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semester 2 2019 > 265 (medical nursing) > Flashcards

265 (medical nursing) Flashcards

1
Q

what is true physiological hypoglycaemia measured at? what is considered hypoglycaemia in diabetes?

A

true physiological hypoglycaemia is a BGL below 3.5mmol but BGL below 4mmol is considered hypo for a diabetic

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2
Q

what is hypo unawareness?

A

when BGLs are below 3.5 mmol but no symptoms are experienced

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3
Q

at what BGL measurement should a person be treated for hypoglycaemia?

A

3.9 mmol

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4
Q

what can cause hypoglycaemia?

A
  1. too much insulin
  2. vigorous exercise without extra carbohydrate
  3. missed or delayed meals
  4. not eating enough carbohydrates
  5. alcohol intake
  6. malnutrition
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5
Q

ketones: normal range?

A

0.0 - 0.6 mmol

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6
Q

signs and symptoms of DKA?

A
  1. High blood glucose levels with ketones present
  2. Tummy pain
  3. Vomiting
  4. Dehydration
  5. Rapid, shallow breathing
  6. Acetone smell on the breath
  7. Confusion
  8. Drowsiness which may lead to coma
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7
Q

when should ketones be checked?

A

when BGL is 15mmol or above

when child is unwell, regardless of BGL

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8
Q

at what level of ketones is action required?

A

when greater than 1 mmol, or 0.6 mmol if using a pump

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9
Q

which insulin should be cloudy?

A

intermediate-acting insulin

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10
Q

what is target BGL range?

A

4.0 - 7.0 mmol/L before main meals

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11
Q

what is target HbA1c range?

A

HbA1c target is < 58 mmol/mol (<7%)

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12
Q

what is a receptor?

A

a protein molecule found on the surface of a cell which receives chemical signals to produce a response from the cell

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13
Q

what is an agonist?

A

a chemical which binds to receptors activates them.

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14
Q

what is an antagonist?

A

a chemical which bind to receptors and prevents them from being activated

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15
Q

what is the difference between a competitive antagonist and a non-competitive antagonist?

A

non-competitive antagonists bind to an allosteric (non-agonist) site on the receptor to prevent activation of the receptor.
(most drugs we will look at will be competitive antagonists)

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16
Q

classic signs of opioid overdose?

A

pinpoint pupils
respiratory depression
oversedation

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17
Q

what systems in the body control all physiological processes? via what mechanisms?

A

endocrine system via hormones

nervous system via neurotransmitters

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18
Q

what neurotransmitter do cholinergic nerves release?

A

ACh

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19
Q

what is the main neurotransmitter adrenergic nerves release?

A

noradrenaline

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20
Q

what are the other important neurotransmitters do adrenergic nerves release?

A

adrenaline

dopamine

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21
Q

adrenoceptors - what division of the ANS are they associated with, what physiology effects do they have?

A

SNS - fight or flight- increase HR, BP, bronchodilation

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22
Q

cholinoceptors - what division of the ANS are they associated with, what physiology effects do they have?

A

PNS - rest and digest - decreased HR, increased urination, defecation, digestion

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23
Q

what NTs are adronreceptors sensitive to?

A

all adrenoceptors are sensitive to adrenaline and noradrenaline

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24
Q

what are the two main types of adrenoreceptors?

A

alpha and beta

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25
Q

where are alpha 1 adrenoceptors found?

A

primarily on blood vessels

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26
Q

alpha 1 receptors mechanism of action

A

vasoconstriction of blood vessels
increase BP
dilate pupils
decrease GIT mobility

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27
Q

alpha 1 receptors effects

A

hypertension
blurred vision
constipation
urinary retention

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28
Q

alpha 1 receptors clinical uses

A

maintenance of BP in hypotension
these receptors can be targeted to reduce BP (prazosin) (alpha-1 receptor antagonist)
can be used as nasal decongestants

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29
Q

where are beta-1 adrenoreceptors primarily found?

