Week 3 Flashcards

Question

small vessel vasculitis what is it

Answer 1

a condition where the smallest blood vessels (arterioles, capillaries, and venules) become inflamed, potentially causing damage to tissues and organs TYPES: Cutaneous small vessel vascultiis eosinophilic granulomatosis with polyangiitis

Answer 2

- Cutaneous small vessel vasculitis - rash

Answer 3

- Reaction, infection, environmental - Rhinosinusitis, asthma, peripheral blood eosinophilia, peripheral neuropathy

Answer 4

a condition where abnormal proteins called cryoglobulins are present in the blood, and these proteins precipitate or clump together at low temperatures

Answer 5

1, Unknown 2, Chronic infection/inflammation 3, Abnormal blood proteins clump together 4, Purpura, arthralgia and weakness

Answer 6

a condition where blood flow through an artery is either partially or completely blocked

Answer 7

- Thrombosis, atherosclerotic plaque, latrogenic, traumatic, arterial embolism

Answer 8

- Associated with atherosclerosis and diabetes - Vasospasm, venous insufficiency, embolism and vasculitis

Answer 9

- Reduced perfusion in peripheral tissues – ischemia and tissue necrosis - Depends upon aetiology and if has underlying peripheral artery disease - Critical limb ischemia - Six Ps of acute ischemia: pain, pallor, poikilothermic, pulselessness, paraesthesia and paralysis

Answer 10

When an artery becomes blocked, tissues downstream lose their oxygen and nutrient supply. Since oxygen is essential for aerobic metabolism, cells must switch to anaerobic metabolism to generate energy. This shift leads to a cascade of harmful biochemical and cellular changes, ultimately resulting in cell death (necrosis)

Answer 11

1. Anaerobic Metabolism and Acidosi Lactic acid accumulation → Tissue acidosis (↓ pH), which; - Disrupts enzyme function - Damages proteins and cell membranes = Leads to oxidative stress and free radical formation Why is this bad? Acidosis worsens cellular dysfunction and contributes to tissue injury 2. ATP Depletion and Ion Pump Failure ATP is needed for ion pumps to maintain cell homeostasis. When ATP is depleted, two critical pumps fail:  Sodium-Potassium (Na⁺/K⁺) Pump Failure: normally, pumps Na⁺ out and K⁺ in to maintain resting potential but failure leads to Na⁺ accumulation inside cells, causing water influx and cell swelling (cellular oedema)  Calcium (Ca²⁺) Pump Failure: normally, keeps Ca²⁺ out of the cytoplasm to prevent enzyme activation but failure leads to Ca²⁺ overload, triggering harmful enzymatic activity inside the cell Why is this bad? Swollen cells disrupt tissue structure and function Excess Ca²⁺ activates destructive enzymes (phospholipases, proteases), which degrade vital cell components 3. Calcium Overload and Muscle Necrosis It leads to irreversible muscle fibre destruction, progressing to gangrene if untreated 4. Release of Cellular Contents into the Bloodstream As cells die, they rupture and release their internal contents into circulation, leading to systemic complications:

Answer 12

- Intermittent or irregular pain during activity and rest - Numbness, coldness or pins and needles in the affected body part - Blue- or purple-tinged skin - Sores or ulcers in the affected body part that do not heal - Blackened areas of skin or loss of skin (gangrene) - Intermittent or irregular pain during activity and rest - Numbness, coldness or pins and needles in the affected body part - Blue- or purple-tinged skin - Sores or ulcers in the affected body part that do not heal - Blackened areas of skin or loss of skin (gangrene)

Answer 13

= an enlargement of an artery resulting in a diameter of more than 1.5 times the normal size - True aneurysms have an intact arterial wall consisting of all three layers (intima, media and adventitia) and occur due to atherosclerosis or degeneration in the artery - False (pseudoaneurysms) lack a complete arterial wall and are related to trauma, iatrogenic injury or infection. - Aneurysms are defined by their location relative to the visceral vessels, involvement of the vessel layer walls, morphology (saccular versus fusiform), and diameter (small versus large

Answer 14

- An aneurysm is a localised dilation or bulging of a blood vessel due to weakening of the arterial wall - The development of aneurysms is influenced by a combination of genetic, degenerative, inflammatory and hemodynamic factors

