Condition Pathophysiology Flashcards
Asthma
bronchi and bronchioles respond stimuli with 3 changes:
* Inflamm mucosa+oedema
* Bronchoconstriction
* Increase secretion mucus
Partial obstruction small bronchi, bronchioles:
air trap, hyper inflation lungs
-residual volume increases = inhaling and coughing difficult
Total obstruction: mucus plugs = O2 deplete =
resp and metab acidosis
COPD
irreversible tissue degeneration
+
obstruction airway lung
Emphysema
- destruction alveolar = overinflated alveolus
- loss septae, capillaries = decrease SFA
- loss elastic fibres = decreased recoil.
- fibrosis, thickening bronchial walls.
- difficulty expiration, air trapping
Chronic Bronchitis
- inflamed , swollen mucosa
- hypertrophy+hyperplasia mucus glands = increase secretions
- chronic irrit, inflam= fibrosis, thick bronchial wall = obstruction
ACPO,HF
heart’s inability effectively fill and/ or eject (pump) blood
Systolic HF “pump dysfunction”
* decreased contractity/force of contraction (eg. myocardial infarction, myocarditis).
* decreased blood supply to the heart (e a coronary artery disease),
* increased afterload (e g. hypertension
*impaired mechanical function (e a. valve disease)
normal preload, but decreased contractility = inadequate emptying of ventricles during systole
Diastolic HF; “filling dysfunction”
* restrictive cardiomyopathy
* valve disease
* hypertension)
noncompliant ventricles - unable fill during diastole = increased filling pressures, decreased preload, normal contractility = decreased SV
SVXHR=CO
- Biventricular heart failure
- Cor pulmonale
secondary to pulmonary arterial hypertension - Left-sided heart failure
« Impaired ability of the left ventricle to maintain adequate cardiac output without an increase in left-sided filling pressures - Right-sided heart failure
«Impaired ability of the right ventricle to deliver of blood flow to the pulmonary circulation and + right atrial pressure.
ACPO:
* heart maintain time, but then = back up blood, fluid collect alveoli ,interstitial area
*hydrostatic pressure become high = shift fluid out capillaries into alveoli
*excess fluid interfere diffusion and effect lungs surfactant
diff expand lungs, end collapse.
Anaphylaxis
T1 allergic reaction, systemic hypersensitivity reaction
IgE bound mast cells;
release histamine chemical mediators
= immediate inflam, pruritis
antigen binds IgE antibodies, large amounts chemical mediators **(histamine) from mast cells in general circulation quick= **
two serious problems
systemic vasodilation w sudden, severe drop BP, increased capillary permeability
nerve endings irritated lungs= oedema, bronchoconstriction (b+b) =obstruction airflows
Addison’s Disease
aka primary adrenal insufficiency, chronic condition
adrenal glands fail produce enough cortisol, mineralocorticoid hormones.
regulate a myriad of physiologic processes, including metabolism, immune function, skeletal growth, cardiovascular function, reproduction, and cognition.
cause autoimmune disorder, infection, damage adrenal glands.
“primary” underlying problem is with adrenal gland
MI
full occlusion coronary artery
three ways:
* thrombus build up
* vasospasm partial occlusion
* thrombus breaks off - emboli lodge
most transmural (3 layers)
point obstruction - heart tissue necrotic, injury, inflamm, ischemia around neurotic zone
- cell destruction, enzymes release from myocardium
- myocardial contractility conduction lost quickly O2 depleted
*gradually nonfunctional scar tissue
Epilepsy/Seizure
neurons - abnormal, excessive, synchronised period electrical activity
clusters of brain neurons temporarily impaired (seconds-minutes)
paroxysmal electrical discharges
result in disordered awareness, behavior, movement
caused -* too much excitatory, too little inhibitory activity
many unknown causes; some known causes (e.g. brain infection):
- increased excitation: long-lasting/fast activation of NIMDA receptor via glutamate
*decreased inhibition: genetic mutations dysfunctional GABA receptors
SE results in impaired respiration and skeletal muscle activity is intense; the combination can lead to severe
hypoxia
hypoglycaemia,
acidosis
decreased BP
potentially resulting in brain damage
Head Injury
increase ICP, cerebral tissues swell in enclosed skull; to ensure adequate CPP body compensates and increases MAP = HTN
Cell damage and bleeding =
* inflammation and vasospasm around injury site
* increased ICP
* further general ischemia, dysfunction.
central area damage undergoes necrosis andreplaced by scar tissue/ cyst
damaged neurons =release of inflammatory neurochemical mediators
mediators alter vessel permeability, oedema, neuronal ischemia, necrosis, and cell death
heightened metabolism in injured brain stimulated by increase in circulating levels of catecholamines contributing to a viscous cycle of ischaemia, cell death and tissue oedema.
Damaged neurons – chemical mediators (vessel permeability, oedema) – further damage –
increase in catecholamines – results further damage.
Heat Stroke
imbalance metabolic prod and subsequent loss heat body
increase core body temp = multiple undesirable effects body systems
systematically increased temperature = swelling ,
degeneration both cellular
and tissue levels
Gastroenteritis
damage villous brush border intestine = malabsorption intestinal contents = osmotic diarrhoea.
release of toxins bind to specific enterocyte receptors = release chloride ions intestinal lumen,= diarrhoea.
Rhabdo:
traumatic/medical injury sarcolemma (myocyte cell membrane) skeletal muscle cells.
intracellular ions
myoglobin
creatine kinase (CK),
urates into circulation =
electrolyte disturbances acidaemia
DIC
renal failure
multi-organ failure.m
Trauma:
coagulation cascade stops bleeding - fibrin mesh stabilises activated platelet
2 pathways;
extrinsic/intrinsic=
activation F X, + conversion prothrombin to thrombin
thrombin converts fibrinogen to fibrin and triggers activation FXIII to cross-link fibrin strands and stabilise clot
stable clot is formed by activated platelets, fibrin and factor XIIIa.
Intrinsic pathway – Results from contact activation (surface damage), internal damage
Extrinsic pathway – Results form (external) trauma/ inflammation= tissue factor release
Tension Pneumothorax
particular pattern damage creates flap tissue/one-way valve effect
opening enlarges on inspiration, promoting airflow into the pleural cavity
expiration, opening sealed preventing removal air from pleural cavity
each inspiration = continual increases air in pleural cavity
pa increases on affected side eventually push mediastinal contents against other lung, compressing other lung and inferior vena cava.
decreased venous return significantly affected by kinking vessels, especially inferior vena cava, as mediastinum pushed towards the contralateral side.
air not released external, heart unable to fill other lung no longer be able to ventilate, inducing cardiac arrest.
Cocaine Toxicity:
cocaine cross blood- brain barrier by proton- coupled cation channel
block re-uptake;
neurotransm dopamine
serotonin and noradrenaline = vasoconstriction ,hypertension.
Sepsis:
cytokines released circulation
multifaceted host response invasion normally sterile tissue by pathogen
recruitment inflammatory cells and acute- phase response normally limited by anti-inflammatory mediators
failure to control the inflammatory cascade=
- loss of capillary integrity
- maldistribution microvascular blood flow
- stimulation nitric oxide production
all lead to organ injury + dysfunction