A

on cardiac cells ( myocardium)

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30
Q

beta-1 receptors mechanism of action (what do they do to the body?)

A

increase heart rate and force of contraction

increased contractility = increased SV = increased CO = inc BP

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31
Q

beta-1 receptors effects

A

tachycardia

hypertension

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32
Q

beta-1 receptors clinical uses

A

used for cardiogenic shock resulting from AMI (positive inotropes)
can be targeted to reduce BP (atenolol)

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33
Q

which beta blockers are likely to cause nightmares, and which aren’t?

A

older beta blockers such as metoprolol and propranolol are lipophilic and therefore can cross the blood brain barrier, leading to the side effect of nightmares. newer generation beta bockers such as atenolol do not cross the BBB

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34
Q

where are beta-2 receptors primarily found?

A

smooth muscles of bronchioles

blood vessels within skeletal muscle, heart, kidneys and brain

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35
Q

beta-2 receptors mechanism of action (what do they do to the body?)

A

bronchodilation
increased skeletal muscle excitability (tremors)
vasodilation of blood vessels in skeletal muscle

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36
Q

beta-2 receptors effects

A

tremors

warmth (flushing)

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37
Q

beta-2 receptors clinical uses

A

used in pts with respiratory conditions to reverse bronchoconstriction

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38
Q

while drugs have some specificity to receptors, they will still bind to similar receptors to some extent.

A

so a beta blocker will be an antagonist significantly at beta-1 receptors, but also have some effect at beta-2 receptors.

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39
Q

main acute complications of DM?

A
  1. hypoglycaemia
  2. hyperglycaemia in very unwell patients
  3. DKA
  4. HHK (hyperosmolar hyperglycaemic state/syndrome)
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40
Q

early signs and symptoms of hypoglycaemia?

A 
BGLs < 4 mmol/L
hunger
trembling
sweating
weakness
headache
dizziness
pallor
cool, clammy skin
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41
Q

later signs and symptoms of hypoglycaemia?

A 
difficulty concentrating
blurred vision/ other vision problems 
anxiety
seizures
altered state of consciousness
coma
death
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42
Q

treatment for a mild hypo episode ( < 4mmol/L)?

A

15-20g fast acting carb
recheck BGL >4mmol/L
20g slow acting carb to maintain BGLs

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43
Q

examples of 15-20g fast-acting carbs?

A

150ml OJ
1/2 can soft drink
6-7 jelly beans
3 tsp sugar or honey

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44
Q

examples of 20g slow-acting carbs?

A 
1 slice bread
1/2 bowl cereal
glass of milk
med sized piece fruit (ie apple, pear)
sml pot of sugary yoghurt
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45
Q

treatment for severe hypo?

A

do not give food if swallowing may be compromised
call for help
position on side
IV dextrose bolus if possible
IM glucagon if no IV access
follow with IV dextrose as soon as possible
once stabilised, follow up with slow-acting carbs

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46
Q

common reaction to IM glucagon?

A

vomiting

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47
Q

why is hyperglycaemia a common complication of DM in patients who are very unwell?

A

because the inflammatory process and immune response cause the release of cortisol, noradrenaline and glycagon, which can cause BGLs to spike

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48
Q

what are diabetic ‘sick day’ rules?

A

because of risk of hyperglycaemia triggered by immune/inflammatory responses, BGLs must be checked much more frequently

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49
Q

how quickly does DKA develop?

A

over a few hours to days

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50
Q

risk factors for developing DKA?

A

new diagnosis
acute stress or illness
missing insulin doses
lack of access to medical care

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51
Q

lab markers for DKA

A 
BGLS > 11 mmol/L
ketones present in blood and urine
pH > 7.3
HCO3 > 15mmol/L
Na+ and K+ changes
high serum osmolality
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52
Q

early signs and symptoms of DKA

A

polyuria
polydipsia
acetone/fruity breath

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53
Q

later signs and symptoms of DKA

A

signs of dehydration such as sunken eyes, tachycardia, dry mucous membranes, headache

kussmaul’s respirations

fatigue and lethargy

abdo pain, nausea and vomiting

seizures

coma

potential heart and kidney issues

54
Q

management of DKA?

