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Nursing Year 2a Flashcards

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1
Q

Pathophysiology of pneumonia

A
  1. infections microorganism reaches alveoli
  2. macrophages overwhelmed, neutrophils recruited
  3. Neutrophils engulf alveoli producing fibrin-rich exudate
  4. Exudate fills infected and neighbouring alveoli
  5. Exudate causes alveoli to stick together, reducing ventilation
  6. Oedema increases diffusion distance for gases, impairing gas exchange
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2
Q

Pathophysiology of COVID-19

A
  1. virus enters respiratory tract binding to epithelial cells
  2. Viral replication and limited immune response begins
  3. Infection is contained at this stage in 80% of patients with viral clearance in 10-14 days
  4. Migration into lower respiratory tract and invasion of the alveoli
  5. Cytokine involvement and immune response causing injury to alveoli
  6. Viral replication continues with damage and apoptosis to host cells
  7. Adjacent healthy alveoli become infected causing death of pneumocystis
  8. Diffuse alveolar damage results in Acute Respiratory Distress Syndrome (ARDS)
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3
Q

Pathophysiology of emphysema

A
  1. irritant
  2. macrophages release inflammatory mediators
  3. neutrophils recruited, releasing elastase
  4. elastase breaks down elastin causing destruction of elastic fibres
  5. alveolar walls lose elasticity, increasing compliance (too stretchy)
  6. Other proteases cause tissue damage too alveolar wall.
  7. pulmonary capillary bed reduced, increasing pressure in pulmonary artery
  8. T- lymphocytes cause further tissue damage
  9. Cell apoptosis (death)
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4
Q

Pathophysiology of asthma

A
  1. Allergen (trigger) such as pollen, exercise, smoke, dust enters respiratory tract
  2. Dendritic cells in epithelial layer engulf pathogen, stimulating immune response
  3. Mast cells in bronchial smooth muscle activated and chemical mediators released
  4. Eosinophils stimulated in bone marrow and attracted to local area
  5. Vasodilation causes fluid to leak from vasculature into tissues = oedema
  6. Airway hyper responsiveness causes bronchospasm
  7. Increase mucous from goblet cells further obstructs air entry
  8. Gas trapping from bronchoconstriction results in hypercapnia
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5
Q

Pathophysiology of embolism

A
  1. Thrombus formation in peripheral circulation dislodges
  2. Thrombus travels to pulmonary circulation, causing partial or complete obstruction of PA
  3. Increased pressure in RV causes dilation and septal deviation to LV
  4. LV preload reduced, causing decreased CO
  5. Systemic arterial hypotension leads to coronary hypo perfusion
  6. RV hypoxia results causing schema and infarction
  7. Further increased myocardial demand causes LV failure
  8. Obstruction to blood flow in pulmonary capillary bed also results in VQ mismatch, worsening hypoxaemia
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6
Q

Objective assessments for respiratory problem

A
  1. vital signs
  2. Peak flow
  3. Chest assessment (IPPA)
  4. COLDSPA (pain)
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7
Q

Best ways to treat Asthma

A
  1. bronchodilators (inhalers/nebuliser)
  2. corticosteroids (oral/IV/inhaled)
  3. Metered dose inhaler (MDI) spacer/neb use
  4. Oxygen therapy
  5. positioning
  6. Reassurance to decrease anxiety which reduces SNS response
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8
Q

What is heart failure

A

An acute or chronic condition in which the heart doesn’t pump blood as well as it should resulting in congestion (CHF) of blood backing up and unable to meet demands of the body

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9
Q

What are the clinical manifestations of Left sided HF

A

dyspnoea (difficulty breathing)
orthopnoea (shortness of breath when lying down)
paroxysmal nocturnal dyspnoea
pulmonary congestion - cough, crackle, wheeze

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10
Q

What are the clinical manifestations of Right sided HF

A 
renal failure
peripheral oedema
ascites
enlarged liver and spleen 
distended JVP
fluid weight gain
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11
Q

