265 (medical nursing) Flashcards
(131 cards)
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
2
Q
what is hypo unawareness?
A
when BGLs are below 3.5 mmol but no symptoms are experienced
3
Q
at what BGL measurement should a person be treated for hypoglycaemia?
A
3.9 mmol
4
Q
what can cause hypoglycaemia?
A
- too much insulin
- vigorous exercise without extra carbohydrate
- missed or delayed meals
- not eating enough carbohydrates
- alcohol intake
- malnutrition
5
Q
ketones: normal range?
A
0.0 - 0.6 mmol
6
Q
signs and symptoms of DKA?
A
- High blood glucose levels with ketones present
- Tummy pain
- Vomiting
- Dehydration
- Rapid, shallow breathing
- Acetone smell on the breath
- Confusion
- Drowsiness which may lead to coma
7
Q
when should ketones be checked?
A
when BGL is 15mmol or above
when child is unwell, regardless of BGL
8
Q
at what level of ketones is action required?
A
when greater than 1 mmol, or 0.6 mmol if using a pump
9
Q
which insulin should be cloudy?
A
intermediate-acting insulin
10
Q
what is target BGL range?
A
4.0 - 7.0 mmol/L before main meals
11
Q
what is target HbA1c range?
A
HbA1c target is < 58 mmol/mol (<7%)
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
13
Q
what is an agonist?
A
a chemical which binds to receptors activates them.
14
Q
what is an antagonist?
A
a chemical which bind to receptors and prevents them from being activated
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)
16
Q
classic signs of opioid overdose?
A
pinpoint pupils
respiratory depression
oversedation
17
Q
what systems in the body control all physiological processes? via what mechanisms?
A
endocrine system via hormones
nervous system via neurotransmitters
18
Q
what neurotransmitter do cholinergic nerves release?
A
ACh
19
Q
what is the main neurotransmitter adrenergic nerves release?
A
noradrenaline
20
Q
what are the other important neurotransmitters do adrenergic nerves release?
A
adrenaline
dopamine
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
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
23
Q
what NTs are adronreceptors sensitive to?
A
all adrenoceptors are sensitive to adrenaline and noradrenaline
24
Q
what are the two main types of adrenoreceptors?
A
alpha and beta
25
where are alpha 1 adrenoceptors found?
primarily on blood vessels
26
alpha 1 receptors mechanism of action
vasoconstriction of blood vessels
increase BP
dilate pupils
decrease GIT mobility
27
alpha 1 receptors effects
hypertension
blurred vision
constipation
urinary retention
28
alpha 1 receptors clinical uses
maintenance of BP in hypotension
these receptors can be targeted to reduce BP (prazosin) (alpha-1 receptor antagonist)
can be used as nasal decongestants
29
where are beta-1 adrenoreceptors primarily found?
on cardiac cells ( myocardium)
30
beta-1 receptors mechanism of action (what do they do to the body?)
increase heart rate and force of contraction
| increased contractility = increased SV = increased CO = inc BP
31
beta-1 receptors effects
tachycardia
| hypertension
32
beta-1 receptors clinical uses
used for cardiogenic shock resulting from AMI (positive inotropes)
can be targeted to reduce BP (atenolol)
33
which beta blockers are likely to cause nightmares, and which aren't?
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
34
where are beta-2 receptors primarily found?
smooth muscles of bronchioles
| blood vessels within skeletal muscle, heart, kidneys and brain
35
beta-2 receptors mechanism of action (what do they do to the body?)
bronchodilation
increased skeletal muscle excitability (tremors)
vasodilation of blood vessels in skeletal muscle
36
beta-2 receptors effects
tremors
| warmth (flushing)
37
beta-2 receptors clinical uses
used in pts with respiratory conditions to reverse bronchoconstriction
38
while drugs have some specificity to receptors, they will still bind to similar receptors to some extent.
so a beta blocker will be an antagonist significantly at beta-1 receptors, but also have some effect at beta-2 receptors.
39
main acute complications of DM?
1. hypoglycaemia
2. hyperglycaemia in very unwell patients
3. DKA
4. HHK (hyperosmolar hyperglycaemic state/syndrome)
40
early signs and symptoms of hypoglycaemia?
```
BGLs < 4 mmol/L
hunger
trembling
sweating
weakness
headache
dizziness
pallor
cool, clammy skin
```
41
later signs and symptoms of hypoglycaemia?
```
difficulty concentrating
blurred vision/ other vision problems
anxiety
seizures
altered state of consciousness
coma
death
```
42
treatment for a mild hypo episode ( < 4mmol/L)?
15-20g fast acting carb
recheck BGL >4mmol/L
20g slow acting carb to maintain BGLs
43
examples of 15-20g fast-acting carbs?
150ml OJ
1/2 can soft drink
6-7 jelly beans
3 tsp sugar or honey
44
examples of 20g slow-acting carbs?
```
1 slice bread
1/2 bowl cereal
glass of milk
med sized piece fruit (ie apple, pear)
sml pot of sugary yoghurt
```
45
treatment for severe hypo?
