NRSG 353 Flashcards

1
Q

Define drug

A

Substance other than food which changes the way the body/mind functions

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2
Q

Pharmacokinetics

A

What the body does to the drug

  • Absorption
  • Distribution
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3
Q

Where are drugs primarily metabolised

A

Liver

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4
Q

Pharmacodynamics

A

What the drug does to the body

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5
Q

SNS VS PSNS (Para)

A
SNS = Fight/flight
PSNS = Rest/digest
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6
Q

SNS/PSNS control

A

Blood vessels
Bronchioles
Heart
Pupils

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7
Q

ANS effector cells

A

CHOLINoceptors –> mimic acetylCHOLINe (relaxation)

ADRENoceptors –> mimic ADRENaline, norADRENaline (stress)- There are 3 types

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8
Q

ADRENorecptor drugs location

A

a1 vessels
B1 heart
B2 bronchi

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9
Q

Inflammation process

A

Injury - inflammation - pain perception

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10
Q

Inflammation release of

A

Histamine (permeability)
Bradykin (pain/vasodilation)
Prostaglandin (vasodilation)

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11
Q

How NSAID’s work

A

Cyco-oxygenase inhibitors, prevent release of prostaglandin which enhances action of other inflammation mediatiors eg. Bradykin

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12
Q

Noiception 4 phases (pain)

A
  1. Transduction (damage)
  2. Transmission (of pain)
  3. Perception
  4. Modulation (suppresses/facilitates pain)
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13
Q

Goblet cell

A

Found in resp and intestinal tracts. secretes mucus

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14
Q

Pneumocytes

A

Alveolar cells
Type 1: Gas exchange
Type 2: Secretion of surfactants to reduce surface tension

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15
Q

Role of medulla and pons

A

Regulate respiration

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16
Q

Factors affecting ventilation

A

Elastic recoil - assist with expiration
Surface tension - expiration
Surfactants - lower ST to allow inspiration

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17
Q

Respiratory function tests

A

Spirometry

Total lung capacity - total amount of air after taking largest breath

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18
Q

Define COPD

A
Lung disease that limit airflow.
Include: 
- Emphysema
- Bronchitis
- Asthma
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19
Q

COPD Pathophysiology

A

Inflammatory response > goblet cell hyperplasia > symptoms eg. hyperventillation

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20
Q

Cor Pulmonare define

A

Pulmonary heart disease. Right ventricular enlargement and failure

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21
Q

Asthma pathophysiology

A
  1. Antigen/trigger
  2. Mast cells degranulate releasing mediators
  3. Mediators cause inflammation, mucus and bronchoconstriction
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22
Q

Respiratory cell receptors

A
a1 = vessels
A2 = nerves
B1 = heart
B2 = bronchi
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23
Q

Relievers vs Preventers

A

Relievers: Anti-muscarinics & Bronchodilators eg. SABA, B2 inhibitors
Preventers: Anti-inflammatory eg. steroids

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24
Q

Define atelectasis

A

Alveoli collapse

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25
Q

Define pleura effusion

A

Fluid in pleural space

26
Q

Underwater seal drain

A
Swinging = respirations
Bubbling = suction
27
Q

pH and hydrogen ion concentration

A

Inverse relationship

28
Q

pH define

A

Measurement of free hydrogen ions

29
Q

Low pH vs high pH

A

Low pH = High H+ = acidosis

High pH = Low H+ = alkalosis

30
Q

Define buffer

A

Substance that combines with hydrogen and removes it

31
Q

Types of acids

A

Volatile - leaves solution, quick, eliminated in lungs with CO2
Fixed - stays in solution, slow, eliminated in kidneys, CO2 stays

32
Q

Acid vs Base

A

A: High H+
B: Low H+

33
Q

ABG define

A

Arterial blood gas

34
Q

Normal range of ABG

A

ACID…BASE
pH 7.35-7.45
paCO2 (resp) 45-35
HCO3 (met) 22-26

35
Q

Kidney functions

A
  • Filter blood
  • Regulate blood pH
  • Regulate blood pressure/volume
  • Produce hormones
36
Q

Body fluid balance

A
Intake = 60% beverages
Output = 60% urine
37
Q

Electrolyte charges

A
Anion = - charged
Cation = + charged
38
Q

Role of electrolytes

A

Ca+ Bone, muscle contraction
Na+ blood volume
K+ Cardiac rhythm, RMP

39
Q

RMP define

A

Resting membrane potential

40
Q

Hypo vs hyper volemia

A

Hypo - fluid depletion

Hyper - fluid overload

41
Q

Renal function tests

A

eGFR

Serum creatinine levels

42
Q

AKI types

A

Pre - arteries
Intra - kidneys
Post - ureters, bladder, prostate gland

43
Q

Pathophysiology of AKI and CKD

A
AKI = Damage to nephrons
CKD = Damage to glomerulus
44
Q

Define gland

A

Structure that makes/secretes hormones

45
Q

Insulin vs glucagon

A

Beta/B-islet cells produce insulin

Alpha cells produce glucagon

46
Q

-ase define

A

Break down of…

47
Q

Define AGE (Advanced glycosylated end)

A

AGE products are harmful compounds formed when protein/fat combines with sugar in blood stream

48
Q

Action potential steps

A
  1. Depolarisation - Na+ inflow
  2. Plateau - Ca inflow, K outflow
  3. Repolarisation - K+ outflow
49
Q

PQRST

A
P - Atrial DEpolarisation
Q
R - Ventricular - DEpolarisation/ Atrial REpolarisation
S
T - Ventricular REpolarisation
50
Q

Cardiac output =

A

Stroke volume x HR

51
Q

Ventricular fibrillation diagnosis

A

No P wave

52
Q

Preload vs Afterload

A

P: Stretching of cardiac cells = ventricular filling
A: Force used to contract

53
Q

Define congestive cardiac failure (CCF)

A

Term used to describe myocardial dysfunction

54
Q

Pathophysiology of CCF

A

Impairment in structure/function which reduces ability of heart to contract/refill

55
Q

COPD Emphysema vs Bronchitis

A

E: Loss of alveoli - alvoli los elastic recoil ‘elastate’
B: Abnormal inflammation - hypetrophy of goblet cell

56
Q

Renal failure clinical manifestations

A
  • AGE products
  • Na and H20 retention = oedema/hypertension
  • Risk of anaemia - kidneys unable to produce erythropoietin
  • Risk of bone breakage - kidneys unable to produce calcitriol
57
Q

Define Calcitriol

A

Produced by kidneys. Form of Vitamin D that helps with calcium uptake

58
Q

define angina

A

Reduced blood glow to coronary arteries = chest pain (can lead to MI)

59
Q

Types of angina

A

Stable - relieved with activity
Unstable - can lead to MI
STEMI - prolonged full blockage
NSTEMI - partial temporary blockage (less infarct to heart)

60
Q

Define infarct

A

Tissue death

61
Q

Use of morphine in angina

A

Vasodilation > decreased cardiac workload

62
Q

Define MI

A

Blockage of coronary artery