265 (medical nursing) Flashcards
what is true physiological hypoglycaemia measured at? what is considered hypoglycaemia in diabetes?
true physiological hypoglycaemia is a BGL below 3.5mmol but BGL below 4mmol is considered hypo for a diabetic
what is hypo unawareness?
when BGLs are below 3.5 mmol but no symptoms are experienced
at what BGL measurement should a person be treated for hypoglycaemia?
3.9 mmol
what can cause hypoglycaemia?
- too much insulin
- vigorous exercise without extra carbohydrate
- missed or delayed meals
- not eating enough carbohydrates
- alcohol intake
- malnutrition
ketones: normal range?
0.0 - 0.6 mmol
signs and symptoms of DKA?
- 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
when should ketones be checked?
when BGL is 15mmol or above
when child is unwell, regardless of BGL
at what level of ketones is action required?
when greater than 1 mmol, or 0.6 mmol if using a pump
which insulin should be cloudy?
intermediate-acting insulin
what is target BGL range?
4.0 - 7.0 mmol/L before main meals
what is target HbA1c range?
HbA1c target is < 58 mmol/mol (<7%)
what is a receptor?
a protein molecule found on the surface of a cell which receives chemical signals to produce a response from the cell
what is an agonist?
a chemical which binds to receptors activates them.
what is an antagonist?
a chemical which bind to receptors and prevents them from being activated
what is the difference between a competitive antagonist and a non-competitive antagonist?
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)
classic signs of opioid overdose?
pinpoint pupils
respiratory depression
oversedation
what systems in the body control all physiological processes? via what mechanisms?
endocrine system via hormones
nervous system via neurotransmitters
what neurotransmitter do cholinergic nerves release?
ACh
what is the main neurotransmitter adrenergic nerves release?
noradrenaline
what are the other important neurotransmitters do adrenergic nerves release?
adrenaline
dopamine
adrenoceptors - what division of the ANS are they associated with, what physiology effects do they have?
SNS - fight or flight- increase HR, BP, bronchodilation
cholinoceptors - what division of the ANS are they associated with, what physiology effects do they have?
PNS - rest and digest - decreased HR, increased urination, defecation, digestion
what NTs are adronreceptors sensitive to?
all adrenoceptors are sensitive to adrenaline and noradrenaline
what are the two main types of adrenoreceptors?
alpha and beta
where are alpha 1 adrenoceptors found?
primarily on blood vessels
alpha 1 receptors mechanism of action
vasoconstriction of blood vessels
increase BP
dilate pupils
decrease GIT mobility
alpha 1 receptors effects
hypertension
blurred vision
constipation
urinary retention
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
where are beta-1 adrenoreceptors primarily found?
on cardiac cells ( myocardium)
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
beta-1 receptors effects
tachycardia
hypertension
beta-1 receptors clinical uses
used for cardiogenic shock resulting from AMI (positive inotropes)
can be targeted to reduce BP (atenolol)
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
where are beta-2 receptors primarily found?
smooth muscles of bronchioles
blood vessels within skeletal muscle, heart, kidneys and brain
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
beta-2 receptors effects
tremors
warmth (flushing)
beta-2 receptors clinical uses
used in pts with respiratory conditions to reverse bronchoconstriction
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.
main acute complications of DM?
- hypoglycaemia
- hyperglycaemia in very unwell patients
- DKA
- HHK (hyperosmolar hyperglycaemic state/syndrome)
early signs and symptoms of hypoglycaemia?
BGLs < 4 mmol/L hunger trembling sweating weakness headache dizziness pallor cool, clammy skin
later signs and symptoms of hypoglycaemia?
difficulty concentrating blurred vision/ other vision problems anxiety seizures altered state of consciousness coma death
treatment for a mild hypo episode ( < 4mmol/L)?
15-20g fast acting carb
recheck BGL >4mmol/L
20g slow acting carb to maintain BGLs
examples of 15-20g fast-acting carbs?
150ml OJ
1/2 can soft drink
6-7 jelly beans
3 tsp sugar or honey
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
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
common reaction to IM glucagon?
vomiting
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
what are diabetic ‘sick day’ rules?
because of risk of hyperglycaemia triggered by immune/inflammatory responses, BGLs must be checked much more frequently
how quickly does DKA develop?
over a few hours to days
risk factors for developing DKA?
new diagnosis
acute stress or illness
missing insulin doses
lack of access to medical care
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
early signs and symptoms of DKA
polyuria
polydipsia
acetone/fruity breath
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
management of DKA?
- correction of dehydration (IVT)
- reverse ketosis by administering insulin
- acid-base and electrolyte corrections
- nurse the patient at 30 degrees to reduce risk of cerebral oedema
- nil by mouth
- strict RIB
- strict FBC
- cardiac monitoring
- treat underlying cause
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)
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
how long should it take to correct dehydration in management of patients with DKA?
24 - 72 hrs
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
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+)
UECs
urea, electrolytes, creatine
when should oral fluids and subcut insulin be reintroduced in DKA?
when DKA has resolved and significant clinical improvement shown
timeframe for development of HHS?
days to weeks
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
characteristics of HHS?
severe hyperglycaemia severe dehydration, hypovolaemia high serum osmolality very unwell no significant ketoacidosis
HHS mortality rate?