What nursing interventions are done with HF

A

fluid balance
IV Frusemide
ACE inhibitors and beta blockers
daily ECG

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12
Q

Pathophysiology of atherosclerosis

A
  1. An irritant is present e.g. lipids (LDL cholesterol), High blood pressure (HTN), toxins (cigarette smoke), diabetes
  2. damage occurs to the endothelium - a crack or fissure is formed
  3. LDL cholesterol deposits accumulate in the artery wall (tunica intima) known as fatty streaks
  4. LDL oxidises (changes), sends signals to immune system and monocytes (WBC) arrive
  5. Monocytes convert to macrophages and consume the cholesterol
  6. Macrophages fill up on cholesterol and die = foam cells
  7. Formation of foam cells = release of cytokines (inflammatory process - vicious circle)
  8. Smooth muscle cells migrate into expanding fatty plaque forming a lipid cap (using collagen and elastin)
  9. Smooth muscle cells also deposit calcium into the fatty plaque, hardening it and causing bulging into the artery lumen
  10. Blood flow is decreased (resistance is increased) and compliance is reduced (less flexibility)
  11. Ongoing inflammation = plaque rupture, thrombogenic material inside the cap is exposed = arriving platelets form a thrombus
  12. A thrombus is formed (either partially or fully) and occludes the artery causing ischaemia, or ultimately infarction
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13
Q

What is VT

A

Ventricular tachycardia, absence of P waves. needs defibrillation

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14
Q

What is VF

A

Ventricular fibrillation, rapid disorganised contraction of the ventricles, needs defibrillating

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15
Q

What is asystole

A

complete absence of electrical activity, cannot defibrillate this

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16
Q

What is AF

A

Atrial fibrillation, no P waves and its irregular

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17
Q

What are cardiovascular diseases

A 
any condition that affects the structure function of the heart and bloods vessels 
CAD - angina, myocardial infarction
CVD
PVD
HF
HTN
Rheumatic heart failure
congenital heart disease
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18
Q

What s ischaemic heart disease

A

insufficient blood flow and blood volume to supply the 02 needs of the myocardium

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19
Q

What is angina

A

is a symptom of reversible myocardial ischaemia, manageable, occurs die to a stable lesion/plaque in the coronary artery

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20
Q

What is the key pathophysiology of IHD

A

ineffective myocardial oxygen perfusion

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21
Q

What is MI

A

myocardial infarction, results from sustained ischaemia or sudden complete blockage of the coronary artery
myocardial tissue distal to the obstruction dies
can be partial thickness (NSTEMI) of full thickness (transmural, STEMI)

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22
Q

What is NSTEMI

A

non ST-elevation myocardial infarction involves partial thickness myocardial wall damage. sudden complete blockage of a coronary artery, ECG finding is definitive

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23
Q

What is STEMI

A

ST-elevation myocardial infarction involves full thickness myocardial wall damage (with/without necrosis). partial blockage of a coronary artery. not visible on an ECG

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24
Q

What is ACS

A

is the term for an imbalance of 02 supply and demand. the underlying pathophysiology is atherosclerosis which can lead to plaque rupture and thrombus formation.
unstable angina pectons
STEMI
non - STEMI

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25
Q

What are the signs and symptoms of IHD and ACS

A 
pale, grey 
confused
tachycardia, chest pain 
hypotensive, hypertensive 
dyspnoea
fatigue, anxiety
palpitations, restlessness
hypoxaemia
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26
Q

What is the difference between a heart attack and a cardiac arrest

A

heart attack is a MI, results from a blocked coronary artery - a circulation problem
Cardiac arrest is a sudden cessation of the hearts functioning triggered by electrical malfunction in the heart that causes an arrhythmia, disrupts the pumping action - an electric problem

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27
Q

What is EF

A

ejection fraction is the amount of blood that is pumped out of the left ventricle with each heart beat. an EF of 40% or less indicates HF

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28
Q

What is Left sided Heart Failure

A

The left ventricle cannot pump blood effectively to the systemic circulation
decrease EF
pulmonary congestion/oedema with dyspnoea
cough
crackle
impaired oxygen exchange

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29
Q

What is Right sided Heart Failure

A

The right ventricle cannot eject sufficient amounts of blood, blood baks up in the venous system and may result in
peripheral oedema
weight gain but anorexia/ nausea may be present
hepatomegaly/ splenomegaly
ascites
jugular vein distension

