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Bachelor of Paramedic Science > PME2 Pathophysiology > Flashcards

PME2 Pathophysiology Flashcards

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1
Q

Acute Thoracic aortic Dissection Pathophysiology

A

Constant high pulsatile pressure weakens tunica intima

blood flows into the intima-media space

false lumen created

can move distally or proximally

can be partial or complete

complete creates true lumen collapse

most common in ascending aorta

will affect left or right coronary artery

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2
Q

Addison Disease Pathophysiology

A

adrenal glands don’t release aldosterone cortisol and adrenal androgens to meet physiologic needs, despite release of ACTH from the pituitary

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3
Q

Adrenal Gland Physiology

A

hypothalamus wakes up the pituitary gland

pituitary gland releases hormones telling adrenal glands to release cortisol and aldosterone

cortisol and aldosterone travel through blood and tell kidneys to react to stress

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4
Q

Aortic Aneurysm Pathophysiology

A

degeneration, of the aortic wall caused by:

smooth muscle cell depletion and disorganisation

elastic fiber fragmentation

excessive deposits of collagen and proteoglycans

allowing the aorta to increase in size and possibly rupture

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5
Q

Allergy Pathophysiology

A

Antigen exposure

TH2 cells produce antibodies

Hypersensitivity reaction produces IgE antibodies

IgE antibodies attach to FCεRI receptors
(on Eosinophils, Mast cells and Basophils)

IgE coated cells now sensitised to antigen

No allergic response occurs

(Molecule capable of inducing allergic response)

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6
Q

Anaphylaxis Pathophysiology

A

Histamine causes Nitric Oxide synthesis leading to systemic vasodilatation

Increased vascular permeability

Bronchial smooth muscle contraction

Increased mucus secretion

Leukotrienes contribute to bronchial smooth muscle contraction

Platelet Activating Factor & CysLTs cause urticaria & erythema

Prostaglandins regulate smooth muscle contraction

Histamine causes GIT symptoms of abdo pain/cramping and nausea and vomiting

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7
Q

asthma pathophysiology

A

immune system activated inflammatory mediators released inflammation of lower airway causing irritation and mucosal oedema causing turbulent air flow bronchoconstriction increases residual volume, PCO2, air trapping and alveolar pressure and reduces oxygen rich air to alveoli causing decreased blood oxygenation

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8
Q

Body’s Response to Profound Dehydration

A

cerebral perfusion pressure decreases

Blood volume decreases

Preload decreases

BP falls

Heart rate increases

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9
Q

Cardiovascular Pathophysiologic Response to Acute Pulmonary Embolism

A

Increased pulmonary vascular resistance and pushing back into RV

Increased right ventricular dilation

Decreased right ventricular contractility and output
(RV not as strong as LV)

Decreased left ventricular preload, therefore low cardiac output

Decreased Systemic BP

Decreased RV coronary perfusion
(as less blood available)

Decreased O2 delivery to right ventricle

Obstructive shock
(secondary to PE)

Death

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10
Q

Function of adrenal androgens

A

no known physiologic role

mediate some secondary sexual characteristics in women (e.g, pubic and axillary hair)

overproduction may result in virilism

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11
Q

Function of Glucocorticoids

A

primarily cortisol

carbohydratemobilizing activity

ubiquitous physiologic regulators influencing a wide variety of bodily functions

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12
Q

Function of Mineralocorticoids

A

principally aldosterone

regulate renal sodium retention influencing electrolyte balance, intravascular volume, and blood pressure

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13
Q

How do pH changes affect potassium?

A

Hydrogen ions accumulate in the intracellular fluid (ICF) during states of acidosis

K+ shifts out to maintain a balance of cations across the membrane

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14
Q

How does the hepatic portal system work?

A

blood flows through spleen, pancreas, gut, intestines

goes through portal vein into liver

sinusoids filter and remove toxins and bacterias

store up to 75% of proteins and carbs

1L blood per minute through liver, inferior vena cava and then through arterial system

3mmHG of pressure in portal system - easy to be damaged

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15
Q

Hyperkalaemia Pathophysiology

A

Membrane hypopolarisation causes an increase in neuromuscular excitability

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16
Q

Hypokalaemia Pathophysiology

A

membrane hyperpolarisation causes a decrease in neuromuscular excitability (resting membrane potential is lower)

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17
Q

Nephrolithiasis (kidney and ureteral stones) Pathophysiology

A

calcium oxalate or calcium phosphate erodes through and creates a plate which gets bigger and stays in kidney or moves