5-10%
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)
acute complications of type 1 DM?
DKA
hypoglycaemia
how many types of insulin are there in australia? what are they?
five
rapid-acting (ultra short) short-acting intermediate-acting long-acting mixed
rapid-acting insulin - examples
novolog
novorapid
apidra
humalog
rapid-acting insulin - onset/peak/duration?
onset - 10 - 30mins
peak - 30mins - 3hrs
duration - 3 - 5hrs
short-acting insulin - examples?
Actrapid
Humulin R
short-acting insulin - onset/peak/duration?
onset - 30mins - 1hr
peak - 2 - 5hrs
duration - 6 - 8hrs
intermediate-acting insulin - examples?
Humulin NPH
Protaphane
intermediate-acting insulin - onset/peak/duration?
onset - 1.5 - 4hrs
peak - 4 - 12hrs
duration - up to 24hrs
long-acting insulin - examples?
Lantus (glargine)
Levemir
long-acting insulin - onset/peak/duration?
onset - 0.8 - 4 hours
peak - minimal peak
duration - up to 24hrs
which insulins are basal insulins?
intermediate-acting
long-acting
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
what are the goals of management of type 2 DM?
prevent complications
optimise quality of life
first line management of type 2 DM?
diet, exercise and education
how many classes of OHAs are there?
seven (though technically one is an injectable)
what are the two main classes of OHAs?
biguanides and sulfonylureas
what drug class is metformin?
biguanides
examples of sulfonylureas?
gliclazide
glimepiride
glibenclamide
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
nursing considerations for sulfonylureas?
can cause hypoglycaemia, sometimes prolonged, especially in the elderly
can cause weight gain
mechanism of action of metformin?
increases insulin sensitivity by increasing peripheral glucose uptake
decreases hepatic glucose production
decreases intestinal absorption of glucose
mechanism of action of sulfonylureas?
increase insulin secretion
advantages of metformin?
doesn’t cause hypoglycaemia
doesn’t cause weight gain, may even help with weight loss
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
what are the chemical mediators that are released as part of the inflammatory process?
prostaglandins
bradykinins
histamines
leukatrienes
what causes pain in inflammation?
chemical mediators (bradykinin and prostaglandin) stimulate nerve endings called nociceptors to produce pain
what is released by the phospholipid bilayer when a cell injury occurs?
arachidonic acid
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
what do thromboxanes do in the body?
encourage clotting - important in platelet aggregation, also vasoconstriction
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
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!
what is arachidonic acid metabolised into by cox enzymes before being converted into prostaglandins and thromboxane?
cyclic endoperoxides
what do leukotrienes do?
cause bronchoconstriction
potent - increase vascular permeability in the inflammatory process
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
symbols for thromboxane and prostaglandins?
TXA2 and PGs
homeostatic role of PGs in clotting?
PGI2 inhibits platelet aggregation (balance between this PG and TXA2 needed to maintain blood clotting homeostasis)
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
what are the steps in the mechanism of nociception?
- transduction
- transmission
- perception
- modulation
what is the mechanism of action on NSAIDs?
cox inhibitors
four major properties of NSAIDs?
analgesic
anti-pyretic
anti-inflammatory
anti-platelet
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
what drug class does asprin belong to? mechanism of action?
salicylates
irreversibly non competitive inhibition of cox enzymes
asprin: adverse effects?
gastric ulceration and bleed
renal damage and failure
increased bleeding time
can promote allergies/respiratory reactions (bronchoconstriction)
tinnitus
reye’s syndrome
how long does it take for platelet function to return to normal after taking asprin?
about 1 week
difference between ibuprofen/naproxen and dicoflenac?
diclofenac much more potent anti-inflammatory effects, but not as well tolerated
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
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
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
mechanism of action of paracetamol?
inhibits PGS in the CNS rather than peripherally
exact mechanism of action is unknown
effects of paracetamol?
excellent anti-pyretic
analgesic
no anti-inflammatory effects because it works in the CNS rather than locally
clinical manifestations of type 1 and type 2 DM: commonalities?
hyperglycaemia
3 Ps - polyphagia, polydipsia and polyuria
fatigue
clinical manifestations of type 1 DM not type 2?
weight loss
anxiety
tremor
clinical manifestations of type 2 DM not type 1?
can be asymptomatic
poor wound healing
blurry vision
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
early signs and symptoms of HHS?
polyuria
polydipsia
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
treatment for HHS?
same as for DKA
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
In patients who have diabetes, at what time of day does a hypoglycaemic state commonly occur?
overnight
what proportion of cases of DM in australia are type 1?
10%
what proportion of cases of DM in australia are type 2?
85%
prevalence of DM in aboriginal and torres strait islanders?
One in five Aboriginal and Torres Strait Islander people > 25 years have diabetes
ethnic groups with higher risk of DM?
Pacific Islander
South Asian
Chinese
ATSI
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
classes of oral hypoglycaemic agents?
Biguanides Sulphonylureas Thiazolidinediones (Glitazones) Alpha-glucosidase Inhibitors. Dipeptidyl peptidase 4 (DPP4) inhibitors Incretin mimetics Sodium-glucose transporter (SGLT2) inhibitors
