Pathophysiology

Pneumonia (4)

1. Congestion (aspiration reaches alveoli, fluid enters alveoli, organism multiplies, inflammatory response with mediators, neutrophils).

2. Red hepatisation (capillaries dilate, alveoli fills with RBC, neutrophils, fibrin. lung becomes red and granular like liver)

3. Grey hepatisation (blood flow decreases, leukocytes and fibrin consolidation. Phagocytosis occurs)

4. Resolution (remaining exudate becomes lysed and processed by macrophages)

COPD

Chronic inflammation and oxidative stress

Fibroblast proliferation = fibrosis of small airways/narrowing

Hyperplasia of mucus cells = increased production

Hypoxaemic vasoconstriction = pulmonary hypertension

Defective immune response = bacteria consolidation

Hyperinflation of chest = gas trapping, reduced TV

Bronchitis = increased mucus production, hyperreactivity of airways, oedema

Emphysema = breakdown of alveolar walls resulting in less surface area.

Asthma

1. hyperresponsiveness (bronchospasm)

2. inflammation = increased mast cells, histamines, WBC, increased fluid/mucus. Systemic IgE production

3. airflow obstruction = narrowed, thickened airways

4. 
   

5. This results in hyperinflation, gas trapping (decreased TV), iWOB, V/Q mismatch, early hypoxaemia, late CO2 retention and resp failure

PE

Thrombus formation (RBC, platelets or fibrin meshwork)

Virchow’s triad promotes thrombus formation (abnormal blood flow, hypercoagulability, altered vessel wall)

Thrombus breaks off wall = embolism —> lungs.

Backlog of blood = increased pulm pressure = increased RV pressure = strain or HF

decreased SV and BP = SNS response to increase HR and vasoconstrict.

HIGH V/Q mismatch = hypoxia, inflammation. Inflammation = bronchoconstriction.

ECG = SI, QIII, TIII

Pneumothorax

Air into pleural space from:

communication between alveolar space and pleural space,

communication between environment and pleural space

presence of gas trapping organism

Traumatic vs spont

Primary spont = unknown cause

secondary spont = lung disease

Heart failure

Classes HFrEF (<50%) or HFpEF (50% or above)

Chronic = sx for 3/12 and received treatment

Acute = decompensated, cardiogenic shock, APO

Decreased CO, reduced organ perfusion, activation of neurohormonal and inflamm systems, worsening cardiac function.

SNS (activated by low CO/BP) = catecholamine release = further increased afterload (alpha 1), increased HR (beta 1), increased contractility (beta 1)

RAAS (activated by decreased blood flow to kidney) = endothelin release, inflammatory markers released, water retention

BNP/ANP proof of counter-regulatory mechanisms due to increased blood volume attempt to diureise

APO (+ lungs kept dry by… [5])

Lungs normally kept dry by:

lymphatic drainage

hydrostatic pressure

capillary oncotic pressure

surfactant

membrane permeability

Cardiogenic = increased pulm capillary hydrostatic pressure (protein poor). low CO despite high SVR

Non-cardiogenic = increased membrane permeability (protein rich). eg. high output states (sepsis, thyrotoxicosis), vasc perm (pancreatitis, DIC, burns, eclampsia), toxins/enviro (submersion, decompression), other (ICH, PE).

Atherosclerosis

Thickening and hardening of arterial wall

Chronic endothelial injury > fatty streak (lipids accumulate) > fibrous plaque (vessel lumen narrows) > complicated lesion (plaque rupture, thrombus formation, narrowing or occlusion)

HDL helps efflux of cholesterol return to the circulation (reduce FOAM cells)

Layers of heart (3)

OUTER = pericardium (serous parietal layer; space with pericardial fluid; serous visceral layer) epicardium contains coronary arteries and fat (physical barrier to infection

MIDDLE = myocardium (muscle)

INNER = endocardium

Cardiac cycle (5)