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30
Q

What are the three key medications in management of acute chest pain

A

GTN spray - abtianginal, relaxes smooth muscle and dilates veins
Morphine - opioid, vasodilation
Aspirin - anti platelet, impedes clotting

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31
Q

What is the role of statins in lipid lowering therapy

A

statins lower total cholesterol low density lipid levels risk factor for development of atherosclerosis, lowering the production of cholesterol in the liver bu inhibiting the enzyme

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32
Q

What do Beta-blockers do

A

Beta-blocker slow conduction (HR) and lessen the force of contraction to balance oxygen supply and demand
metoprolol

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33
Q

What do ACE inhibitors do

A

ACE inhibitors promote vasodilation and diuresis by decreasing after load and preload the decreasing the workload of the heart
cilazapril, enalapril

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34
Q

What is the kidney responsible for

A
  1. acid-base balance
  2. water balance
  3. electrolyte regulation
  4. toxin removal
  5. BP regulation
  6. Erythropoietin production - RBD production in the bone marrow
  7. vitamin D activation
35
Q

What is an Acute Kidney Injury (AKI)

A

occurs when the kidneys are unable to remove the body metabolic waste or perform their seven regulatory functions

36
Q

What nursing assessments are done with kidney problems

A 
daily weight
assess skin integrity
vital signs 
cap refil 
palpate or scan of the bladder
37
Q

What is the three different types of traumatic brain injury

A

focal - localised to impact site to skull
contrecoup - brain shifting within the skull and meninges during acceleration/deceleration movement
diffuse - movement of he brain within cranial cavity causing widespread neural damage

38
Q

Types of stroke

A

a stroke is an altered blood supply to the brain causing death of neutrons due to decreased 02.
ischaemic - thrombotic atherosclerosis severly reduces blood flow due to a blood clot, transient ischaemic attacks (TIAs)
Haemorrhagic - inter cranial haemorrhage, very little blood flow to neutrons deprived of 02

39
Q

What is Parkinson’s Disease

A

A chronic progressive neurologic condition that affects the pigmented dopaminergic neutrons of the substantiated nigra and locus ceruteus of the basal ganglia. degeneration of neutrons are associated with impaired motor function

40
Q

What is autonomic dysreflexia

A

strong discomfort/pain sending signals into spinal cord via intact peripheral nerves below T6 lesion
CNS senses this input as it travels up the spinal cord evoking a massive peripheral sympathetic response through spinal reflexes, vessels vasoconstrictor below T6 injury
vessels continue to constrict as they try to send signals to the brain peripheral artery hypertension occurs
brain detects hypertensive crisis through baroreceptors in carotid and aortic arch CANT get the signals to relax decreases blood pressure in the lower extremities
brain attempts two manoeuvres to haunt hypertensive crisis
1. shut down sympathetic surge by decreasing inhibitory impulses
2. decrease peripheral BP by slowing HR through an intact vagus nerve
nerves above the level of injury vasodilate and the nerves below the level of injury vasoconstrict

41
Q

Symptoms of autonomic dysreflexia

A 
hypertension
bradycardia
sweating
flushing
pupillary constriction
nasal congestion
pale cool skin
42
Q

Pathophysiology of raised ICP

A

rise in ICP greater than CPP causes reduced blood flow to the brain. reduced blood flow means less 02/glucose delivery to tissue causing cerebral ischaemia
cerebral ischaemia stimulates a sympathetic response in order to increase blood flow
parasympathetic response initiated by raised BP is detected by baroreceptors. this results in an attempt to reduce BP by HR
Ongoing high BP causes further rise in ICP and further restriction of blood flow. switch from aerobic to anaerobic respiration results in lower ATP production
Breakdown od NA/K pump causes water to enter the cell, resulting in cell death. cerebral oedema worsens the brain stem is compressed causing irregular respiration before death is imminent

43
Q

Signs and symptoms of ICP

A

level of consciousness - drowsiness, dizziness, lethargy
speech - slurred, delayed word finding, no speech
motor strength - weakness, sensation changes, swallowing difficulty
behaviour - personality change, emotional, disinhibition
pupil changes - unequal, sluggish, oral, pinpoint
cognition - poor memory, inability to sequence, confusion,