A
  1. correction of dehydration (IVT)
  2. reverse ketosis by administering insulin
  3. acid-base and electrolyte corrections
  4. nurse the patient at 30 degrees to reduce risk of cerebral oedema
  5. nil by mouth
  6. strict RIB
  7. strict FBC
  8. cardiac monitoring
  9. treat underlying cause
55
Q

why must dehydration be corrected slowly in management of DKA?

A

to avoid cerebral oedema (rapid rehydration could cause a dramatic shift of fluid from the extracellular space to the intracellular space, resulting in cerebral oedema)

56
Q

why must dehydration be corrected before administration of insulin in management of DKA?

A

inadequate blood volume = inadequate perfusion of tissues = poor transport of insulin to tissues = insulin unable to be utilised by body

57
Q

how long should it take to correct dehydration in management of patients with DKA?

A

24 - 72 hrs

58
Q

what should be administered alongside IV insulin in management of DKA?

A

IV dextrose, to avoid risk of hypoglycaemia, with or without potassium chloride depending on their lab values

59
Q

what is involved with correcting acid-base and electrolyte imbalances in management of DKA?

A

1/24 BGLs and 1-4/24 ABGs (blood gases)

checking ketones in urines

close monitoring of UandEs (especially K+ and Na+)

60
Q

UECs

A

urea, electrolytes, creatine

61
Q

when should oral fluids and subcut insulin be reintroduced in DKA?

A

when DKA has resolved and significant clinical improvement shown

62
Q

timeframe for development of HHS?

A

days to weeks

63
Q

which tends to be more serious - DKA or HHS? which is more common?

A

HHS is rarer but higher mortality

dehydration and metabolic issues are more severe

64
Q

characteristics of HHS?

A 
severe hyperglycaemia
severe dehydration, hypovolaemia
high serum osmolality
very unwell
no significant ketoacidosis
65
Q

HHS mortality rate?

A

5-10%

66
Q

risk factors for HHS?

A

Elderly – reduced thirst or fluid intake

Non-compliance or missed doses

Poorly controlled Type 2 diabetes

Infection and illness (MI, stroke, sepsis) – hyperglycaemia

Drugs that reduce insulin action (glucocorticoids)

67
Q

acute complications of type 1 DM?

A

DKA

hypoglycaemia

68
Q

how many types of insulin are there in australia? what are they?

A

five

rapid-acting (ultra short)
short-acting
intermediate-acting
long-acting
mixed
69
Q

rapid-acting insulin - examples

A

novolog
novorapid
apidra
humalog

70
Q

rapid-acting insulin - onset/peak/duration?

A

onset - 10 - 30mins
peak - 30mins - 3hrs
duration - 3 - 5hrs

71
Q

short-acting insulin - examples?

A

Actrapid

Humulin R

72
Q

short-acting insulin - onset/peak/duration?

A

onset - 30mins - 1hr
peak - 2 - 5hrs
duration - 6 - 8hrs

73
Q

intermediate-acting insulin - examples?

A

Humulin NPH

Protaphane

74
Q

intermediate-acting insulin - onset/peak/duration?

A

onset - 1.5 - 4hrs
peak - 4 - 12hrs
duration - up to 24hrs

75
Q

long-acting insulin - examples?

A

Lantus (glargine)

Levemir

76
Q

long-acting insulin - onset/peak/duration?

A

onset - 0.8 - 4 hours
peak - minimal peak
duration - up to 24hrs

77
Q

which insulins are basal insulins?

A

intermediate-acting

long-acting

78
Q

why might a person with type 2 DM need to take insulin?

A

acute illness or stress eg. surgery, pregnancy etc

oral hypoglycaemic agents become less effective in maintaining normal BGL over time

pancreas becomes unable to produce sufficient insulin due to the increasing insulin resistance

non-adherence to diet and exercise can lead to persistent hyperglycaemia that requires insulin

79
Q

what are the goals of management of type 2 DM?