1. Atrial systole (depolarisation = contraction. Atrial kick = 25-30% CO)

2. Isovolumetric contraction (increase pressure, AV valves close, volume constant)

3. Ventricular systole (vent pressure increases, semilunar valves open, blood ejected)

4. Isovolumetric relaxation (closure of semilunar valves before AV valves open = all valves closed)

5. Ventricular diastole (vent pressure falls below atrial pressure = AV valves open & passive filling)

Aortic valve disorders (2)

1. Regurgitation = closing problem. tachy, CP, HTN, hypoxia, APO

2. stenosis = opening problem. tachy, CP, hypoxia, APO, HYPOtension *SENSITIVE TO NITRATES/PRELOAD DEPENDENT

Infective endocarditis + sx

Risk factors (trauma, procedure, valve disease) = endothelial damage, inflammation & thrombus formation (sterile thrombotic endocarditis)

+introduction of bacteria (IVDU, PIVC, UTI) = bacterial adherence, thrombus formation, formation of vegetations.

= emboli, murmurs, HF, petechiae, abscess, arrhythmias, TIA

Pericarditis, sx + 2 major investigations

Inflammation of pericardium (often from viral illness)

-Symptoms = tachycardia, palpitations, febrile (high risk of bacteria), chest pain IMPROVED WHEN LEANING FORWARD

-          ECHO to rule out effusion (PERICARDIAL SAC NON-COMPLIANT) (pulsus pardoxus SpO2 or QRS alternans – tamponade risk)

-          ECG abnormalities = widespread concave STE and PR depression. Sinus tachy

-          TREAT WITH NSAIDS + treat arrythmias

Myocarditis + treatment

-          Inflammation of heart MUSCLE

-          CAN GO INTO CARDIOGENIC SHOCK

-          Treat as per cardiogenic shock if needed. Inotropes, analgesia, treat cardiac failure, +/- OT2, ACE inhibitors, treat arrhythmias

Aortic aneurysms + dissection types + treatment

Enlargement of the aorta caused by a weakness in the arterial wall.

Thoracic or abdominal

Dissection =

Type A, I = ascending and descending, Type A II = ascending only, Type B = descending

Treat = esmolol, art line, surgical repair

Anaphylaxis

Severe, systemic hypersensitivity reaction

Mediated by IgE

Allergen > mast cell and basophil de-granulation > histamine, leukotreins, prostaglandins, cytokins

= mass vasodilation (hypotension)

increased vasc permeability (angioedema)

bronchoconstriction (wheeze)

mucosal oedema (airway narrowing)

»»DISTRIBUTIVE SHOCK

Bronchiolitis

<1year old

LRTI (inflammation of bronchioles)

Oedema of bronchioles, increased mucus, cellular debris (causing obstruction/increased resistance), air trapping, atelectasis

NO BRONCHOSPASM therefore bronchodilators ineffective

Croup

Subglottic upper airway oedema/inflammation

turbulent flow = stridor

increased negative intrathoracic pressure = retractions

Pertussis

Whooping/100 day cough

Bordetella pertussis attaches to ciliated resp epithelium = impairs ciliary function.

Inflammation, increased mucus production, decreased airway clearance (secondary pneumonia + pulmonary hypertension)

Epiglottitis

Bacterial upper airway infection (epiglottis and supraglottic structures) = drooling/unable to swallow. Stridor. IVABs

Foreign body upper vs lower sx

Upper = stridor, distress++

Lower (bronchi) = unilateral wheeze, asymmetrical air entry, hyperinflation (ball-valve effect)

SVT

Abnormal electrical circuit above ventricles (eg WPW/AVRT or AVNRT)

= decreased ventricular filling time, decreased SV, decreased CO

INFANTS vulnerable as SV is fixed so HR dependant → fatigue, HF, cardiogenic shock

Acute rheumatic fever

autoimmune response to group A strep

antibodies cross-react with cardiac tissue (molecular mimicry)

damage to myocardium, endocardium, valves = regurgitation, reduced efficiency

REPEATED EPISODES = rheumatic heart disease

Epileptic seizures

Abnormal excessive electrical activity. Synchronous, excessive neuronal firing within cortical networks.

