priority cards Flashcards
where are alpha 1 adrenoceptors found?
primarily on blood vessels
what are the two main types of adrenoreceptors?
alpha and beta
what does activation of alpha 1 receptors cause?
vasoconstriction of blood vessels
increase BP
dilate pupils
decrease GIT mobility
what are the negative effects of too much activation of alpha 1 receptors?
hypertension
blurred vision
constipation
urinary retention
effects of meds that target alpha 1 receptors?
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
what are the negative effects of too much activation of beta-1 receptors?
tachycardia
hypertension
effects of meds that target beta-1 receptors?
used for cardiogenic shock resulting from AMI (positive inotropes) (agonist)
can be targeted to reduce BP (atenolol) (antagonist)
where are beta-2 receptors primarily found?
smooth muscles of bronchioles
blood vessels within skeletal muscle, heart, kidneys and brain
what does activation of beta-2 receptors cause?
bronchodilation
increased skeletal muscle excitability (tremors)
vasodilation of blood vessels in skeletal muscle
what are the negative effects of too much activation of beta-2 receptors?
tremors
warmth (flushing)
effects of meds that target beta-2 receptors?
used in pts with respiratory conditions to reverse bronchoconstriction
causes of type 1 diabetes?
autoimmune,
genetic factors,
idiopathic,
viral infections/other damage to beta cells
causes of type 2 diabetes?
obesity, sedentary lifestyle,
pathophysiology of type 1 diabetes?
- immune response leads to destruction of pancreatic beta cells
- no insulin produced,
- GLUT-4 receptors cannot be activated
- no glucose uptake into cells (high BGLs)
- increased hepatic production/release of stored glucose, increased release of stored glucose from muscles
- increased BGLs - (positive feedback loop worsens hyperglycaemia)
pathophysiology of type 2 diabetes?
- increased adipose tissue leads to increase in FFAs
- leads to chronic low grade inflammation
- leads to oxidative stress, cell damage
- increases insulin resistance at a cellular level
- impaired insulin uptake and utilisation = excess hepatic glucose production/use of stored glycogen from muscles
- hyperglycaemia -> type 2 DM
- ongoing insulin resistance causes beta cell dysfunction in pancreas, less insulin produced, vicious cycle
pathophysiology behind the 3Ps is type 1 diabetes?
polyuria - high filtrate osmolarity, increased water loss through kidneys
polydipsia - dehydration from increased water loss at kidneys + high BGL = high blood osmolarity = increased thirst
polyphagia - brain signals body to eat because cells are starving for glucose
signs and symptoms of type 2 diabetes?
often asymptomatic, but will manifest the 3Ps to a lesser extent, also fatigue
acute complications of type 1 diabetes?
hypoglycaemia, DKA
acute complications of type 2 diabetes?
HHS (hyperosmolar hyperglycaemic state), hypoglycaemia
management of type 1 diabetes?
insulin, monitoring of BGLs
management of type 2 diabetes?
lifestyle changes (diet, exercise), OHAs, insulin
routes of admin for insulin?
subcut, IV
signs and symptoms of type 1 diabetes?
polyuria polyphasia polydipsia weight loss fatigue headache weakness nausea and vomiting abdominal pain
what are the mechanisms of insulin resistance in type 2 DM?
insulin resistance due to the following mechanisms:
- a reduction in the number of insulin binding sites or a decrease in the amount of insulin binding to receptors
- decreased beta cell responsivity to increased glucose levels = decreased insulin production
how does DKA occur?
- insulin deficiency - absolute or relative
- persistent hyperglycaemia
- glucosuria, concurrent loss of water and electrolytes in urine
- leads to dehydration, hypovolaemia
- increases lactate (direct contributor to acidiosis), also increases breakdown of fats into FFAs which are broken down into ketones and acetone, causing acidosis
how many points would you make in an answer to a question worth five marks?
5
management of DKA or HHS?
- correction of dehydration (IVT)
- reverse hyperglycaemia by administering insulin
- acid-base and electrolyte corrections
- cardiac monitoring
- 1/24 obs, 1-4/24 ABGs
- nurse the patient at 30 degrees to reduce risk of cerebral oedema
- nil by mouth
- strict RIB
- strict FBC
- treat underlying cause
treatment for a mild hypo episode ( < 4mmol/L)?
15-20g fast acting carb
recheck BGL >4mmol/L
20g slow acting carb to maintain BGLs
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
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
Why would a patient with poorly managed diabetes be at risk of recurrent infections?
