Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bachelor of Paramedic Science > SPOPs Pathophysiology > Flashcards

SPOPs Pathophysiology Flashcards

You may prefer our related Brainscape-certified flashcards:
NREMT® Paramedic flashcards NREMT® EMT flashcards Biology 101 flashcards
1
Q

Pre-Eclampsia Pathophysiology

A

defective spiral artery remodelling causing placental hpoperfusion

diseased placenta releases proinflammatory proteins into maternal circulation

inflammatory markers attack endothelial cells

systemic vasoconstriction and endothelial dysfunction

hypertension and end-organ damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

HELLP Pathophysiology

A

believed to be an immunological response caused when maternal cells come into contact with a genetically distinct fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Breech Delivery Pathophysiology

A

foetus has not turned into normal cephalic presentation

head emerges last and can become entrapped as cervix not fully dialated

can result in foetal asphyxiation and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Primary PPH Pathophysiology

A

During pregnancy the maternal blood volume increases by approx 50%

greater increase in plasma volume relative to RBC’s, leading to a fall in haemoglobin concentration and haematocrit

estimated blood flow at term to the uterus is 500-800 ml/min (10-15% of cardiac output), with most traversing the placental bed

failure of the uterine myometrial fibres to contract and retract with resultant continuation of bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathophysiology of post delivery uterine contractions.

A

uterine vessels supplying placental site traverse a weave of myometrial fibres which contract after birth resulting in myometrial retraction. This results in the uterine blood vessels becoming compressed and kinked, occluding blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathophysiology of Secondary PPH

A

infection resulting from retained piece of placenta or membrane, causing a failure of uterine contraction and retraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Croup Pathophysiology

A

virus causes swelling of the larynx and trachea causing the airways to narrow and breathing to become more difficult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

RSV Pathophysiology

A

starts as an upper respiratory infection, with familiar cold symptoms

has ability to quickly spread down from the nose and throat into the lower respiratory tract

it infects and causes inflammation in the tissues of the lungs (causing pneumonia) and the tiny bronchial air tubes (causing bronchiolitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Bronchiolitis Pathophysiology

A

inflammation of the lining of the epithelial cells of the bronchioles causing mucus production, inflammation and cellular necrosis

these cells can then obstruct the airway cause wheezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pathophysiology of Asthma

A

The smooth muscles of bronchials are exposed to an antigen

Mast cells within the lung degranulate, spilling their contents which initiates an inflammatory mediated response causing bronchial smooth muscle constriction, mucosal oedema and mucosal plugging from thick tenacious fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pathophysiology of Sepsis

A

inflammatory stimulus (eg, a bacterial toxin) triggers production of proinflammatory mediators

mediators cause neutrophil–endothelial cell adhesion, activate the clotting mechanism
and generate microthrombi

microthrombi opposed by anti-inflammatory mediators, causing a negative feedback mechanism

arteries and arterioles dilate, decreasing peripheral arterial resistance and cardiac output increases (Initial stages of shock)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pathophysiology of Septic Shock

A

sepsis not treated

cardiac output decreases, BP falls (with or without an increase in
peripheral resistance) causing typical features of shock

Vasoactive mediators cause blood flow to bypass capillary exchange vessels (a distributive defect)

Poor capillary flow from this shunting and capillary obstruction by microthrombi decreases oxygen delivery, impairing removal of carbon dioxide and waste products

Decreased perfusion causes dysfunction and sometimes failure of one or more organs, including the kidneys, lungs, liver, brain, and heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lanugo

A

fine hair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Vernix

A

white coating thought to protect skin whilst in tummy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Fertilisation Steps

A

200 - 500 million sperm enter vagina

acid in vaginal kills all but a few hundred

sperm travel through vagina, cervix, uterus and fallopian tube

sperm try to attach to the egg’s zona palucida

egg snaps shut to stop sperm entering

zygote froms from chromosomes and DNA

baby formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pronuclei

A

formed by fusion of egg and sperm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cleavage

A

zygote divides into 2, 4 then 8 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Morula

A

zygote with 16 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Blastocyst

A

has embryoblast and trophoblast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Placental Formation

A

Blastocyst implants into uterine wall

trophoblast invade endometrial lining for baby to get nutrients

special glands secrete glucose

placenta starts at 8-12 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Aim of Physiological Changes During Pregnancy