@ Cellular level this is an imbalance between: excitatory neurotransmission (glutamate) and inhibitory neurotransmission (GABA)

Structural, genetic (channel disorder), metabolic, infection, trauma

Metabolically demanding (O2, glucose, lactate production)

Febrile seizures simple vs complex (4) + patho

Simple = GTC, <15min, recovery within 1hr, once in 24hrs

Complex = focal features, >15mins, aLOC >1hr, reoccurs in 24hrs

Fever increases neuronal excitability through:

cytokine-mediated inflammatory changes, altered ion channel activity, increased metabolic demand (age-dependent brain susceptible)

Meningitis

Inflammation of the meninges (often bacterial)

Neonates present systemic due to immature immune systems (rely on maternal antibodies, more permeable blood brain barrier, etc.)

Appendicitis

Luminal obstruction → intraluminal pressure increases → venous congestion develops (abdo pain, fever, nausea) → gut flora proliferate rapidly – neutrophilic infiltration → cytokines and inflammatory mediators released (visceral peritoneal irritation, systemic inflammatory response ie febrile, tachy) → atrial supply becomes compromised (ischemic tissue) → mucosal breakdown allows bacterial translocation → perforation risk → full tissue necrosis = rupture and contents spill into peritoneal cavity

Mesenteric adenitis

Inflammation of mesenteric lymph nodes most often RLQ

Stretching of mesentery, local inflammatory response.

Often follows URTI, Gastro or other viral illness. Pathogens stimulate immune response

Intussusception

Bowel telescopes into adjacent distal segment (most often ileum into caecum)

Pulls mesentery, blood vessels and lymphatics in

Compression of mesenteric vessels = venous congestion, bowel wall oedema, progessive obstruction

Atrial supply compromised, mucosal sloughing occurs, bloody/mucusy stool (red currant jelly)

Gastoenteritis

Viral pathogens infect enterocytes in small intestine

Leads to = villous atrophy, impaired absorption sodium and glucose, osmotic diarrhoea, enterotoxins increase chloride secretion water follows sodium into the lumen

LOSE SODIUM, POTASSIUM, BICARBONATE

Scrotal pain (3)

1. Torsion = rotation of testes and loss of blood supply. No relief with lifting testicles. Loss of cremasteric reflex (testicles pull up when inner thigh stroked)

2. Epididymo-orchitis and orchitis = infection of epididymis and sometimes teste (or just teste) normally infection. Pain relieved when lifting testes

3. Incarcertated hernia = intestines protrude into groin or scrotum and are unable to be pushed back in

Renal calculi (2 risks)

Hard deposits of minerals and salts in urinary tract

Risk: hydronephrosis, damage to tubular epithelium

Priapism (2)

Prolonged erection >4hrs with no sexual arousal

1. high flow = unregulated flow of blood

2. low flow = ischaemia risk (must aspirate)

Phimosis and paraphimosis

1. phimosis = foreskin can’t be pulled back

2. paraphimosis = foreskin can’t be pulled forward over head. Ischaemic risk. (medical handling, infection, trauma, skin conditions)

Rhabdomyolysis

Break down of skeletal muscle - contents spill into blood stream

(K+, myoglobins, phosphate, CK, uric acid)

Myoglobins large and can obstruct/damage tubules

RISK: AKI, Arrhythmias (hyper K+)

Cause: long lie, crush injury, ischameia, hyperthermia, exercise

AKI patho and causes (pre 4, intra 4, post 4)

Decline in GFR, accumulation of waste products (urea, creatinine)

a. Pre-renal = dehydration, shock, V/Ds, excessive diuresis

b. intra-renal = structural ie tubular injury, necrosis (ischaemic or nephrotoxic), nephritis, vascular injury

c. post-renal = urine outflow obstructed ie. constipation, enlarged prostate, kidney stones, tumour

