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semester 2 2019 > priority cards > Flashcards

priority cards Flashcards

1
Q

where are alpha 1 adrenoceptors found?

A

primarily on blood vessels

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2
Q

what are the two main types of adrenoreceptors?

A

alpha and beta

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3
Q

what does activation of alpha 1 receptors cause?

A

vasoconstriction of blood vessels

increase BP

dilate pupils

decrease GIT mobility

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4
Q

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

A

hypertension
blurred vision
constipation
urinary retention

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5
Q

effects of meds that target alpha 1 receptors?

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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6
Q

where are beta-1 adrenoreceptors primarily found?

A

on cardiac cells ( myocardium)

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7
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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8
Q

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

A

tachycardia

hypertension

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9
Q

effects of meds that target beta-1 receptors?

A

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

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

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10
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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11
Q

what does activation of beta-2 receptors cause?

A

bronchodilation

increased skeletal muscle excitability (tremors)

vasodilation of blood vessels in skeletal muscle

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12
Q

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

A

tremors

warmth (flushing)

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13
Q

effects of meds that target beta-2 receptors?

A

used in pts with respiratory conditions to reverse bronchoconstriction

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14
Q

causes of type 1 diabetes?

A

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

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15
Q

causes of type 2 diabetes?

A

obesity, sedentary lifestyle,

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16
Q

pathophysiology of type 1 diabetes?

A
  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)
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17
Q

pathophysiology of type 2 diabetes?

A
  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
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18
Q

pathophysiology behind the 3Ps is type 1 diabetes?

A

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

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19
Q

signs and symptoms of type 2 diabetes?

A

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

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20
Q

acute complications of type 1 diabetes?

A

hypoglycaemia, DKA

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21
Q

acute complications of type 2 diabetes?

A

HHS (hyperosmolar hyperglycaemic state), hypoglycaemia

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22
Q

management of type 1 diabetes?

A

insulin, monitoring of BGLs

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23
Q

management of type 2 diabetes?

A

lifestyle changes (diet, exercise), OHAs, insulin

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24
Q

routes of admin for insulin?

A

subcut, IV

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25
Q

signs and symptoms of type 1 diabetes?

A 
polyuria
polyphasia
polydipsia
weight loss
fatigue
headache
weakness
nausea and vomiting
abdominal pain
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26
Q

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

A

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
27
Q

how does DKA occur?

A
  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
28
Q

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

A

5

29
Q

management of DKA or HHS?

A
  1. correction of dehydration (IVT)
  2. reverse hyperglycaemia by administering insulin
  3. acid-base and electrolyte corrections
  4. 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
30
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

31
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

32
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

33
Q

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

A
  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
34
Q

Long term diabetes monitoring?

A
  • Retinal screening
  • Feet checks
  • HbA1c
  • Urine ACR
  • GFR
  • BP
  • Lipid profile
  • Dental health
  • Mental health
35
Q

rapid-acting insulin - examples

A

novolog
novorapid
apidra
humalog

36
Q

short-acting insulin - examples?

A

Actrapid

Humulin R

37
Q

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

A

10-15 minutes prior to eating a meal

Must eat immediately after administration

38
Q

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

A

30 minutes prior to eating a meal

39
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

40
Q

mechanism of action of metformin?

A

increases insulin sensitivity by increasing peripheral glucose uptake

decreases hepatic glucose production

decreases intestinal absorption of glucose

41
Q

mechanism of action of sulfonylureas?

A

increase insulin secretion

42
Q

difference between atherosclerosis and arteriosclerosis?

A

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.

43
Q

assessments to consider in a short answer question

A

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

44
Q

fluid resus formula?

A

20 - 30mls per kg initially.

45
Q

MAP formula

A

(SBP + 2xDBP) divided by 3

46
Q

what does MAP represent?

A

how well-perfused the tissues are

47
Q

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

A

Disability:

level of consciousness
speech
pain

48
Q

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

A

Exposure:

body temperature

skin integrity

signs of pressure injury

wounds, dressings or drains, invasive lines

ability to transfer and mobilise

bowel movements

49
Q

pathophysiology of atherosclerosis?

A

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;

50
Q

common side effects of ACE inhibitors?

A 
dizziness
headache
drowsiness
diarrhea
low BP
weakness
cough
rash
51
Q

common side effects of beta blockers?

A 
dizziness
headache
weakness.
drowsiness or fatigue.
cold hands and feet.
dry mouth, skin, or eyes.
upset stomach.
diarrhea or constipation
52
Q

common side effects of calcium channel blockers?

A 
dizziness
headache
constipation,
rash,
nausea,
flushing,
oedema (fluid accumulation in tissues),
drowsiness,
low BP
53
Q

MOA of calcium channel blockers?

A

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

54
Q

indications for CCBs?

A

HTN

angina

abnormal heart rhythms

subarachnoid haemorrhage

55
Q

why are CCBs indicated for abnormal heart rhythms?

A

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

56
Q

MOA of ace inhibitors?

A

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

57
Q

indications for ACE inhibitors?

A 
HTN
congestive heart failure
prevention of stroke
diabetic nephropathy
left ventricular dysfunction following MI
58
Q

MOA of beta-blockers?

A

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

59
Q

indications for beta-blockers?

A 
HTN
angina
heart failure
arrhythmias
\+ more
60
Q

what are the factors that affect myocardial oxygen demand?

A
  1. heart rate
  2. blood volume (preload)
  3. blood pressure (afterload)
  4. left ventricular muscle size
  5. muscle contractility
61
Q

MOA of ARBs?

A

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

62
Q

five clinical manifestations of asthma?

A 
expiratory wheeze
dyspnoea
tachycardia
hypoxaemia
chest tightness
SOB
cough
63
Q

why is AKI potentially life-threatening?

A

dues to electrolyte imbalances

64
Q

common causes of AKI?

A

low fluid volume - dehydration, haemorrhage, CHF

nephrotoxic drugs - certain ABs, NSAIDs

semester 2 2019 (16 decks)

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