A

maximise nutrition and oxygen to the developing fetus and help the maternal system adjust to the extra stress and demands of pregnancy to:

support foetus

protect foetus

prepare uterus for lablour

protect mother from cardiovascular injury at delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Human Chorionic Gonadotrophin (HcG)

A

Detected in blood 9 days and in urine 10-12 days after fertilisation

Linked to maternal changes in first trimester

causes nausea and vomiting in first trimester

changes to smell, taste, saliva

Prevents degeneration of the corpus luteum and stimulates production of oestrogen and progesterone until placenta takes over

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Oestrogen Function During Pregnancy

A

Produced by corpus luteum, until the placenta takes over

Stimulates growth of tissues including vascularisation of the uterus

Causes swelling and softening of connective tissues (cervix, nipples, ligaments) by increasing water content in extracellular mix

Increased fluid retention

Later in pregnancy can block insulin and affect glucose uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Progesterone Function During Pregnancy

A

Secreted by the corpus luteum until the placenta takes over

thickens and nourish the uterus walls

Uterotonic inhibitor – lowers smooth muscle excitability to prevent uterine contractions, not only in the uterus but, in the ureters, stomach, and intestines

Increases the sensitivity of the maternal chemoreceptors to carbon dioxide, stimulatingventilation at lower atrial pressures

inhibits lactation during pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Prolactin Function During Pregnancy

A

inhibits lactation during pregnancy

enlarges mammary glands and prepares them for milk production

produces breast milk

26
Q

Relaxin Function During Pregnancy

A

inhibits uterus contraction to prevent premature birth

relaxes blood vessles, increasing blood flow to placenta and kidneys

relaxes joints of the pelvis

softens and lengthens cervix during birth

27
Q

Oxytoxin Function During Pregnancy

A

stimulates contraction of uterus muscles during labour

triggers production of prostaglandins to increase contractions

can be used to induce labour

28
Q

Uterus Changes During Pregnancy

A

uterus leaves the pelvis and ascends into the abdominal cavity

uterus can grow up to 5 times its normal size

abdominal contents become displaced

fundus increases in size until 38 weeks and then descends in preparation for delivery

Uterus blood flow increases from 50mL/min at 10 weeks to 500mL/min at term

29
Q

Cervix Changes Druing Pregnancy

A

mucous glands secrete operculum (mucous plug) which seals the uterus and protects from infection

30
Q

Vaginal Changes During Pregnancy

A

blood supply increases due to uterus and embryo demands

blood causes colour changes in the vulva leading to a bluish discoloration

feeling of fullness and heaviness

increased discharge

31
Q

Musculoskeletal Postural Changes During Pregnancy

A

equilibrium of the spine and pelvis

centre of gravity no longer falls over the feet

need to lean backwards to gain equilibrium resulting in disorganisation of spinal curves

32
Q

Musculoskeletal Muscle Changes During Pregnancy

A

alterations in collagen metabolism due to altered levels of relaxin, oestrogen and progesterone

connective tissue more pliable and laxative

reduced joint stability especially in symphysis pubis and sacroiliac joints

elongation of abdominal muscles can cause pelvic girdle pain and linea alba (abdominal separation)

33
Q

Haematological Changes During Pregnancy

A

major alteration to blood composition to protect against:

normal blood loss during delivery (round 500ml)

maintain cardiac output despite widespread vasodilation

promote rapid haemostasis during placental separation

bacterial infection

34
Q

Haemodilution

A

blood volume increase by 30-40% (approx. 1500mL) between 7 and 34 weeks

plasma increases at a faster rate than other cellular components

plasma increase begins around 7 weeks, rapidly during second trimester, reaching 40-50% by 32 weeks

RBC volume increases slower, reaching 2-30% increase

RBC increase is less than the total plasma increase = physiological aneamia

blood viscosity reduced by 20% which decreases heart’s workload

haemoglobin concentration falls due to haemodilution - can be concern due to increased iron requirements

WBC (neutrophil) increases to protect against bacterial infections

hypercoagulability due to increase in clotting factors incl fibrinogen

35
Q

Cardiovascular Changes During Pregnancy

A

progesterone decreases BP causing decreased systemic vascular resistance

cardiac output increases by 30 – 50% peaking in 3rd trimester due to increased blood volume

HR increases 15% and stroke volume 30%

IVC compression at later stages (25-30% drop in CO lying supine)

can all lead to dizziness, light headedness, palpitations, decreased exercise tolerance.