- Impaired vision due to retinal changes
- Neuropathy →decreased pain sensation → reduced early warning systems
- Skin breaks → hypoxia and decreased perfusion → reduced inflammatory response
- Increased glycosylated Hb impedes release of O2 to tissues
- High glucose environment excellent for sustaining microorganisms
Long term diabetes monitoring?
- Retinal screening
- Feet checks
- HbA1c
- Urine ACR
- GFR
- BP
- Lipid profile
- Dental health
- Mental health
rapid-acting insulin - examples
novolog
novorapid
apidra
humalog
short-acting insulin - examples?
Actrapid
Humulin R
how soon after taking rapid-acting insulin should a meal be eaten?
10-15 minutes prior to eating a meal
Must eat immediately after administration
how soon after taking short-acting insulin should a meal be eaten?
30 minutes prior to eating a meal
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
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
difference between atherosclerosis and arteriosclerosis?
Arteriosclerosis is the stiffening or hardening of the artery walls.
Atherosclerosis is the narrowing of the artery because of plaque build-up.
Atherosclerosis is a specific type of arteriosclerosis.
assessments to consider in a short answer question
rapid ABCD assessment should be done for all patients when you commence care - provides you with baseline
respiratory Ax -
peak expiratory flow rate to assess asthma severity & response to treatment
GSC/neuro obs should be done if there has been hypoxia
pain Ax - especially if pain including chest tightness has been mentioned
history taking - for example, medication history around asthma meds will indicate control/need for education
FBC
serum lactate
blood gases - arterial or venous
cultures - blood, sputum, urine, wound
UECs
CRP (c-reactive protein) - how inflamed the body is
clotting screen
fluid resus formula?
20 - 30mls per kg initially.
MAP formula
(SBP + 2xDBP) divided by 3
what does MAP represent?
how well-perfused the tissues are
what is assessed under D in an A-E assessment?
Disability:
level of consciousness
speech
pain
what is assessed under E in an A-E assessment?
Exposure:
body temperature
skin integrity
signs of pressure injury
wounds, dressings or drains, invasive lines
ability to transfer and mobilise
bowel movements
pathophysiology of atherosclerosis?
increased release of inflammatory cells which leads to increased vascular permeability –> monocytes and LDLs move into the endothelial layer –> macrophages engulf these –> foam cells produced –> plaque formation;
common side effects of ACE inhibitors?
dizziness headache drowsiness diarrhea low BP weakness cough rash
common side effects of beta blockers?
dizziness headache weakness. drowsiness or fatigue. cold hands and feet. dry mouth, skin, or eyes. upset stomach. diarrhea or constipation
common side effects of calcium channel blockers?
dizziness headache constipation, rash, nausea, flushing, oedema (fluid accumulation in tissues), drowsiness, low BP
MOA of calcium channel blockers?
they inhibit the influx of calcium into muscle cells of the heart and arteries, which interferes with the electrical signal which causes myocardial contraction, and prevents constriction of arteries
vasodilation reduces = decreased afterload = reduced oxygen requirements for heart
electrical conduction within myocardial cells = decreased contractility = reduced oxygen requirements
indications for CCBs?
HTN
angina
abnormal heart rhythms
subarachnoid haemorrhage
why are CCBs indicated for abnormal heart rhythms?
they slow electrical conduction through the heart and thereby correct abnormal rapid heartbeats
MOA of ace inhibitors?
they reduce the activity of ACE, preventing the conversion of angiotensin I into angiotensin II, leading to dilation of blood vessels, and thereby reducing blood pressure
also decreases aldosterone production = less fluid retention = decreased BP
indications for ACE inhibitors?
HTN congestive heart failure prevention of stroke diabetic nephropathy left ventricular dysfunction following MI
MOA of beta-blockers?
block adrenaline and noradrenaline from binding to beta-adrenergic receptors, decreasing heart rate and contractility = reduced cardiac workload
also, blocks beta-receptors in the kidneys, which decreases renal blood pressure and therefore release of renin
indications for beta-blockers?
HTN angina heart failure arrhythmias \+ more
what are the factors that affect myocardial oxygen demand?
- heart rate
- blood volume (preload)
- blood pressure (afterload)
- left ventricular muscle size
- muscle contractility
MOA of ARBs?
blocks angiotensin II receptors on vascular smooth muscle and adrenal cortex, reducing vasoconstriction and increasing renal blood flow
five clinical manifestations of asthma?
expiratory wheeze dyspnoea tachycardia hypoxaemia chest tightness SOB cough
why is AKI potentially life-threatening?
dues to electrolyte imbalances
common causes of AKI?
low fluid volume - dehydration, haemorrhage, CHF
nephrotoxic drugs - certain ABs, NSAIDs