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18
Q

Pathophysiology of Autonomic Dysreflexia

A
  • nociceptors stimulated below T6
  • lateral spinothalamic tract carries message to T6 where cord severed
  • creates overexaggerated reflex stimulus by simpathetic nervous response
  • leads to massive arterial resistance (constriction) due to splantnic circulation (abdomen supply)
  • 1/4 blood volume sent to below T6
  • arterial constriction causes massive significant rise to system BP resulting in vasalspasm hypotension and pallor of skin
  • BP stimulates baroreceptors in carotids
  • message sent to CNIX and CNX to try to reduce BP, leading to vasodilation above T6 and reflex bradycardia and flushed skin, headaches
  • uncontrolled hypertension as splantnic circulation not controlled
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19
Q

Pathophysiology of Bowel Obstruction

A

Obstruction

Dilation due to air and gas

wall swells

Bowel absorption function reduced

Fluid sequestered into the lumen

Ischemia

Necrosis

Perforation

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20
Q

Pathophysiology of DKA

A

glucose not converted to energy as not enough insulin or insulin resistance which increases BGL (glucose can’t get into cell)

fat breakdown for energy produces ketone acids

metabolic acidosis develops when BGL extremely high

kidney produces excess urine causing polyruia and thirst

person can’t drink enough to maintain fluid levels causing dehydration and hypovolaemia

respiratory rate increases to blow off excess CO2 caused by ketones

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21
Q

Pathophysiology of Gall Stones

A

too much cholesterol or not enough bile salts that allow cholesterol to crystalise and form gall stones (biliary calculi)

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22
Q

Pathophysiology of Central Vertigo

A

Issue with vestibular Occular Reflex:

Vestibular nuclei in brainstem

Cerebellum (voluntary movement,coordination, balance, speech)

Parietal lobes (proprioception and visualinfo)

23
Q

Pathophysiology of meningococcal septicaemia

A

bacteria changes permeability structure and degrades endothelial cells leading to fluid and electrolyte loss into interstitial space causing severe
hypotension and decreased cardiac output

24
Q

Pathophysiology of migraine headache

A

neurons in trigeminovascular system triggered
neuropeptides increase and act on mast cells
peripheral and central sensitization
migraine

25
Q

Pathophysiology of MODS

A

infection penetrates the blood

systemic inflammation response

vasodilation and capillary permeability causing relative hypovolemia whilst

vascular damage causes DIC and rash

MODS acidosis

death

26
Q

Pathophysiology of normal response to a stimulus

A

stimulus
nociceptor - pain receptor
peripheral nerve - afferent pain fibre (dorsal ganglion and dorsal root)
synapse
spinal decussation
lateral spinothalamic tract (pain)
reticular formation (in pons and medulla - awareness, alert)
thalamus (sensory relay centre)
somatosensory cortex - parietal lobe - locate pain
hypothalamus - stress response (sympathetic)
limbic system - emotional response

27
Q

Pathophysiology of Pancreatitis

A

large pooling of pancratic juices in the pancreas which overwhelms trypsin inhibitor

too much trypsin in pancreas will start eating pancreas

can cause multi organ dysfunction secondary to cytokine cascade

death occurs rarely

28
Q

Pathophysiology of perciardial effusion and cardiac tamponade

A

stretch is speed dependent, eg:
slow effusion = > ability to stretch
effusion results in too much fluid in pericardial cavity
increases pericardial pressure

cardiac tamponade results when increased pericardial pressure creates cardiac dysfunction

29
Q

Pathophysiology of Peripheral Vertigo

A

Vestibular system

Cranial nerve VIII

30
Q

Pathophysiology of portal hypertension

A

restricted blood flow, leading to increase in pressure leading to oesophageal varices and varices ascites

31
Q

Pathophysiology of protein breakdown

A

acinar cells release trypsinogen and trypsin inhibitors in pancreas
go through pancreatic duct into duodenem
then transformed into tryptin by enteropeptidase which removes amino
acids and creates trypsin to break down proteins
trypsin activated peptide can then be used as a tool to screen for pancreatitis

32
Q

Pathophysiology of Rabdomyolysis

A

bilipid layer of cell impermable to K and NA

Sodium K pump keeps concentration gradient in homeostasis

pump fails and lets K leak out of the cell causing hyperkalaemia

sodium enters cell taking a lot of water with it and cell ruptures

33
Q

Pathophysiology of renin angiotensin system shock compensation

A

kidneys pick up drop in BP

Renin release converts angiotensin 1 to angiotensin II in lungs

II is potent vasoconstrictor, increases antidiuretic hormones and aldosterone (to increase water uptake)

34
Q

Pathophysiology of Second Contact with Antigen

A

Antigen binds to sensitised IgE

Activates signalling cascade

Eosinophils, Mast cells & Basophils degranulate

Release cellular inflammatory mediators
Histamine 
Platelet Activating Factor
CysLT
Tryptase
Prostoglandins
Cytokine/Chemokine