CKD, stages

Decreased GFR <60 for 3/12. Progressive and irreversible

Stage 1 (polyuria due to inability to concentrate urine) - Stage 5 (oliguria and anuria)

Diabetes (3)

-          T1DM = autoimmune disease, pancreatic cell destruction. Little to no insulin production

-          T2DM = Insulin resistance = decreased glucose uptake by muscle. Increased hepatic glucose production (gluconeogenesis and glycogenolysis). Initially pancreatic b cells increase insulin secretion to compensate, over time b cells unable to increase insulin output

-          Gestational diabetes = placenta produces hormones for the baby to develop and grow – these hormones block the action of the woman’s insulin and cause insulin resistance

DKA

Hyperglycaemic, Acidotic, Ketotic.

Dehydrated, electrolyte imbalance.

Lack of insulin = gluconeogenesis + glycogenolysis

Ketones (byproduct of alternative energy production) = lower pH

Osmotic diuresis

HHS

Hyperglycaemic, dehydrated, electrolyte imbalances (slower onset, sicker)

Stress event → catecholamines and cortisol increased hepatic glucose production.

Enough insulin to supress ketones

Shock pathophysiology and stages (3)

INADEQUATE PERFUSION due to decreased CO, inadequate glucose/O2

-          Compensatory = mechanisms (SNS) activated by baroreceptors and chemoreceptors. Release of catecholamines. Blood flow maintained to heart, brain, lungs. Decreased flow to kidneys (activates RAAS + ADH release)

-          Progressive = compensatory mechanisms fail, decreased ATP, hypoxia of organs, decreased perfusion, failure of Na+/K+ pump, altered membrane permeability, metabolic acidosis, Ischaemia

-          Irreversible/refractory = compensatory mechanisms overwhelmed. Tissue hypoxia, ischaemia, necrosis and death of cell. Build up of toxins, MODS

Distributive shock

Maldistribution of circulation

1. Neurogenic = Spinal cord injury, disrupts SNS. Loss of tone, mass vasodilation, fluid shift, INADEQUATE PERFUSION

2. Anaphylactic = allergen → vasoactive mediators → mass vasodilation and increased membrane permeability → fluid shift, INADEQUATE PERFUSION [Adrenaline B2 effects]

3. Septic = infection → inflammatory response → Mediators cause vasodilation (selective vasoconstriction), increased membrane permeability, fluid shift. + Microemboli + hypermetabolic state and increased O2 demand, INADEQUATE PERFUSION [Norad alpha effects]

Hypovolaemic shock (4 eg)

Decreased venous return → decreased ventricular filling → decreased SV → decreased CO = INADEQUATE PERFUSION

Causes: diaphoresis, haemorrhage, Vs/Ds, burns

Cardiogenic shock (4 causes)

Ineffective forward motion of blood → decreased SV → decreased CO = INADEQUATE PERFUSION (+APO) [dobutamine inotrope/chronotrope without vasoconstrictio/increased workload]

1. Arrhythmia (VT, brady, rAF)

2. Reduced contractility (diastolic dysfunction, RV infact)

3. Failure of forward flow (valve dysfunction, septum rupture)

4. Inadequate filling (MI, cardiomyopathy, toxins)

Obstructive shock (3)

Tamponade, Tension, PE

= structural compression → decreased venous return → decreased SV/CO = INADEQUATE PERFUSION

Inotrope receptors

alpha = vasoconstriction

b1 = increased HR, increased contractility

b2 = bronchodilation, some vasodilatory effects

V1/V2 = vasoconstriction + anti-diuresis

Pancreatitis (3)

1. duct obstruction (gall stone, ETOH, trauma)

2. premature enzyme activation (normally occurs in intestines)

3. autodigestion of pancreatic tissue. necrosis, vessel damage (haemorrhage risk)

4. inflammatory resposne

5. pancreatic oedema, tissue necrosis, haemorrhage, increased membrane permeability