care available: consult for mx

68
Q

HONK/HHNK Patho

A
  • relative insulin deficiency
  • hyperglycaemia
  • exceeds ability of kidneys to reabsorb glucose
  • osmotic diuresis
  • dehydration
69
Q

Seizure Patho

A

Occurs as a result of a brief disturbance to the brain which causes abnormal excessive electromechanical activity. There is an increase in membrane permeability which allows greater amounts of sodium and potassium to diffuse across membranes - increased ability of neurons to cause APs - imbalance between excitation and inhibition (defects in GABA/inhibition and glutamate/excitation) - uncontrolled electrical activity.

70
Q

Types of sedatives

A

GHB
Alcohol
Benzos

71
Q

Types of psychostimulants

A

Ecstasy
Cocaine
PCP
Amphetamines

72
Q

Sedatives patho

A

Act by increasing the activity of GABA, which is a major inhibitory neurotransmitter in the CNS
Sedatives bind to GABA A receptors which facilitates binding of GABA to the receptor sites - increases GABA neurotransmisssion - sedation, muscle relaxation, anti-convulsant effects, decrease anxiety

73
Q

Sedative signs and symptoms

A
Drowsy
Agitated
Muscle relaxation
Confusion
Dizzy
Blurred vision 
Weakness 
Slurred speech
74
Q

Psychostim patho

A

Simulates activity of CNS - In toxic levels - Severe agitation and psychotic behaviour
Overstimulation of SNS - MI, HT, hyperthermia, rhabdo

75
Q

Psychostim signs and symptoms

A

nervous, anxious, confused, irritable, aggressive, violent, palpitations, headache, dizzy, seizure, stroke

76
Q

Causes of Thrombolytic stroke

A

blood clot or thrombus which forms in the brain, blocking blood flow through effected vessel OR embolism that has broken free and become lodged in cerebral artery

77
Q

Causes of haemorrhagic stroke

A

ruptured blood vessels which causes adjacent brain tissue to be displaced and compressed - disrupting blood flow and o2 supply - ischaemia

78
Q

Signs and symptoms of ICH

A
  • severe headache
  • N+V
  • pupil abnormalities
  • resp abnormalities
  • slow pulse and HT
  • GCS<10
79
Q

Types of haemorrhagic stroke

A

subarachnoid - bleeding in space around brain

intracerebral - bleeding within brain tissue