Answer 15

- In Australia, the prevalence and incidence of aneurysms vary based on type, age, sex, and ethnicity. - It is estimated that 2–3% of the adult population may develop an aneurysm over their lifetime, though many remain asymptomatic and undetected - Congenital Factors: Connective tissue disorders (e.g., Marfan syndrome, Ehlers-Danlos syndrome) - Degenerative Changes: Atherosclerosis (causing weakening of arterial wall); hypertension (increases mechanical stress on vessel walls); aging (reduces elasticity and integrity of vessel) - Inflammatory and Infectious Causes: Vasculitis (e.g., Takayasu arteritis, Giant cell arteritis); autoimmune disorders and infections (due to bacterial or fungal infections e.g., tuberculosis) - Trauma and Iatrogenic Causes: Blunt or penetrating trauma; surgical or endovascular interventions (e.g., coronary angiogram) leading to pseudoaneurysm formation - Lifestyle and Environmental Factors: Tobacco smoking (promotes oxidative stress and vascular damage); dyslipidaemia (contributes to atherosclerosis) and other risk factors linked to development of atherosclerosis and hypertension such as diet, being sedentary and the environment (e.g., air pollution and heatwaves)

Answer 16

- Depend on size and location, may be asymptomatic - Brain: asymptomatic unless it ruptures - Thoracic: substernal, back and neck pain, dyspnoea, stridor, brassy cough - Abdominal: pulsating mass, mild-severe mid-abdominal or lumbar discomfort to severe abdominal or back pain

Answer 17

- Asymptomatic or symptomatic

Answer 18

- Inadequate muscle pump function - Incompetent valves (reflux) - Venous thrombosis or non-thrombotic venous obstruction - Anatomic, physiologic and histologic changes leading to vein dilation, skin changes and/or skin ulceration

Answer 19

- Superficial veins - Remodelling of vessel wall - Possible genetic link - More common in women > men

Answer 20

- Oedema, skin changes, venous ulceration - Chronic venous insufficiency - Superficial and/or deep venous reflex and/or obstruction

Answer 21

The formation of a blood clot (thrombus) within a blood vessel, either an artery or a vein

Answer 22

= refers to inflammation of a vein associated with thrombus (blood clot) formation - Thrombus in vein + inflammation - Superficial or deep veins - Secondary to other conditions

Answer 23

- VTE is associated with conditions that increase the risk of clotting, including those that lead to decreased venous flow and pooling, abnormalities of coagulation or fibrinolysis and endothelial dysfunction - Each year in Australia, about 1 in 1000 people develop a first episode of VTE, which approximates to about 20,000 cases - More than half of these episodes occur during or soon after a hospital admission, which makes them potentially preventable

Answer 24

- Asymptomatic until clot moves to another organ – lungs - Signs and symptoms are related to inflammation  Pain, swelling, deep muscle tenderness  Fever, malaise, elevated WBC  Site of thrombosis determines symptoms

Answer 25

- Known as deep venous thrombosis (DVT) - If untreated can result in complications e.g., pulmonary emboli

Answer 26

improper functioning of the vein valves in the leg, causing swelling and skin changes

Answer 27

- Venous hypertension results from structural factors (e.g., venous obstruction, valvular dysfunction) and functional factors (e.g., obesity, heart failure, weak calf muscles - The risk factors for developing chronic venous disease include:  Advancing age, female sex, family history of venous disease, ligamentous laxity, prolonged standing, increased body mass index, smoking, lower extremity trauma, prior venous thrombosis (ie, post-thrombotic) and certain hereditary conditions. - Impaired venous return leads to persistent ambulatory venous pressures of 60–90 mmHg, causing venous dilation and progressive damage. A genetic predisposition is suspected, though no single gene has been identified

Answer 28

- Chronic venous disease (CVD) is one of the most common vascular conditions, affecting up to 39% of the Australian population - The risk of chronic venous disease increases with age and has a 3 to 1 female predominance

Answer 29

Symptoms include: - Pain, leg heaviness, aching, swelling, skin dryness, tightness, itching, irritation, and muscle cramps - Venous claudication - a severe deep pain and tightness typically in the thigh muscles with vigorous exercise, can occur in the setting of acute, severe venous obstruction or longstanding venous obstruction Signs include: - Dilated veins (e.g., varicose veins - subcutaneous dilated, tortuous veins >3mm in diameter); chronic venous insufficiency is an advanced stage of CVD and is associated with oedema, skin changes and/or venous ulcers