A

prevent complications

optimise quality of life

80
Q

first line management of type 2 DM?

A

diet, exercise and education

81
Q

how many classes of OHAs are there?

A

seven (though technically one is an injectable)

82
Q

what are the two main classes of OHAs?

A

biguanides and sulfonylureas

83
Q

what drug class is metformin?

A

biguanides

84
Q

examples of sulfonylureas?

A

gliclazide
glimepiride
glibenclamide

85
Q

nursing considerations for metformin

A

should be withheld during acute illness

should be stopped 24hrs prior to investigations using contrast

shouldn’t be used in pts with renal impairment (where GFR < 30)

can cause GIT side effects

86
Q

nursing considerations for sulfonylureas?

A

can cause hypoglycaemia, sometimes prolonged, especially in the elderly

can cause weight gain

87
Q

mechanism of action of metformin?

A

increases insulin sensitivity by increasing peripheral glucose uptake

decreases hepatic glucose production

decreases intestinal absorption of glucose

88
Q

mechanism of action of sulfonylureas?

A

increase insulin secretion

89
Q

advantages of metformin?

A

doesn’t cause hypoglycaemia

doesn’t cause weight gain, may even help with weight loss

90
Q

what is an AVPU assessment?

A

Alert
responds to Verbal commands
responds to Pain
Unresponsive

modified version GCS to test for LOC, usually in emergency situations

91
Q

what are the chemical mediators that are released as part of the inflammatory process?

A

prostaglandins
bradykinins
histamines
leukatrienes

92
Q

what causes pain in inflammation?

A

chemical mediators (bradykinin and prostaglandin) stimulate nerve endings called nociceptors to produce pain

93
Q

what is released by the phospholipid bilayer when a cell injury occurs?

A

arachidonic acid

94
Q

what is the role of arachidonic acid in the inflammatory process?

A

it’s metabolised by cox-1 and cox-2 enzymes to make thromboxanes and prostaglandins

it’s metabolised by LOX enzymes to make leukotrienes

95
Q

what do thromboxanes do in the body?

A

encourage clotting - important in platelet aggregation, also vasoconstriction

96
Q

what do prostaglandins do in the inflammatory process?

A

powerful vasodilators

cause fever

hyperalgesic (augment the effect of bradykinin to increase pain)

enhance effect of bradykinin and histamine

97
Q

what are some of the other roles of prostaglandins in the body?

A

production of stomach mucus
reduction of stomach secretions
regulation of renal blood flow
inhibition of platelet aggregation

DIFFERENT PROSTAGLANDINS DO DIFFERENT THINGS IN THE BODY!

98
Q

what is arachidonic acid metabolised into by cox enzymes before being converted into prostaglandins and thromboxane?

A

cyclic endoperoxides

99
Q

what do leukotrienes do?

A

cause bronchoconstriction

potent - increase vascular permeability in the inflammatory process

100
Q

what happens to the production of prostaglandins and thromboxanes during inflammatory response?

A

synthesis is increased

these chemicals are normally present in the body to allow for normal function though

101
Q

symbols for thromboxane and prostaglandins?

A

TXA2 and PGs

102
Q

homeostatic role of PGs in clotting?

A

PGI2 inhibits platelet aggregation (balance between this PG and TXA2 needed to maintain blood clotting homeostasis)

103
Q

difference between cox-1 and cox-2 enzymes?

A

cox-1 is responsible for producing PGs that are involved in normal homeostatic processes

cox-2 is only produced in inflammation and produces the inflammatory PGs

104
Q

what are the steps in the mechanism of nociception?

A
  1. transduction
  2. transmission
  3. perception
  4. modulation
105
Q

what is the mechanism of action on NSAIDs?

A

cox inhibitors

106
Q

four major properties of NSAIDs?

A

analgesic
anti-pyretic
anti-inflammatory
anti-platelet

107
Q

what effect does taking NSAIDs have on leukotrienes? what effect may this have on the body?

