PME2 Pathophysiology Flashcards
Acute Thoracic aortic Dissection Pathophysiology
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
Addison Disease Pathophysiology
adrenal glands don’t release aldosterone cortisol and adrenal androgens to meet physiologic needs, despite release of ACTH from the pituitary
Adrenal Gland Physiology
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
Aortic Aneurysm Pathophysiology
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
Allergy Pathophysiology
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)
Anaphylaxis Pathophysiology
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
asthma pathophysiology
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
Body’s Response to Profound Dehydration
cerebral perfusion pressure decreases
Blood volume decreases
Preload decreases
BP falls
Heart rate increases
Cardiovascular Pathophysiologic Response to Acute Pulmonary Embolism
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
Function of adrenal androgens
no known physiologic role
mediate some secondary sexual characteristics in women (e.g, pubic and axillary hair)
overproduction may result in virilism
Function of Glucocorticoids
primarily cortisol
carbohydratemobilizing activity
ubiquitous physiologic regulators influencing a wide variety of bodily functions
Function of Mineralocorticoids
principally aldosterone
regulate renal sodium retention influencing electrolyte balance, intravascular volume, and blood pressure
How do pH changes affect potassium?
Hydrogen ions accumulate in the intracellular fluid (ICF) during states of acidosis
K+ shifts out to maintain a balance of cations across the membrane
How does the hepatic portal system work?
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
Hyperkalaemia Pathophysiology
Membrane hypopolarisation causes an increase in neuromuscular excitability
Hypokalaemia Pathophysiology
membrane hyperpolarisation causes a decrease in neuromuscular excitability (resting membrane potential is lower)
Nephrolithiasis (kidney and ureteral stones) Pathophysiology
calcium oxalate or calcium phosphate erodes through and creates a plate which gets bigger and stays in kidney or moves
Pathophysiology of Autonomic Dysreflexia
- 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
Pathophysiology of Bowel Obstruction
Obstruction
Dilation due to air and gas
wall swells
Bowel absorption function reduced
Fluid sequestered into the lumen
Ischemia
Necrosis
Perforation
Pathophysiology of DKA
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
Pathophysiology of Gall Stones
too much cholesterol or not enough bile salts that allow cholesterol to crystalise and form gall stones (biliary calculi)
Pathophysiology of Central Vertigo
Issue with vestibular Occular Reflex:
Vestibular nuclei in brainstem
Cerebellum (voluntary movement,coordination, balance, speech)
Parietal lobes (proprioception and visualinfo)
Pathophysiology of meningococcal septicaemia
bacteria changes permeability structure and degrades endothelial cells leading to fluid and electrolyte loss into interstitial space causing severe
hypotension and decreased cardiac output
Pathophysiology of migraine headache
neurons in trigeminovascular system triggered
neuropeptides increase and act on mast cells
peripheral and central sensitization
migraine
Pathophysiology of MODS
infection penetrates the blood
systemic inflammation response
vasodilation and capillary permeability causing relative hypovolemia whilst
vascular damage causes DIC and rash
MODS acidosis
death
Pathophysiology of normal response to a stimulus
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
Pathophysiology of Pancreatitis
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
Pathophysiology of perciardial effusion and cardiac tamponade
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
Pathophysiology of Peripheral Vertigo
Vestibular system
Cranial nerve VIII
Pathophysiology of portal hypertension
restricted blood flow, leading to increase in pressure leading to oesophageal varices and varices ascites
Pathophysiology of protein breakdown
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
Pathophysiology of Rabdomyolysis
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
Pathophysiology of renin angiotensin system shock compensation
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)
Pathophysiology of Second Contact with Antigen
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
Pathophysiology of Sepsis
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)
Pathophysiology of Septic Shock
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
Pathophysiology of shock
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
Pathophysiology of Nonperforated and Perforated Appendicitis
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
Pathophysiology of Hyperosmolar hyperglycaemic syndrome (HHS)
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
Pneumonia Pathophysiology
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
Potassium Notes
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
Respiratory Pathophysiologic Response to Acute Pulmonary Embolism
V/Q mismatch dead space
Splantnic Circulation Pathophysiology
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
Vertigo Pathophysiology
mismatch between visual, proprioceptive and vestibular inputs
What causes lysis?
Anaerobic metabolism
ATP
Chemotherapy
Major Burns
Rabdomyolysis
Sodium potassium pump
What do prostaglandins do?
inhibit acid secretions and stimulate mucous production and bicarbonate and protect against damaging compounds
What happens to potassium in cell lysis?
potassium leaks out of the cell
What happens when the portal system gets to 10 mmHG or more?
oesophageal varices and varices ascites develops
What influences serum potassium levels?
Aldosterone
Catecholamines
Insulin
renal regulation of potassium secretion
What is the digestive process?
mouth - mechanical breakdown
propulsion due to peristalsis in oesophagus and bowel
digestion within small bowel (pancreas helps)
defecation
What is the hormonal control of extrinsic control in renal filtration?
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
What is the pressure of the portal system?
3 mmHG
What is the role of potassium K+?
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)
Cardiogenic APO Pathophysiology
- The left ventricular fails
- Congestion of the pulmonary vasculature=increased hydrostatic pressure
- Overwhelmed osmotic/oncotic pressure (homeostatic forces are no longer equal)
- Plasma is fored through the vessel wall into the interstitial space then to the alveoli
- The surfactant that holds the alveoli open is diluted and the alveoli collapse
- Gaseous echange is severly limited then hypoxia rapidly ensues