Answer 30

Anatomic changes: - Valvular incompetence causes venous reflux and dilation, creating a vicious cycle of vessel wall distortion and worsening valve failure - Chronic venous obstruction can lead to fibrosis and post-thrombotic syndrome Physiologic changes: - Normally, precapillary arterioles constrict upon standing to protect the capillary bed - In venous hypertension, this reflex is lost, allowing direct transmission of high venous pressure - Reduced shear stress triggers endothelial dysfunction, inflammation, and vessel wall remodelling, leading to venous insufficiency

Answer 31

a bulge in the wall of the aorta, the body's main artery, caused by weakening of the artery wall

Answer 32

- Occurs in the upper part of the aorta - The majority (~95%) of patients are asymptomatic until a serious event, such as aortic dissection or rupture, occurs - This makes it difficult to determine the true prevalence of TAAs - However, estimates suggest an incidence of 5–10 cases per 100,000 person-years, with numbers increasing due to both population aging and improved detection - TAAs are more common in men - However, possibly due to decline in oestrogen levels during menopause, which may reduce the protective effects of oestrogen on the aortic wall, women over the age of 50 have a faster aneurysm progression

Answer 33

- Defined as a localised enlargement of the abdominal aorta to a diameter of ≥30 mm (on abdominal US or CT) and are a degenerative disease of ageing - Approximately 4–7% of men and 1–2% of women over the age of 65 are affected

Answer 34

- In an aortic aneurysm, this normal architecture becomes compromised, leading to progressive weakening and dilation - The key initiating event is often the dysfunction and loss of vascular smooth muscle cells (VSMC), which are responsible for maintaining the extracellular matrix (ECM) and regulating vascular tone - As these cells become dysfunctional and die off, the ability of the aortic wall to repair itself diminishes, increasing its susceptibility to progressive dilation and rupture The process is complex: - At the core of aneurysm formation is VSMC dysfunction - they lose their contractile properties and undergo programmed cell death, reducing the strength of the aortic wall. This dysfunction occurs in response to chronic inflammation, oxidative stress and mechanical strain, and the VSMC start producing matrix metalloproteinases (MMPs), cytokines, and reactive oxygen species (ROS). - The ECM is crucial for maintaining the strength and elasticity of the aortic wall. It consists of elastin, which allows the aorta to stretch and recoil, and collagen, which provides tensile strength. In an aneurysm, these proteins undergo excessive degradation due to the overactivity of the MMPs, which break down the elastin and collagen, leading to loss of structural support and an increase in aortic wall compliance Chronic inflammation - Originates from chronic damage to the aortic wall, primarily due to high blood pressure, oxidative stress and atherosclerosis leading to small injuries in the vessel wall. These injuries trigger an immune response, where macrophages, T cells, and neutrophils infiltrate the aortic tissue to repair the damage. However, instead of resolving the injury, these immune cells prolong inflammation by releasing cytokines and enzymes (MMPs) that degrade elastin and collagen, and over time, this weakens the aortic wall, making it more susceptible to dilation and rupture Oxidative stress - From e.g., endogenous - aging, metabolic disorders, diabetes; exogenous - tobacco smoking, pollution, poor diet) further fuels this process by producing free radicals (ROS) that damage smooth muscle cells (VSMCs) and extracellular matrix (ECM) proteins. Normally, VSMCs help repair tissue damage, but in aneurysms, they become dysfunctional and fail to regenerate the damaged wall. This creates a cycle where the aortic wall continues to degrade, stimulating even more immune cell recruitment and inflammation Mechanical stress - The aorta is constantly under pressure from blood flow. In aneurysms, this stress is even higher than normal because the aortic wall is already weak. Hypertension and/or turbulent blood flow e.g., from atherosclerosis narrowing the arteries, cause tiny injuries and inflammation to the endothelial wall Chronic inflammation - Originates from chronic damage to the aortic wall, primarily due to high blood pressure, oxidative stress and atherosclerosis leading to small injuries in the vessel wall. These injuries trigger an immune response, where macrophages, T cells, and neutrophils infiltrate the aortic tissue to repair the damage. However, instead of resolving the injury, these immune cells prolong inflammation by releasing cytokines and enzymes (MMPs) that degrade elastin and collagen, and over time, this weakens the aortic wall, making it more susceptible to dilation and rupture Oxidative stress - From e.g., endogenous - aging, metabolic disorders, diabetes; exogenous - tobacco smoking, pollution, poor diet) further fuels this process by producing free radicals (ROS) that damage smooth muscle cells (VSMCs) and extracellular matrix (ECM) proteins. Normally, VSMCs help repair tissue damage, but in aneurysms, they become dysfunctional and fail to regenerate the damaged wall. This creates a cycle where the aortic wall continues to degrade, stimulating even more immune cell recruitment and inflammation Mechanical stress - The aorta is constantly under pressure from blood flow. In aneurysms, this stress is even higher than normal because the aortic wall is already weak. Hypertension and/or turbulent blood flow e.g., from atherosclerosis narrowing the arteries, cause tiny injuries and inflammation to the endothelial wall