44
Q

What are type types of stokes

A

Ischaemic and Haemorrhagic

45
Q

What are the two different types of Ischaemic stroke

A

cerebral embolism is a blood clot or debris formed elsewhere in the body which travels to the brain. if it cannot pass through the lumen it will occlude the vessel interrupting blood flow causing tissue ischaemia
cerebral thrombosis is a narrowing of the cerebral arteries caused by plaque build-up. A clot then forms on the plaque, occluding the vessels lumen and restricting blood flow to an area of the brain

46
Q

What are the type of Haemorrhagic strokes

A

intracerebral and subarachnoid haemorrhage.
a burst blood vessel will cause blood to leak into brain tissue and surrounding structures, causing a rise in intracranial pressure and damage to brain tissue

47
Q

What is a TIA

A

Transient Ischaemic Attack
A temporary focal loss of neurological function caused by ischaemia results from inadequate blood flow to brain from partial or complete occlusion of an artery

48
Q

Pathophysiology of Ischaemic stroke

A

ischaemic cascade - disrupted blood flow, anaerobic respiration, lactic acid, insufficient ATP
Ion imbalance - increase in intracellular calcium, increased glutamate, vasoconstriction
enlarged area of infarction into penumbra - cell membrane and proteins break down, formation of free radicals, protein production decreased, cell injury and death

49
Q

Pathophysiology of Haemorrhagic stroke

A

ruptured vessel - explosive eruption of blood from vessel into surrounding brain tissue and structure, haematoma develops, exposure of brain to blood and increase in intracranial pressured caused by sudden entry of blood into the tissue
Ion imbalance - mismatch between blood flow and metabolic demand, breakdown of sodium/potassium pump maintaining cellular function, anaerobic respiration to produce ATP, increased production of lactic acid
Cell death
Altered pH
Cell membrane and proteins breakdown

50
Q

Right side brain injury symptoms

A

paralysed left side
special perceptual deficits
quick, impulsive, behavioural style
memory deficits

51
Q

left side brain injury symptoms

A

paralysed right side
speech and language deficits
slow, cautious behavioural style
memory deficits

52
Q

physiology of brain injury

A

brain suffers traumatic injury
brain swelling or bleeding increases intracranial volume
rigid cranium allows no room for expansion of contents so intracranial pressure increases
pressure on blood vessels within the brain causes blood flow to the brain to slow
cerebral hypoxia and ischaemia occur
intracranial pressure continues to rise, brain may herniate
cerebral blood flow ceases

53
Q

Types of spinal cord injury

A 
transient confusion (reversible)
contusion
laceration
compression
transection (irreversible)
54
Q

What is a secondary spinal injury

A

ischaemia
hypoxia
oedema
inflammatory process

55
Q

functions lost in complete spinal injuries

A

voluntary movement
sensation of pain, temp, pressure and proprioception
bowel and bladder function
loss of reflexes

56
Q

some functions may be preserved in incomplete spinal cord injuries

A

central cord syndrome
anterior cord syndrome
brown-squared cord syndrome

57
Q

Level of patients injury

A

C5 top of shoulder
T4 nipple line
T10 umbilicus
L4 great toe

58
Q

What level is Quadriplegia (tetraplegia)

A

C1-C6

59
Q

What level is Paraplegia

A

T1-L

60
Q

Specific complications of SCI

A

spinal shock
neurogenic shock
autonomic dysreflexia

61
Q

What is spinal shock

A

areflexia (sudden depression reflex activity)
muscles paralysed, flaccid and without sensation below level in injury
bowel and function lost
gastric stasis
paralytic ileus

62
Q

What is neurogenic shock

A

is a condition in which you have trouble keeping your heart rate, blood pressure and temperature stable because of damage to your nervous system after a spinal cord injury.

