priority cards

Question 1

where are alpha 1 adrenoceptors found?

Answer 1

primarily on blood vessels

Question 2

what are the two main types of adrenoreceptors?

Answer 2

alpha and beta

Question 3

what does activation of alpha 1 receptors cause?

Answer 3

vasoconstriction of blood vessels

increase BP

dilate pupils

decrease GIT mobility

Question 4

what are the negative effects of too much activation of alpha 1 receptors?

Answer 4

hypertension
blurred vision
constipation
urinary retention

Question 5

effects of meds that target alpha 1 receptors?

Answer 5

maintenance of BP in hypotension

these receptors can be targeted to reduce BP (prazosin) (alpha-1 receptor antagonist)

can be used as nasal decongestants

Question 6

where are beta-1 adrenoreceptors primarily found?

Answer 6

on cardiac cells ( myocardium)

Question 7

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

Answer 7

increase heart rate and force of contraction

increased contractility = increased SV = increased CO = inc BP

Question 8

what are the negative effects of too much activation of beta-1 receptors?

Answer 8

tachycardia

hypertension

Question 9

effects of meds that target beta-1 receptors?

Answer 9

used for cardiogenic shock resulting from AMI (positive inotropes) (agonist)

can be targeted to reduce BP (atenolol) (antagonist)

Question 10

where are beta-2 receptors primarily found?

Answer 10

smooth muscles of bronchioles

blood vessels within skeletal muscle, heart, kidneys and brain

Question 11

what does activation of beta-2 receptors cause?

Answer 11

bronchodilation

increased skeletal muscle excitability (tremors)

vasodilation of blood vessels in skeletal muscle

Question 12

what are the negative effects of too much activation of beta-2 receptors?

Answer 12

tremors

warmth (flushing)

Question 13

effects of meds that target beta-2 receptors?

Answer 13

used in pts with respiratory conditions to reverse bronchoconstriction

Question 14

causes of type 1 diabetes?

Answer 14

autoimmune,
genetic factors,
idiopathic,
viral infections/other damage to beta cells

Question 15

causes of type 2 diabetes?

Answer 15

obesity, sedentary lifestyle,

Question 16

pathophysiology of type 1 diabetes?

Answer 16

1. immune response leads to destruction of pancreatic beta cells
2. no insulin produced,
3. GLUT-4 receptors cannot be activated
4. no glucose uptake into cells (high BGLs)
5. increased hepatic production/release of stored glucose, increased release of stored glucose from muscles
6. increased BGLs - (positive feedback loop worsens hyperglycaemia)

Question 17

pathophysiology of type 2 diabetes?

Answer 17

1. increased adipose tissue leads to increase in FFAs
2. leads to chronic low grade inflammation
3. leads to oxidative stress, cell damage
4. increases insulin resistance at a cellular level
5. impaired insulin uptake and utilisation = excess hepatic glucose production/use of stored glycogen from muscles
6. hyperglycaemia -> type 2 DM
7. ongoing insulin resistance causes beta cell dysfunction in pancreas, less insulin produced, vicious cycle

Question 18

pathophysiology behind the 3Ps is type 1 diabetes?

Answer 18

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

Question 19

signs and symptoms of type 2 diabetes?

Answer 19

often asymptomatic, but will manifest the 3Ps to a lesser extent, also fatigue

Question 20

acute complications of type 1 diabetes?

Answer 20

hypoglycaemia, DKA

Question 21

acute complications of type 2 diabetes?

Answer 21

HHS (hyperosmolar hyperglycaemic state), hypoglycaemia

Question 22

management of type 1 diabetes?

Answer 22

insulin, monitoring of BGLs

Question 23

management of type 2 diabetes?

Answer 23

lifestyle changes (diet, exercise), OHAs, insulin

Question 24

routes of admin for insulin?

Answer 24

subcut, IV

Question 25

signs and symptoms of type 1 diabetes?