Allergic response occurs

35
Q

Pathophysiology of Sepsis

A

Infection penetrates the blood causing dysregulated inflammation response and body is overwhelmed by release of anti-inflammatory mediators increasing vascular permeability causing fluid shifts and cellular hypoxia. Fluid loss into interstitium causes increase in peripheral vascular resistance worsening tissue ischemia and increasing lactate. Within sepsis response microcirculatory dysfunction resulting in circulatory dysfunction and DIC)

36
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

37
Q

Pathophysiology of shock

A

after initial injury

HR increases to maintain volume circulating

As HR gets faster (>150/180), myocardium won’t stretch and preload not there

BP declines as HR can only do so much

refractory shock

death

38
Q

Pathophysiology of Nonperforated and Perforated Appendicitis

A

lumen obstructed by faeces, tumour, foreign body

E. coli and bacteroids fragilis overgrowth causing secretions

secretions don’t drain, intraluminal pressure increases

venous and arterial blood flow restricted, mucosa ulcerates, bacteria causes inflammation and oedema, restricted blood flow causes tissue death and gangrene

appendix splits open and faecal matter leaks into perineum

39
Q

Pathophysiology of Hyperosmolar hyperglycaemic syndrome (HHS)

A

insulin can’t get into cell due to insulin resistance

BGL increases

enough sugar getting into cell to provide energy, therefore no fat breakdown (keto acidosis)

big cells draw fluid into circulation to help dilute glucose levels

diuresis occurs

40
Q

Pneumonia Pathophysiology

A

pathogen multiplication - invade from naso or oropharyngeal pathway and aspirate into lungs

local inflammation - macrophages overwhelmed, cytokines create inflammation and increase microvascular permeability and flooding of WBC into alveolar space causing diffusion issue

systemic inflammation - cytokines in alveolar space spread into systemic system creating systemic response of increased WBC, temp, cardiac output

dysregulation

41
Q

Potassium Notes

A

Major intracellular cation 90%

Concentration maintained by Na+/ K+ pump

Regulates intracellular Na+ and H+ electrical neutrality

Transmits and conducts nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction

42
Q

Respiratory Pathophysiologic Response to Acute Pulmonary Embolism

A

V/Q mismatch dead space

43
Q

Splantnic Circulation Pathophysiology

A

blood flows through spleen, pancreas, gut, intestines then goes through portal vein into liver
sinusoids filter and remove toxins and bacterias, store up to 75% of proteins and carbs
Liver has 1L blood flow every minute then through inferior vena cava and then through arterial system

44
Q

Vertigo Pathophysiology

A

mismatch between visual, proprioceptive and vestibular inputs

45
Q

What causes lysis?

A

Anaerobic metabolism

ATP

Chemotherapy

Major Burns

Rabdomyolysis

Sodium potassium pump

46
Q

What do prostaglandins do?

A

inhibit acid secretions and stimulate mucous production and bicarbonate and protect against damaging compounds

47
Q

What happens to potassium in cell lysis?

A

potassium leaks out of the cell

48
Q

What happens when the portal system gets to 10 mmHG or more?

A

oesophageal varices and varices ascites develops

49
Q

What influences serum potassium levels?

A

Aldosterone

Catecholamines

Insulin

renal regulation of potassium secretion

50
Q

What is the digestive process?

A

mouth - mechanical breakdown

propulsion due to peristalsis in oesophagus and bowel

digestion within small bowel (pancreas helps)

defecation

51
Q

What is the hormonal control of extrinsic control in renal filtration?

A

renin angiotensin system:

renin (enzyme) secreted by juxtoglomerular cells converts angiotensinogen to angiotensin I

angiotensin converting enzyme transforms angiotensin I into angiotensin II, stimulating aldosterone in adrenal glands causing sodium reabsorption, which draws in water to increase blood volume and increases systemic blood pressure

52
Q

What is the pressure of the portal system?

A

3 mmHG

53
Q

What is the role of potassium K+?

A

major intracellular cation

Concentration maintained by sodium/Potassium pump

Regulates intracellular electrical neutrality in relation to Na+ and H+

Essential for transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction

(90-98% inside cell)

54
Q

Cardiogenic APO Pathophysiology

A
  1. The left ventricular fails
  2. Congestion of the pulmonary vasculature=increased hydrostatic pressure
  3. Overwhelmed osmotic/oncotic pressure (homeostatic forces are no longer equal)
  4. Plasma is fored through the vessel wall into the interstitial space then to the alveoli
  5. The surfactant that holds the alveoli open is diluted and the alveoli collapse
  6. Gaseous echange is severly limited then hypoxia rapidly ensues

Bachelor of Paramedic Science (19 decks)

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