36
Q

Respiratory Changes During Pregnancy

A

changes in ventilation due to:

BMR increase causes increased oxygen consumption (20%)

progesterone increases sensitivity of chemoreceptors to CO2 and leads to 40% ventilation increase

40% increase in tidal volume by end of first trimester (from 500ml – 700ml)

35-45% decrease in chest wall compliance, decreasing functional residual capacity (FRC) and residual volume (RV)

Progesterone production enhances response to hypercapnia and water retention

37
Q

Gastrointestinal Changes During Pregnancy

A

progesterone relaxes muscles decreasing GI motility and lower oesophageal sphincter tone causing:

reflux

nausea and vomiting

constipation

38
Q

Renal Changes During Pregnancy

A

Systemic vasodilation early in pregnancy increases renal plasma volume and GFR

dilation of the kidney’s collecting system causes retention of electrolytes necessary for foetal growth limiting proteins, glucose and amino acids in urine

increase in total body sodium increases plasma volume

progesterone dilates kidneys and potentially kinks the ureters from 10 weeks and can cause urinary stasis and increased risk of infection

39
Q

Integumentary Changes During Pregnancy

A

Melanocyte stimulating hormone increases and causes deeper pigmentation of the skin leading to:

patchy mask on the face (chloasma)

pigmented line on the abdomen from the pubis to the umbilicus (linea niagra)

Areola darken and toughen up

Stretch marks in the collagen layer of the skin causing red stripes (stria gravidarum)

40
Q

Hyperemesis Gravidarum (HG)

A

Onset 6 – 8 weeks and in some settles around 21 weeks, others until full term

causes chronic dehydration and malnutrition and can lead to excessive weight loss

if Pts don’t receive aggressive and consistent management they are at extreme risk of:

loss of > 5-10% of pre-pregnancy body weight

dehydration and production of ketones

nutritional deficiencies

metabolic imbalances

severe fatigue and debility

depression/anxiety and trauma

premature labour/delivery

41
Q

Morning Sickness (NVP)

A

usually begin at 6 – 8 weeks, peaking at 9 weeks and settles at 14 weeks

lose little if any, weight

don’t impact ability to eat/drink normally

vomit infrequently and the nausea is episodic but not severe or constant

diet or lifestyle changes are enough most of the time

typically improve after first trimester, but may have brief period of it later in pregnancy

still able to work most days and fulfill normal life duties

42
Q

Role of oxytocin during labour

A

love hormone

causes feelings of euphoria

helps uterine contractions

helps bonding with baby

responsible for milk ejection

43
Q

Role of prolactin during labour

A

the ‘mothering’ hormone

major hormone of breastfeeding

may play a role in helping baby

adjust to life outside the womb

peaks at the start of labour

44
Q

Role of endorphins during labour

A

causes feelings of euphoria

natural pain relief

increased with feelings of love

works on same area of our brain as morphine and heroin

45
Q

Role of adrenaline during labour

A

fight or flight response

initially slows labour, natural reaction to birth

gives sudden rush of energy before delivery

46
Q

Role of melatonin during labour

A

improves and initates oxytoxin function to work more effectively

makesg contractions longer and labour quicker

higher levels at night - why more labour at night

47
Q

Respiratory Distress Syndrome (RDS) Pathophysiology

A

surfactant deficiency, especially in immature lungs which increases the surface tension in small airways and alveoli, reducing the lungs compliance

48
Q

What effect does Asthma have?

A

Decreased flow rates and reduced gas exchange

Air gets into lungs due to decreased intrapulmonary pressure on inspiration, but struggles to get out on expiration due to the increased pressures and further narrowing

Lung stretch receptors sense hyperinflation and trigger hyperventilation

More air is trapped and CO2 builds up

Decrease in alveoli perfusion

Intrathoracic pressure impedes venous return

49
Q

Asthma Mortality

A

rare

3 major contributing factors of severity, management and psychological factors

50
Q

Stages of Cognitive Development

A

Stage 1 - Sensorimotor Period

Stage 2 - Preoperational Period

Stage 3 - Concrete Operational Period

Stage 4 - Formal Operational Period

51
Q

Paget’s Stage 1 Sensorimotor Period

A

Birth to 2 years

coordination of sensory input and motor responses

development of object permanence

52
Q

Paget’s Stage 2 Preoperational Period

A

2 to 7 years

development of symbolic thought marked by irreversibility, centration, and egocentrism