Answer 25

``` polyuria polyphasia polydipsia weight loss fatigue headache weakness nausea and vomiting abdominal pain ```

Question 26

what are the mechanisms of insulin resistance in type 2 DM?

Answer 26

insulin resistance due to the following mechanisms: 1. a reduction in the number of insulin binding sites or a decrease in the amount of insulin binding to receptors 2. decreased beta cell responsivity to increased glucose levels = decreased insulin production

Question 27

how does DKA occur?

Answer 27

1. insulin deficiency - absolute or relative 2. persistent hyperglycaemia 3. glucosuria, concurrent loss of water and electrolytes in urine 4. leads to dehydration, hypovolaemia 5. increases lactate (direct contributor to acidiosis), also increases breakdown of fats into FFAs which are broken down into ketones and acetone, causing acidosis

Question 28

how many points would you make in an answer to a question worth five marks?

Answer 28

5

Question 29

management of DKA or HHS?

Answer 29

1. correction of dehydration (IVT) 2. reverse hyperglycaemia by administering insulin 3. acid-base and electrolyte corrections 8. cardiac monitoring 5. 1/24 obs, 1-4/24 ABGs 6. nurse the patient at 30 degrees to reduce risk of cerebral oedema 7. nil by mouth 8. strict RIB 9. strict FBC 10. treat underlying cause

Question 30

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

Answer 30

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

Question 31

treatment for severe hypo?

Answer 31

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

Question 32

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

Answer 32

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

Question 33

Why would a patient with poorly managed diabetes be at risk of recurrent infections?

Answer 33

1. Impaired vision due to retinal changes 2. Neuropathy →decreased pain sensation → reduced early warning systems 3. Skin breaks → hypoxia and decreased perfusion → reduced inflammatory response 4. Increased glycosylated Hb impedes release of O2 to tissues 5. High glucose environment excellent for sustaining microorganisms

Question 34

Long term diabetes monitoring?

Answer 34

* Retinal screening * Feet checks * HbA1c * Urine ACR * GFR * BP * Lipid profile * Dental health * Mental health

Question 35

rapid-acting insulin - examples

Answer 35

novolog novorapid apidra humalog

Question 36

short-acting insulin - examples?

Answer 36

Actrapid | Humulin R

Question 37

how soon after taking rapid-acting insulin should a meal be eaten?

Answer 37

10-15 minutes prior to eating a meal | Must eat immediately after administration

Question 38

how soon after taking short-acting insulin should a meal be eaten?

Answer 38

30 minutes prior to eating a meal

Question 39

nursing considerations for metformin

Answer 39

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

Question 40

mechanism of action of metformin?

Answer 40

increases insulin sensitivity by increasing peripheral glucose uptake decreases hepatic glucose production decreases intestinal absorption of glucose

Question 41

mechanism of action of sulfonylureas?

Answer 41

increase insulin secretion

Question 42

difference between atherosclerosis and arteriosclerosis?

Answer 42

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.

Question 43

assessments to consider in a short answer question

Answer 43

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

Question 44

fluid resus formula?

Answer 44

20 - 30mls per kg initially.

Question 45

MAP formula

Answer 45

(SBP + 2xDBP) divided by 3

Question 46

what does MAP represent?

Answer 46

how well-perfused the tissues are

Question 47

what is assessed under D in an A-E assessment?

Answer 47

Disability: level of consciousness speech pain

Question 48

what is assessed under E in an A-E assessment?

Answer 48

Exposure: body temperature skin integrity signs of pressure injury wounds, dressings or drains, invasive lines ability to transfer and mobilise bowel movements

Question 49

pathophysiology of atherosclerosis?

Answer 49

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;

Question 50

common side effects of ACE inhibitors?

Answer 50

``` dizziness headache drowsiness diarrhea low BP weakness cough rash ```

Question 51

common side effects of beta blockers?

Answer 51

``` dizziness headache weakness. drowsiness or fatigue. cold hands and feet. dry mouth, skin, or eyes. upset stomach. diarrhea or constipation ```

Question 52

common side effects of calcium channel blockers?

Answer 52

``` dizziness headache constipation, rash, nausea, flushing, oedema (fluid accumulation in tissues), drowsiness, low BP ```

Question 53

MOA of calcium channel blockers?

Answer 53

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

Question 54

indications for CCBs?

Answer 54

HTN angina abnormal heart rhythms subarachnoid haemorrhage

Question 55

why are CCBs indicated for abnormal heart rhythms?

Answer 55

they slow electrical conduction through the heart and thereby correct abnormal rapid heartbeats

Question 56

MOA of ace inhibitors?

Answer 56

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

Question 57

indications for ACE inhibitors?

Answer 57

``` HTN congestive heart failure prevention of stroke diabetic nephropathy left ventricular dysfunction following MI ```

Question 58

MOA of beta-blockers?

Answer 58

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

Question 59

indications for beta-blockers?

Answer 59

``` HTN angina heart failure arrhythmias + more ```

Question 60

what are the factors that affect myocardial oxygen demand?

Answer 60

1. heart rate 2. blood volume (preload) 3. blood pressure (afterload) 4. left ventricular muscle size 5. muscle contractility

Question 61

MOA of ARBs?

Answer 61

blocks angiotensin II receptors on vascular smooth muscle and adrenal cortex, reducing vasoconstriction and increasing renal blood flow

Question 62

five clinical manifestations of asthma?

Answer 62

``` expiratory wheeze dyspnoea tachycardia hypoxaemia chest tightness SOB cough ```

Question 63

why is AKI potentially life-threatening?

Answer 63

dues to electrolyte imbalances

Question 64

common causes of AKI?

Answer 64

low fluid volume - dehydration, haemorrhage, CHF nephrotoxic drugs - certain ABs, NSAIDs