A

increases synthesis of leukotrienes as more arachadonic acid is available for conversion.

leukotrienes increase bronchoconstriction, and may exacerbate asthma or COPD

108
Q

what drug class does asprin belong to? mechanism of action?

A

salicylates

irreversibly non competitive inhibition of cox enzymes

109
Q

asprin: adverse effects?

A

gastric ulceration and bleed

renal damage and failure

increased bleeding time

can promote allergies/respiratory reactions (bronchoconstriction)

tinnitus

reye’s syndrome

110
Q

how long does it take for platelet function to return to normal after taking asprin?

A

about 1 week

111
Q

difference between ibuprofen/naproxen and dicoflenac?

A

diclofenac much more potent anti-inflammatory effects, but not as well tolerated

112
Q

how can the adverse effects of ibuprofen and other NSAIDs on the GIT be reduced?

A

by using in combination with paracetamol, in order to reduce the doses required

113
Q

when should selective cox-2 inhibitors (coxibs) be avoided and why?

A

in pts at risk of cardiac disease/history

increases production of thromboxanes which makes blood more liable to clotting, increasing risk of MI

114
Q

what are coxibs?

A

selective cox-2 inhibitors

they block the production of PGs with inflammatory effects without affecting the synthesis of PGs that regulate GIT/kidney etc

115
Q

mechanism of action of paracetamol?

A

inhibits PGS in the CNS rather than peripherally

exact mechanism of action is unknown

116
Q

effects of paracetamol?

A

excellent anti-pyretic
analgesic

no anti-inflammatory effects because it works in the CNS rather than locally

117
Q

clinical manifestations of type 1 and type 2 DM: commonalities?

A

hyperglycaemia
3 Ps - polyphagia, polydipsia and polyuria
fatigue

118
Q

clinical manifestations of type 1 DM not type 2?

A

weight loss
anxiety
tremor

119
Q

clinical manifestations of type 2 DM not type 1?

A

can be asymptomatic
poor wound healing
blurry vision

120
Q

lab markers of HHS?

A 
BGL > 30mmol/L
Ketones can be present/absent 
pH > 7.3, 
HCO3- >15mmol/L
K+ and Na+ changes
High serum osmolality
121
Q

early signs and symptoms of HHS?

A

polyuria

polydipsia

122
Q

later signs and symptoms of HHS?

A 
Sunken eyes 
Tachycardia 
Hypotension
Dry skin 
Headache 
Weakness
Cramps
Fatigue and lethargy 
Abdominal pain, 
N+V 
Seizures
Altered LOC
Coma
123
Q

treatment for HHS?

A

same as for DKA

124
Q

how are sick days managed in type 1 DM?

A 
continue (possibly increase) insulin
frequent monitoring of BGLs
monitor ketones
increased fluids
ketones + vomiting = trip to hospital
important to keep up carb intake
125
Q

In patients who have diabetes, at what time of day does a hypoglycaemic state commonly occur?

A

overnight

126
Q

what proportion of cases of DM in australia are type 1?

A

10%

127
Q

what proportion of cases of DM in australia are type 2?

A

85%

128
Q

prevalence of DM in aboriginal and torres strait islanders?

A

One in five Aboriginal and Torres Strait Islander people > 25 years have diabetes

129
Q

ethnic groups with higher risk of DM?

A

Pacific Islander
South Asian
Chinese
ATSI

130
Q

risk factors for type 2 DM?

A

non-modifiable:
genetics
age
ethnicity

modifiable:
obesity (especially abdominal adiposity)
sedentary lifestyle
poor diet
calorie intake greater than energy expenditure
131
Q

classes of oral hypoglycaemic agents?

A 
Biguanides
Sulphonylureas
Thiazolidinediones (Glitazones)
Alpha-glucosidase Inhibitors.
Dipeptidyl peptidase 4 (DPP4) inhibitors
Incretin mimetics
Sodium-glucose transporter (SGLT2) inhibitors

semester 2 2019 (16 decks)

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