Answer 35

dilations that occur at weak points along the arterial circulation within the brain

Answer 36

- Global prevalence of cerebral aneurysms is approx. 3.2%, with a mean age of 50 and an overall 1:1 gender ratio - This ratio changes after age 50, with an increasing female predominance approaching 2:1. CAs can vary in size (small < 0.5 mm, large>25 mm), are saccular (berry) and asymptomatic

Answer 37

- CAs most frequently develop in areas where blood flow causes high wall shear stress, which is why they commonly occur at vessel bifurcations - In cerebral aneurysms, VSMCs produce pro-inflammatory molecules that lead to localised weakening, rather than widespread wall loss as seen in aortic aneurysms - Whereas AAAs are driven by chronic inflammation, CAs have increased endothelial dysfunction and local cytokine activation - Whereby AAA expands progressively over time, CAs rupture unpredictably, even at smaller sizes, due to localised weakening at high-flow bifurcations

Answer 38

- Aneurysms occurring in the arteries of the lower limb are the most common peripheral aneurysms -

Answer 39

- They share common mechanisms with aortic aneurysms, including inflammation, ECM degradation and haemodynamic stress, but they also have unique contributors such as higher atherosclerotic involvement, localised mechanical stress, and genetic predisposition - Peripheral arteries experience more shear stress and turbulent blood flow in areas of arterial branching (such as the popliteal artery) which contribute to localised wall weakening and aneurysm formation

Answer 40

- The clinical presentations of aneurysms depend on their location, size, and whether they have ruptured - Aneurysms in different locations manifest differently but share common risks of rupture and ischaemic complications - Aortic aneurysms are often silent until rupture, cerebral aneurysms present catastrophically with SAH, and peripheral aneurysms are prone to embolism and limb ischemia

Answer 41

high blood pressure, where blood pressure is permanently higher than normal

Answer 42

- Systolic blood pressure of 140 mmHg or more - Diastolic blood pressure of 90mmHg or more - Receiving medication for high blood pressure

Answer 43

- 45% in 75 and older both female and male ' - higher rates in males - same for both lower and higher socio

Answer 44

- Blood pressure reacts to changes in the environment to maintain organ perfusion over a wide variety of conditions - The primary factors determining the blood pressure are the sympathetic nervous system, the renin-angiotensin-aldosterone system (RAAS), and the plasma volume (largely mediated by the kidneys) - However, the pathophysiology of hypertension involves complex interactions between environmental and behavioural factors, genes, hormonal networks and multiple organ systems (renal, cardiovascular, and central nervous system), as indicated in the image below

Answer 45

1. RENAL - Pressure natriuresis relationship and RAAS 2. Vascular mechanisms - small arteries remodelling and large 3. neural mechanisms - baroreceptor dysfunction, overactivation of SNS control centre 4. hormonal mechanisms - RAAS, aldosterone, ostreogen, testosterone

Answer 46

microvascular remodelling LVH Myocardial infraction CAD endothelial dysfunction arthlerosclerosis arterial stiffness microbleeds in brain

Answer 47

chronic elevation of BP with no identifiable cause - Dysfunction in RAAS, SNS and renal sodium balance leads to sustained BP elevation

Answer 48

- In AUS, more than 34% of adults have high BP and majority (90-95%) have primarily hypertension with a multifactorial gene-environment aetiology

Answer 49

Primary hypertension results from genetic and environmental factors affecting cardiovascular and renal function Key mechanisms include: - SNS overactivity: increased norepinephrine raises heart rate and vasoconstriction - RAAS dysregulation: Excess angiotensin II and aldosterone increase vascular resistance and fluid retention - Endothelial dysfunction: Reduced nitric oxide and increased oxidative stress promote vasoconstriction - Salt sensitivity leads to volume expansion and increased BP