53
Q

Paget’s Stage 3 Concrete Operational Period

A

7 - 11 years

Mental operations applied to concrete events

mastery of conservation, hierarchical classification

54
Q

Paget’s Stage 4 Formal Operational Period

A

11 through to adulthood

Mental operations applied to abstract ideas; logical, systematic thinking

55
Q

Neurological Differences in Paediatric Patients

A

Undeveloped temperature regulation

Large head in relation to body size
(More susceptible to head injuries)

Incomplete motor development
(Increased risk of falls)

Thinner cranial bones
(increased risk of head trauma)

Presence of fontanelles at birth
(Anterior fontanelle closes 12-18months, Posterior closes 2-3 months)

(Neonates and infants increased risk of hypothermia)

56
Q

Anatomical Respiratory Differences in Paediatric Patients

A

Narrower airways

Large tongue with smaller mouth|
(Greater risk of obstructions)

Soft cricoid cartiledge
(External pressures can obstruct airway)

Larynx is higher and more anterior
(More difficult airway management)

Trachea is soft and compressible and smaller in diameter
(Hyperextension or hyperflexion of neck can fully compress airway and difficult airway management)

(Greater risk of obstructions -Swelling (inhalation burns, croup etc), -Foreign bodies, -Nasal mucous (RSV))

57
Q

Physiologicaly Respiratory Differences in Paediatric Patients

A

Higher basal metabolic rate

Smaller and fewer alveoli
(Smaller area for gas exchange and increased dead space - must breathe faster to achieve adequate minute ventilation)

Infants are obligatory nasal breathers
(partially blocked results in increased resistance, laboured breathing and difficult feeding)

Infants use abdominal muscles for breathing
(Any distention of injury can quickly lead to respiratory distress)

(Naturally higher respiratory rates and oxygen consumption resulting in greater loss of water from lungs)

58
Q

Cardiovascular Differences in Paediatric Patients

A

Large body surface area

Decreased contractile efficiency of heart
(Difficulting manipulating their cardiac stroke volume - increased HR to increase stroke volume.)

Smaller volumes of circulating blood
(Small amounts of blood loss constitute a large percentage of their volume.)

Cardiac output, oxygen consumption and delivery are higher
(Anything that causes an increase in oxygen consumption and a decrease in delivery can cause decompensation)

Smaller veins and more subcutaneous tissue
(Difficult cannulation)

Higher metabolic rate
(Increased cardiac workload and HR)

(Greater fluid losses through evaporation. Require greater fluid requirements to maintain adequate circulating volume.)

59
Q

Gastrointestinal Differences in Paediatric Patients

A

Increased glucose requirements with poor glycogen stores

Reliance on others for fluid and nutrition
(Hard for caregivers to meet the childs needs, especially when sick)

Higher metabolic rate
(ncreased waste production and increased nutrition and fluid requirements)

Cylindrical abdomen
(Poor protection of vital organs)

Proportionally longer intestinal length
(Greater fluid losses)

Immature lower oesophageal sphincter tone (up to 12 months)
(Regurgitation)

(Can rapidly develop hypoglycemia and muscular fatigue)

60
Q

Musculoskeletal Differences in Paediatric Patients

A

Lack of tone, muscle and power

Bones are soft until puberty
(Bones will break and bend more easily)

Bones are more flexible
(Serious internal injuries can result without fractures present)

Growth plates are still active
(Fractures to these long bones can have significant impacts on growth)

Babies born with more bones than adults
(Many of these will fuse together as they grow)

(Rely on others to keep stable and safe, Large head held by weak neck so more prone to head and spinal injuries, cannot initiate shivering with poor muscle tone)

61
Q

Renal Differences in Paediatric Patients

A

Immature tubular function

Decreased ability to concentrate urine
(loss of water)

Age related changes in pharmokinetics and pharmodynamics
(slower excretion of some drugs)

(sodium wasting)

62
Q

Other Differences in Paediatric Patients

A

body to surface area ratio is 4 times that of adults and heat production is only 1 and a half times as high

nerve endings in the retinas are not fully developed
(Blurred images and shapes seen in the first few weeks - will start to smile at you when clearly sees you smiling)

(More prone to accidental hypothermia)

Bachelor of Paramedic Science (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions