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Nursing science 2 > MCQ - Exam prep > Flashcards

MCQ - Exam prep Flashcards

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1
Q

What is the functional tissue of an organ called?

A

parenchyma - distinguid from the connective and supportive tissue

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2
Q

What is sulphonylureas used for?

A

An anti-diabetic drug, widely used in the management of diabetes mellitus type 2

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3
Q

The accumulation of cells, lipids and tissue in the intimal lining of arteries is what disease?

A

Atherosclerosis

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4
Q

Structure of arteries and veins
Tunica Adventitia
Tunic Media
Tunica Intima

A

Adventitia -Strong and fibrous - holds vessel open
Media - smooth muscle and elastic - permits diameter changes
Intima - endothelium - lesions develop here

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5
Q

Atherosclerosis - 5 Modifiable Risk factors

A 
Obesity
Hyperlipidaemia
Smoking
Diabetes (lifestyle related)
Insufficient physical activity
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6
Q

Atherosclerosis - 5 Non-modifiable risk factors

A 
Age
Premature menopause in females
Indigenous Australian
Low socioeconomic groups
Family history of close relative with the disease under 60
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7
Q

An autoimmune, neuromuscular disease caused by Ab-mediated loss of nicotinic ACh receptors at the NMJ

A

myasthenia gravis

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8
Q

Myasthenic crisis symptoms

A

Severe muscle weakness -> Quadriplegia, SOB, Difficulty swallowing
Can occur 3-4 hours after too little or too much medication
Can be stress induced -> Infection, pregnancy, cold exposure, sugary

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9
Q

Myasthnia gravis Tx

A
  • Neostigmin & Pyridostigmine (Anticholinesterases)
  • Corticosteroids
  • Ciclosporin & Azathioprine (Immunosupressant)
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10
Q

Bradykinesia

A

Slowness of movement

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11
Q

Thiopentone (thiopental) - IV

A
  • Induction Agent
  • Enhances/mimics action of GABA in CNS by inhibiting excitatory neurotransmission.
  • No analgesic effects
  • Resp and CVS effects (depresses/decreases)
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12
Q

GABA (Gamma aminobutyric acid)

A
  • CNS inhibitory neurotransmitter
  • Most widely distributed
  • Reduces neuronal excitability in the nervous system
  • Produced in presynaptic neurone and acts on postsynaptic GABA receptors.
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13
Q

Propofol - IV

A
  • Induction agent; suitable for maintenance and sedation
  • Activates GABAa receptor
  • Shortens opening time of nicotinic AChR and NA+ channels in cortex
  • Rapid onset and fast recovery
  • No analgesic properties
  • Min CVS effects
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14
Q

Ketamine - IV

A
  • Induction agent; and maintenance
  • NMDA rector antagonist (reduces neuronal excitability)
  • Potent analgesic
  • CVS stimulant
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15
Q

Induction IV

A
  • Thiopentone
  • Propofol
  • Ketamine
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16
Q

What are some Inhalant anaesthesia agents?

A

‘flurane’
Sevoflurane
Desflurane
Isoflurane
fluranes are all volatile agents and can trigger Malignant Hyperthermia!
- Also N20 can be an induction and maintenance inhalant. No reversal for inhaled agents.

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17
Q

Neuromuscular Blocking Agents (muscle relaxant) fall into which two categories?

A

Depolarising vs Non-depolarising

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18
Q

Suffix -> aines are responsible for?

A

-Local anaesthsia
eg Lignocaine and Bupivacaine
-Block conduction of PNS impulses -> block sodium channels => no threshold potential
-Considerations for age, wt, health, liver function for dosage used.

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19
Q

Bier’s block

A

Regional anaesthesia - local anaesthetic is given intravenously with a tourniquet applied to stop it from spreading systemically.

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20
Q

Acute respiratory distress syndrome (ARDS)

Clinical presentation?

A
  • Rapid onset (12-18 hours)
  • ^ RR
  • Metabolic acidosis
  • Hypoxaemia refractory to O2 therapy
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21
Q

What do drugs ending in ‘ole’ do?

A

Proton Pump Inhibitors (PPI) - Inhibit the formation of Hydrochloric acid
eg Pantoprazole, Omeprazole, Esomeprazole(Nexium)
Adverse effects - headache, dry mouth, GI upset (N,V,D)

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22
Q

Cimetidine

A
  • Histamine receptor antagonist - Used in Pyloric obstruction
  • Blocks acid secretions
  • Interacts with CYP -> metformin, warfarin etc
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23
Q

Is Penicillin more effective against gram positive or gram negative bacteria?

A

Gram +++++++++++

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24
Q

What is the mechanism of action of Penicillin?

A

Inhibits synthesis of bacterial cell wall - binds with proteins -> defective cell wall destroys the organism
Also called Beta-Lactam Antibacterials

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25
Q

Is Penicillin given IV or oral?

A

IV - as it is destroyed by gastric acid

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26
Q

What are some common Beta-Lactam Antibacterials?

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

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27
Q

What are three common asthma medications

A
  • Prednisolone
  • Aminophylline
  • Salbutamol
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27
Q

What are three common asthma medications

A
  • Prednisolone
  • Aminophylline
  • Salbutamol
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28
Q

Stroke risk factors

A
  • Smoking
  • lifestyle (ethanol, obesity, cholesterol)
  • HTN
  • DM 1 & 2
  • Heart disease
  • Family Hx
  • Chlamydia pneumonia
  • ^Age
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29
Q

What is bioavailability of a drug?

A

Amount of active drug that reaches systemic circulation.

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30
Q

What affects the bioavailability of a drug?

A

Absorption
Intestinal motility
First pass hepatic metabolism
(IV = 100% bioavailability)

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31
Q

What are treatment options for genital herpes?

A

Antiviral agents - DNA polymerase inhibitors

  • Aciclovir
  • Famciclovir
  • Valaciclovir (best)
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32
Q

What are Desflurane, Isoflurane and Sevoflurane used for?

A

Inhaled Induction agents

33
Q

What are the 4 phases of wound healing?

A
  1. Haemostasis (Immediate)
  2. Inflammation (0-3 days)
  3. Proliferation (2-24 days)
  4. Maturation (24 days-1year)
34
Q

What are the cells in the first stage of wound healing?

A
  1. Haemostasis - Platelets are activated from exposed collagen and begin clotting. Platelets recruit Neutrophils (WBCs) and Monocytes(blood) to the site.
35
Q

What are the cells in the second phase of wound healing?

A
  1. Inflammation
    Neutrophils and Macrophages phagocytosis bacteria and necrotic tissue. Macrophages release cytokines. Mast cells secrete histamine (causing vasodilation)
36
Q

What are cells in the third stage of wound healing?

A
  1. Proliferation
    Fibroblasts produce the ExtraCellularMatrix(ECM) and collagen to form Granulation tissue as a framework. Macrophages continue to remove debris
37
Q

What are cells in the fourth stage of wound healing?

A
  1. Maturation
    Fibroblasts continue to release a stronger and more organised collagen and create a stronger framework with 70-80% tensile strength recovered.
38
Q

What are the three processes of wound healing?

A

Primary - Margins aligned
Secondary - left open, longer inflammation
Tertiary - Delayed primary, left open and closed later

39
Q

What may cause wounds to become chronic?

A

Repeated trauma
Ischemia
Infection

40
Q

What health conditions influence wound healing?

A 
Diabetes
CVS conditions
Blood disorders (Anaemia)
Auto-immune disorders
Obesity or very thin
Stress
Phychiatric disorders 
Medications
Smoking
41
Q

What are the changes that age causes to skin?

A
  • Dermis loses 80% thickness
  • 40% Less collagen
  • Less small blood vessels
  • Epidermis and dermis seperate more easily
  • Reduces sensory nerves
42
Q

What is Suxamethonium used for?

A

IV, Depolarising NM Blocking agent aka Muscle relaxant for intubation.
Mimics the action of ACh -> agonist on nicotinic receptor on motor end plate DEPOLARISING +++ => Paralysis. Short acting ~5min

43
Q

How do Non-depolarising agents work?

A

Act as a competitive antagonist to ACh at the nicotinic ACh receptor on NMJ to PREVENT DEPOLARISATION, Require reversal as they have CVS changes (decrease HR and BP)

44
Q

What are medications ending in ‘ium’ used for? e.g Atracurium

A

Non-depolarising Neuromuscular Blocking Agent aka muscle relaxant.
Atracurium, Pancuronium, Rocuronium, Vecuronium.

45
Q

What is the Loeser Model?

A

Pain model that puts the pain in context with biophysical and behaviour of pain.
Nocicoeption>Pain>Suffering>Pain behaviour

46
Q

What are the 3 categories of Nociceptor pain receptors?

A

Mechanical receptor - myelinated
Thermal receptor - Myelinated
Polymodal receptor - Un-myelinated

47
Q

What are the two different types of afferent nociceptors?

A

Myelinated - Delta - Fast 30m/sec

Un-myelinated - C - Slow 12m/sec

48
Q

What are 2 neurotransmitters involved in pain transmission?

A

Substance P - send signal to higher brain areas, opioids block this.
Glutamate

49
Q

What is angina?

A

Reversible myocardial ischaemia

-Caused from increase in myocardial O2 demand eg stress and exercise

50
Q

What is Prinzmetal angina?

A

Coronary spasm, reversible myocardial ischaemia that happens at random, usually at night. Pathology unclear, possibly altered Ca+ channels

51
Q

What is unstable angina?

A

Unpredicatable, no clear cause from stress etc.

Intermediate b/t stable angina and MI

52
Q

What are diagnostic tests for angina Sx?