Answer 50

Non-modifiable: - Age: BP increases with arterial stiffening - Genetics: Family history contributes to 30% of BP variations - Race: Higher prevalence and severity - Reduced Nephron Number: Genetic and prenatal factors impact renal function Modifiable: - High sodium intake: Excess sodium retention raises BP - Obesity and metabolic syndrome: Insulin resistance leads to vascular dysfunction - Physical inactivity: Reduced vascular flexibility and SNS overactivity - Excess alcohol and smoking: Increases vasoconstriction and endothelial damage - Chronic stress and poor sleep: SNS hyperactivity raises BP - Social and environmental factors: Low socioeconomic status, pollution and stress contribute to hypertension

Answer 51

Asymptomatic in early stages, or morning headaches, dizziness, fatigue and vision changes Advanced-Stage: target organ damage leads to: - Cardiovascular: Heart failure, myocardial infarction - Cerebrovascular: Stroke, vascular dementia - Renal: Chronic kidney disease, nephropathy - Ophthalmic: Hypertensive retinopathy, vision loss - Peripheral Arteries: Atherosclerosis, limb ischaemia

Answer 52

Elevated blood pressure due to an identifiable underlying cause, only 10% of hypertension cases

Answer 53

- A number of common and uncommon medical conditions may increase BP and lead to secondary hypertension - In many cases, these causes may coexist with risk factors for primary hypertension and are significant barriers to achieving adequate BP control

Answer 54

The kidneys play a key role in BP regulation through fluid balance and electrolyte homeostasis. 1. Chronic Kidney Disease (CKD): In renal parenchymal disease, damaged nephrons fail to effectively excrete sodium and water, leading to intravascular volume expansion and elevated BP. Additionally, the kidneys respond to impaired perfusion by inappropriately activating the RAAS which further raises BP by promoting vasoconstriction and sodium retention. Hypertension accelerates kidney damage, creating a vicious cycle that increases the risk of end-stage renal disease (ESRD). 2. Renovascular Hypertension: Narrowing of the renal arteries (stenosis) reduces blood flow to the kidneys, triggering excessive RAAS activation as a compensatory response. Angiotensin II, a potent vasoconstrictor, increases systemic vascular resistance, while aldosterone promotes sodium and water retention, elevating BP. Secondary hyperaldosteronism in renal artery stenosis exacerbates hypertension and volume overload. 3. Role of Fluid Balance in BP Control: In advanced CKD, BP regulation becomes highly dependent on intravascular volume. Excess fluid accumulation (volume overload) worsens hypertension and contributes to pulmonary congestion and heart failure. Diuretics and sodium restriction are essential in controlling BP in CKD patients

Answer 55

- Primary Hyperaldosteronism: Excess aldosterone secretion (usually from an adrenal adenoma or bilateral adrenal hyperplasia) leads to sodium retention, potassium excretion and volume expansion, causing hypertension. - Pheochromocytoma: A tumour of the adrenal medulla that secretes excess catecholamines (epinephrine and norepinephrine) which causes episodic or sustained hypertension by increasing heart rate and CO and constricting blood vessels, raising systemic vascular resistance - Cushing’s Syndrome: Excess cortisol increases BP via RAAS activation and vasoconstriction - Thyroid Disorders: Hypothyroidism and hyperthyroidism can both elevate BP via altered vascular resistance - Acromegaly: Excess growth hormone increases sodium retention and cardiac output

Answer 56

Vascular Causes: Coarctation of Aorta: Congenital narrowing increases upper body BP while lowering lower limb BP Neurological Causes: Increased Intracranial Pressure e.g. from brain tumours, head trauma or hydrocephalus increases BP via the Cushing reflex Medication-Induced Hypertension: NSAIDs, corticosteroids, oral contraceptives, sympathomimetics and cyclosporine can elevate BP. Recreational Drugs (Cocaine, Amphetamines) can cause acute or chronic hypertension. Obstructive Sleep Apnea (OSA): Chronic hypoxia and SNS activation increase BP variability and risk of resistant hypertension Pregnancy-Related Hypertension: Preeclampsia and Eclampsia: Endothelial dysfunction, vasoconstriction, and fluid retention elevate BP

Answer 57

decrease in systemic blood pressure below accepted low values, typically recognised as less than 90/60 mmHg - classified into different types, including absolute, relative, orthostatic, and profound hypotension