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
46
common reaction to IM glucagon?
vomiting
47
why is hyperglycaemia a common complication of DM in patients who are very unwell?
because the inflammatory process and immune response cause the release of cortisol, noradrenaline and glycagon, which can cause BGLs to spike
48
what are diabetic 'sick day' rules?
because of risk of hyperglycaemia triggered by immune/inflammatory responses, BGLs must be checked much more frequently
49
how quickly does DKA develop?
over a few hours to days
50
risk factors for developing DKA?
new diagnosis
acute stress or illness
missing insulin doses
lack of access to medical care
51
lab markers for DKA
```
BGLS > 11 mmol/L
ketones present in blood and urine
pH > 7.3
HCO3 > 15mmol/L
Na+ and K+ changes
high serum osmolality
```
52
early signs and symptoms of DKA
polyuria
polydipsia
acetone/fruity breath
53
later signs and symptoms of DKA
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
management of DKA?
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
why must dehydration be corrected slowly in management of DKA?
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
why must dehydration be corrected before administration of insulin in management of DKA?
inadequate blood volume = inadequate perfusion of tissues = poor transport of insulin to tissues = insulin unable to be utilised by body
57
how long should it take to correct dehydration in management of patients with DKA?
24 - 72 hrs
58
what should be administered alongside IV insulin in management of DKA?
IV dextrose, to avoid risk of hypoglycaemia, with or without potassium chloride depending on their lab values
59
what is involved with correcting acid-base and electrolyte imbalances in management of DKA?
1/24 BGLs and 1-4/24 ABGs (blood gases)
checking ketones in urines
close monitoring of UandEs (especially K+ and Na+)
60
UECs
urea, electrolytes, creatine
61
when should oral fluids and subcut insulin be reintroduced in DKA?
when DKA has resolved and significant clinical improvement shown
62
timeframe for development of HHS?
days to weeks
63
which tends to be more serious - DKA or HHS? which is more common?
HHS is rarer but higher mortality
dehydration and metabolic issues are more severe
64
characteristics of HHS?
```
severe hyperglycaemia
severe dehydration, hypovolaemia
high serum osmolality
very unwell
no significant ketoacidosis
```
65
HHS mortality rate?
5-10%
66
risk factors for HHS?
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
acute complications of type 1 DM?
DKA
| hypoglycaemia
68
how many types of insulin are there in australia? what are they?
five
```
rapid-acting (ultra short)
short-acting
intermediate-acting
long-acting
mixed
```
69
rapid-acting insulin - examples
novolog
novorapid
apidra
humalog
70
rapid-acting insulin - onset/peak/duration?
onset - 10 - 30mins
peak - 30mins - 3hrs
duration - 3 - 5hrs
71
short-acting insulin - examples?
Actrapid
| Humulin R
72
short-acting insulin - onset/peak/duration?
onset - 30mins - 1hr
peak - 2 - 5hrs
duration - 6 - 8hrs
73
intermediate-acting insulin - examples?
Humulin NPH
| Protaphane
74
intermediate-acting insulin - onset/peak/duration?
onset - 1.5 - 4hrs
peak - 4 - 12hrs
duration - up to 24hrs
75
long-acting insulin - examples?
Lantus (glargine)
| Levemir
76
long-acting insulin - onset/peak/duration?
onset - 0.8 - 4 hours
peak - minimal peak
duration - up to 24hrs
77
which insulins are basal insulins?
intermediate-acting
| long-acting
78
why might a person with type 2 DM need to take insulin?
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
what are the goals of management of type 2 DM?
prevent complications
optimise quality of life
80
first line management of type 2 DM?
diet, exercise and education
81
how many classes of OHAs are there?
seven (though technically one is an injectable)
82
what are the two main classes of OHAs?
biguanides and sulfonylureas
83
what drug class is metformin?
biguanides
84
examples of sulfonylureas?
gliclazide
glimepiride
glibenclamide
85
nursing considerations for metformin
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
nursing considerations for sulfonylureas?
can cause hypoglycaemia, sometimes prolonged, especially in the elderly
can cause weight gain
87
mechanism of action of metformin?
increases insulin sensitivity by increasing peripheral glucose uptake
decreases hepatic glucose production
decreases intestinal absorption of glucose
88
mechanism of action of sulfonylureas?
increase insulin secretion
89
advantages of metformin?
doesn't cause hypoglycaemia
doesn't cause weight gain, may even help with weight loss
90
what is an AVPU assessment?
Alert
responds to Verbal commands
responds to Pain
Unresponsive
modified version GCS to test for LOC, usually in emergency situations
91
what are the chemical mediators that are released as part of the inflammatory process?
prostaglandins
bradykinins
histamines
leukatrienes
92
what causes pain in inflammation?
chemical mediators (bradykinin and prostaglandin) stimulate nerve endings called nociceptors to produce pain
93
what is released by the phospholipid bilayer when a cell injury occurs?
arachidonic acid
94
what is the role of arachidonic acid in the inflammatory process?