63
Q

What is a venous wound

A

gaiter area of the leg or affect the dorm of the foot. pitting oedema, irregular edge, often painless unless infected, copious exudate, brown pigmentation of the surrounding skin

64
Q

What is a arterial ulcer

A

feet, heels and toes, often over bony prominences, ulcer appears punched out with well marked edges
painful, skin dusky or pale, skin hairless thin and brittle with shiny texture, reduced or absent peripheral pulse

65
Q

What are factors contributing to gastrointestinal tract conditions

A 
bleeding, trauma, perforation, obstruction
inflammation, infections, infestations
tumors, benign and malignant
congenital disorder
circulatory and nervous system faults
ageing 
high levels of stress
66
Q

signs and symptoms of gastrointestinal tract conditions

A 
change in appetite 
weight gain or loss
dysphagia 
intolerance to certain foods
nausea and vomiting 
change in bowel habit
abdominal pain 
flatus
67
Q

What is cholecystitis

A

gall bladder inflammation

A mixture of particulate solids precipitated from bile.

68
Q

What is Crohn’s disease

A

subacute, chronic inflammation of all layers of colon (transmural) Affects the lining of the colon

69
Q

What is volvulus

A

twisting of part of intestine around itself

70
Q

What is a left semi colectomy

A

removal of diseased are of bowel and length of normal bowel either side, removal of any potentially diseased areas.
two ends of healthy bowel are joined together

71
Q

What is an ostomy

A

is a surgical opening that connects an organ or underlying structure directly to the skin
there are different types of ostomies for different areas of the body they are named after the organ or structure they connect to
e.g. tracheostomy is an opening through the neck connecting the trachea allowing the patient to breath

72
Q

What is a stoma

A

a stoma the end of the organ or structure on the skin surface
can be reversible or permanent

73
Q

Types of Gastrointestinal stomas

A

colostomy - part of the colon is brought through the surface of the skin through an opening on to the abdomen
urostomy - permanent diversion of the urinary tract involving a stoma, It re-directs urine away from a bladder that’s diseased, has been injured, or isn’t working as it should.
ileal conduit - the ureter is implanted into a segment of the ileum that is led out through the abdominal wall. the loop of ileum is a passageway for the urine to pass

74
Q

specific indications for stomas

A

colostomy - cancer sigmoid colon, inflammatory bowl disease, trauma, volvulus, may be created to rest a portion of bowel
ileostomy - when removal of the colon is required, most commonly for inflammatory bowel disease

75
Q

Pathophysiology of atelectasis

A

partial or complete collapse of a lobe or the entire lung
reduced ventilation or blockage
obstruction of air to an from alveoli
trapped air absorbed into bloodstream, blockage stops further air entering alveoli
area of lung becomes airless
lung collapse
respiratory distress

76
Q

What is DVT

A

Deep vein thrombosis
decreased or mechanically altered blood flow
trauma to blood vessels stimulates the clotting cascade
platelets aggregate at the site, especially where venous states is present
platelets and fibrin form initial clot
decreased blood flow leads to decreased oxygenation and increase in hematocrits
RBC are trapped in the fibrin network
clot may completely occlude blood vessels or embolus may travel to other parts to the body

77
Q

What are the components of Virchows triad

A

Hyper-coagulability of blood - cancer, thrombophila, inflammatory disease
Stasis of blood - immobility, varicose veins, venous obstruction
Vessel wall injury - Surgery, chemical, irritation, inflammation

78
Q

What is paralytic ileus

A

hypo mobility of the GI tract in the absence of mechanical bowel obstruction, most often occurs post operatively
SNS activated intra operatively and bowel mobility inhibited
increase in cytokines and inflammatory mediators decrease bowel motility
peristalsis slows then stops
this leads to decreased movement of faecal matter through the bowels

79
Q

What is compartment syndrome

A

A painful and dangerous condition caused by pressure build-up from internal bleeding or swelling of tissues.
fluid enters a fixed volume compartment
increase in tissue and venous pressure
capillaries collapse
muscle and nerve ischaemia occurs
OR
external compression (plaster cast)
decrease in size of compartment
increase in intra-compartment pressure and decrease in arteriolar pressure
leads to muscle and nerve ischaemia occurs

80
Q

What is ischaemia

A

reduced blood flow

81
Q

What is metastasis

A

The spread of cancer cells from the place where they first formed to another part of the body

82
Q

What is intermittent claudication

A

muscle pain that happens when you’re active and stops when you rest

83
Q

What is Empyema

A

a collection of pus in the cavity between the lung and the membrane that surrounds it (pleural space).

nursing science (4 decks)

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