Answer 58

- Blood pressure regulation is primarily dependent on cardiac output and systemic vascular resistance - Any pathology affecting these factors can result in hypotension Cardiac output reduction: - Heart failure (systolic/diastolic dysfunction) - Arrhythmias (bradycardia, tachycardia) - Myocardial infarction - Valvular heart diseases - Cardiac tamponade Hypovolaemia: - Haemorrhage - Dehydration (vomiting, diarrhoea, excessive diuresis) - Adrenal insufficiency (e.g., Addison’s disease) Decreased systemic vascular resistance: - Septic shock (due to bacterial endotoxins) - Anaphylactic shock (severe allergic reaction) - Neurogenic shock (spinal cord injury) - Certain medications (vasodilators, beta-blockers, calcium channel blockers) Endocrine disorders: - Hypothyroidism (leading to reduced cardiac contractility) - Adrenal insufficiency (loss of vasopressor effects of cortisol) Neurological disorders: - Autonomic dysfunction (Parkinson’s disease, Dementia with Lewy bodies; diabetic neuropathy which affects peripheral nerves; older age as these decreases in baroreceptor sensitivity) - Prolonged bed rest (deconditioning of baroreceptors)

Answer 59

Hypotension results from the disruption of one or more of the following physiological mechanisms: Decreased cardiac output: - CO is the product of stroke volume (amount of blood ejected per heartbeat) and heart rate. Any condition that impairs myocardial contractility, reduces preload (blood returning to the heart), or affects heart rate can lead to reduced CO and hypotension - Conditions include heart failure, myocardial infarction, severe bradycardia and cardiac tamponade Reduced systemic vascular resistance (SVR): - Blood pressure is determined by the diameter of blood vessels. Vasodilation decreases SVR, leading to a drop in BP - This is seen in distributive shock (septic, anaphylactic or neurogenic shock), where excessive vasodilation occurs due to the release of inflammatory mediators or autonomic dysfunction Impaired baroreceptor reflex: - Baroreceptors in the carotid sinus and aortic arch sense changes in BP and trigger compensatory mechanisms via the autonomic nervous system. In normal physiology, a drop in BP triggers sympathetic activation, increasing heart rate and vasoconstriction - Conditions such as autonomic neuropathy, prolonged bed rest or neurodegenerative diseases impair this reflex, resulting in orthostatic hypotension Fluid and electrolyte imbalance: - Hypovolaemia due to dehydration, haemorrhage or excessive diuresis reduces intravascular volume, decreasing stroke volume and CO - Electrolyte imbalances, such as hyponatraemia or adrenal insufficiency, can exacerbate hypotension by impairing fluid balance and vascular tone Endocrine dysregulation: - Adrenal insufficiency leads to decreased production of cortisol and aldosterone, impairing sodium retention and vascular tone regulation. - Hypothyroidism decreases cardiac contractility and heart rate, contributing to low blood pressure Medication effects: - Antihypertensives (beta-blockers, ACE inhibitors, diuretics) can cause excessive blood pressure reduction. - Vasodilators, sedatives, and anaesthetics can contribute to hypotension by decreasing vascular tone and myocardial contractility Autonomic nervous system dysfunction: - REVISION: Autonomic nervous system regulates BP through the balance between sympathetic and parasympathetic activity. Sympathetic activation increases HR and vascular resistance, raising BP. Parasympathetic activation lowers HR and dilates vessels, decreasing BP. - Dysfunction in autonomic regulation (e.g., diabetic autonomic neuropathy, Parkinson’s disease, spinal cord injury) results in inadequate BP compensation, leading to hypotension, particularly orthostatic hypotension

Answer 60

Symptoms depend on the severity and cause of hypotension General symptoms: - Dizziness, light-headedness - Fatigue - Blurred vision - Nausea - Syncope (fainting) Neurological symptoms (due to reduced cerebral perfusion) - Confusion, difficulty concentrating - Seizures in severe cases Sign of Shock - Cold - Clammy skin - Rapid pulse - Low urine output - Metabolic acidosis - Mutli organ failure in prolonged cases

Answer 61

- Absolute Hypotension: Defined as a systolic BP lower than 90 mmHg or a mean arterial pressure (MAP) lower than 65 mmHg, indicating inadequate perfusion. - Relative Hypotension: A significant drop in BP from baseline despite being within normal ranges. This can occur in patients who usually have high blood pressure but experience a sudden reduction - Profound Hypotension: Medication-dependent or associated with life-threatening conditions requiring intensive management. - Shock (Severe Hypotension with Organ Hypoperfusion) - Orthostatic Hypotension: A decrease in systolic pressure of 20 mmHg or more, or diastolic pressure of 10 mmHg or more upon standing. This is commonly experienced in physiotherapy clinical practice, particularly among hospitalised patients, and among patients who are elderly, has diabetes and or are on antihypertensives, and caused by autonomic dysfunction, volume depletion or medications