A

Hx, vitals, ECG, CXR, Blood test, Echocardiogram, Angiogram, exercise stress test.

53
Q

What are 4 pharmacological management options for unstable angina?

A

O2, GTN, Aspirin, Morphine

54
Q

What are ‘olol’s used for?

A 
Beta blockers! for stabel angina
-Decrease HR,
-Decrease force of contraction
= decrease BP
Adverse effects are Brady cardia and orthostatic HTN
55
Q

What are ‘pril’s used for?

A

ACE Inhibitors! Inhibit Angiotensin Converting enzyme, which prevents Angiotensin I converting to Angiotensin II. Leading to reduced peripheral resistance,

56
Q

What is the term for incomplete or partial paralysis?

A

Paresis

57
Q

What does Hemiparesis mean?

A

Incomplete paralysis affecting one side of the body

58
Q

What does Hemiplegia mean?

A

Paralysis of one side of the body

59
Q

What is the term for the loss of the ability to speak or write?

A

Aphasia

60
Q

What does Apraxia mean?

A

Inability to execute motor acts

61
Q

What is the term for poorly articulated speech?

A

Dysarthria

62
Q

What is Dysphagia?

A

Difficulty swallowing

63
Q

What is Agnosia?

A

loss of recognition ability; people or shapes

64
Q

What is Hemianopia?

A

Blindness in half the field of vision

65
Q

What is Cerebral Blood Flow mainly regulated by?

A

In response to changes in O2, H+ and CO2

66
Q

What is Cerebrovascular Disease?

A

A neurological disorder defined as the abnormality of the brain, caused by a pathological process in the blood vessels.

67
Q

What is a common clinical manifestation of CVD?

A

Stroke (Cerebrovascular accident)

68
Q

What are the risk factors for Stroke?

A
  • Smoking.
  • Lifestyle (Obesity, cholesterol)
  • HTN
  • Type 1&2 DM
  • Heart disease eg AF
  • Hx or Family Hx of stroke
  • Chlamydia pneumonia
  • Age
  • Gender - higher in Men
69
Q

What are four types of Ischemic Stroke?

A
  • TIA (Transient ischaemic attack), temporary and intermittent blockages.
  • Thrombotic stoke, artery occlusion from thrombus in cerebral arteries.
  • Embolic stroke, fragments from outside the brain.
  • Lacunar stroke, micro-infants in smaller arteries
70
Q

What is an area of irreversibly damaged tissue called?

A

Infarct

71
Q

What is Type I Acute Respiratory failure classified as?

A

Hypoxaemia with normal CO2

Reduced O2 in the blood

72
Q

What is Type II Acute Respiratory Failure

A

Hypoxaemia and Hypercapnia

Reduced blood O2 and increased blood CO2

73
Q

COPD Patients should aim to have SpO2 between what %?

A

88-92% to allow effective CO2 removal. If over-titrating supplemental O2, can cause impact on the transportation and removal of CO2

74
Q

What is the main cause of Acute Pulmonary Oedema (APO)?

A

Cardiogenic causes related to an increase in Left Atrial Pressure. Leads to increase pulmonary hydrostatic pressure -> oncotic pressure ->fluid moves into interstitial space that exceeds lymphatic drainage.

75
Q

What is the mechanism of action of Frusemide? And some adverse effects?

A

Its a diuretic. It inhibits the reabsorption of Na+ and Cl- in the ascending limb of loop of Henle. This results in less water being reabsorpted => more water excreted.
Adverse effects are electrolyte disturbance, polyuria, orthostatic hypotension. Hyponatraemia and hypokalaemia

76
Q

What is Atelectasis? and what are the common causes?

A

Collapse of lung tissue. Can be caused by:

  • Pleural effusion
  • Any surgery
  • Blocked airway
  • Respiratory distress syndrome
77
Q

What is Acute Respiratory Distress Syndrome (ARDS)?

A

Damage to capillary/alveolar membrane resulting in leaking of fluid into alveolar space. Massive inflammatory response - Synthesis and release of inflammatory mediators: Neutrophils, macrophages, endotoxin, IL-1, TNF, ROS.
Leads to pulmonary oedema+++

78
Q

What is the most common cause of respiratory failure in children?

A

Respiratory distress syndrome - due to lack of surfactant leading to alveolar collapse.

79
Q

What are risk factors for pneumonia?

A
  • Age
  • Immunocompromised
  • Underlying pulmonary disease (COPD, asthma)
  • Alcohol, smoking
  • Prolong immobilisation
80
Q

Where are Beta 2 receptors located? and what does a secondary messenger do when activated by medication?

A

Located mainly in the lungs (Some in heart (mainly B1)). Drugs like salbutamol and salmeterol stimulate Beta 2-adrenergic receptors causing relaxation of bronchial smooth muscle. The receptors have a secondary messenger system of increasing the production of cyclic AMP (cAMP) which also produces bronchodilation.

Nursing science 2 (2 decks)

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