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
what do thromboxanes do in the body?
encourage clotting - important in platelet aggregation, also vasoconstriction
96
what do prostaglandins do in the inflammatory process?
powerful vasodilators
cause fever
hyperalgesic (augment the effect of bradykinin to increase pain)
enhance effect of bradykinin and histamine
97
what are some of the other roles of prostaglandins in the body?
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
what is arachidonic acid metabolised into by cox enzymes before being converted into prostaglandins and thromboxane?
cyclic endoperoxides
99
what do leukotrienes do?
cause bronchoconstriction
potent - increase vascular permeability in the inflammatory process
100
what happens to the production of prostaglandins and thromboxanes during inflammatory response?
synthesis is increased
these chemicals are normally present in the body to allow for normal function though
101
symbols for thromboxane and prostaglandins?
TXA2 and PGs
102
homeostatic role of PGs in clotting?
PGI2 inhibits platelet aggregation (balance between this PG and TXA2 needed to maintain blood clotting homeostasis)
103
difference between cox-1 and cox-2 enzymes?
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
what are the steps in the mechanism of nociception?
1. transduction
2. transmission
3. perception
4. modulation
105
what is the mechanism of action on NSAIDs?
cox inhibitors
106
four major properties of NSAIDs?
analgesic
anti-pyretic
anti-inflammatory
anti-platelet
107
what effect does taking NSAIDs have on leukotrienes? what effect may this have on the body?
increases synthesis of leukotrienes as more arachadonic acid is available for conversion.
leukotrienes increase bronchoconstriction, and may exacerbate asthma or COPD
108
what drug class does asprin belong to? mechanism of action?
salicylates
irreversibly non competitive inhibition of cox enzymes
109
asprin: adverse effects?
gastric ulceration and bleed
renal damage and failure
increased bleeding time
can promote allergies/respiratory reactions (bronchoconstriction)
tinnitus
reye’s syndrome
110
how long does it take for platelet function to return to normal after taking asprin?
about 1 week
111
difference between ibuprofen/naproxen and dicoflenac?
diclofenac much more potent anti-inflammatory effects, but not as well tolerated
112
how can the adverse effects of ibuprofen and other NSAIDs on the GIT be reduced?
by using in combination with paracetamol, in order to reduce the doses required
113
when should selective cox-2 inhibitors (coxibs) be avoided and why?
in pts at risk of cardiac disease/history
increases production of thromboxanes which makes blood more liable to clotting, increasing risk of MI
114
what are coxibs?
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
mechanism of action of paracetamol?
inhibits PGS in the CNS rather than peripherally
exact mechanism of action is unknown
116
effects of paracetamol?
excellent anti-pyretic
analgesic
no anti-inflammatory effects because it works in the CNS rather than locally
117
clinical manifestations of type 1 and type 2 DM: commonalities?
hyperglycaemia
3 Ps - polyphagia, polydipsia and polyuria
fatigue
118
clinical manifestations of type 1 DM not type 2?
weight loss
anxiety
tremor
119
clinical manifestations of type 2 DM not type 1?
can be asymptomatic
poor wound healing
blurry vision
120
lab markers of HHS?
```
BGL > 30mmol/L
Ketones can be present/absent
pH > 7.3,
HCO3- >15mmol/L
K+ and Na+ changes
High serum osmolality
```
121
early signs and symptoms of HHS?
polyuria
| polydipsia
122
later signs and symptoms of HHS?
```
Sunken eyes
Tachycardia
Hypotension
Dry skin
Headache
Weakness
Cramps
Fatigue and lethargy
Abdominal pain,
N+V
Seizures
Altered LOC
Coma
```
123
treatment for HHS?
same as for DKA
124
how are sick days managed in type 1 DM?
```
continue (possibly increase) insulin
frequent monitoring of BGLs
monitor ketones
increased fluids
ketones + vomiting = trip to hospital
important to keep up carb intake
```
125
In patients who have diabetes, at what time of day does a hypoglycaemic state commonly occur?
overnight
126
what proportion of cases of DM in australia are type 1?
10%
127
what proportion of cases of DM in australia are type 2?
85%
128
prevalence of DM in aboriginal and torres strait islanders?
One in five Aboriginal and Torres Strait Islander people > 25 years have diabetes
129
ethnic groups with higher risk of DM?
Pacific Islander
South Asian
Chinese
ATSI
130
risk factors for type 2 DM?
non-modifiable:
genetics
age
ethnicity
```
modifiable:
obesity (especially abdominal adiposity)
sedentary lifestyle
poor diet
calorie intake greater than energy expenditure
```
131
classes of oral hypoglycaemic agents?
```
Biguanides
Sulphonylureas
Thiazolidinediones (Glitazones)
Alpha-glucosidase Inhibitors.
Dipeptidyl peptidase 4 (DPP4) inhibitors
Incretin mimetics
Sodium-glucose transporter (SGLT2) inhibitors
```
