Assessments:

• Mini exam 1 15% Monday July 29th

• Mini exam 2 15% Monday August 19th

• Mini exam 3 15% Monday September 2nd

• Final Exam 55% Thursday Nov 28th

Cell Adaptation

(1) Describe four types of cellular adaptations

(2) List examples of hypertrophy, hyperplasia, atrophy, metaplasia and dysplasia

(3) Compare and contrast apoptosis and necrosis

(4) Define dysplasia and discuss its consequences

(5) Outline common agents that cause cell injury

(1) Describe four types of cellular adaptations

The 4 types of cellular adaptations are:

• Hypertrophy

  • is an increase in cell size

  • caused by increased functional demand and hormonal stimulation

  • causes an increase in cell size & cell function

  • results in an increase in tissue mass due to increased protein synthesis

  • seen in cardiac, skeletal, and muscle tissue

• hyperplasia

  • is an increase in cell number

  • occurs as a response to a stimulus and ceases when stimulus is removed

  • restricted to cells capable of mitosis like the epidermis, intestinal epithelium, and glandular tissue

  • Common types of hyperplasia: breast enlargement in pregnancy, benign prostatic hyperplasia

• atrophy

  • is a decrease in cell size

  • due to workload or adverse environmental conditions

  • is adaptive and reversible

  • Types:

    • Disuse atrophy (paralysis)

    • Degeneration (MS)

    • Ischaemic atrophy (kidney, heart

    • Malnutrition atrophy (starvation)

    • Endocrine stimulation loss (uterine, breast)

• metaplasia

  • change in cell type

  • reversible replacement of one mature cell type by another (usually a less differentiated cell type)

  • A response to a persistent irritation and inflammation to cells

  • May predispose to cancer

• Atypical hyperplasia (dysplasia)

  • Deranged cell growth resulting in mature cells of varying size, shape, and appearance

    • may be associated with chronic irritation or inflammation

    • may be reversible if offending agent is removed

  • Dysplasia is considered a strong precursor of cancer

    • e.g Cervical cancer

    • Dysplasia is not a truly adaptive process but is related to hyperplasia

These adaptations allow cells to survive and maintain their function in response to various stimuli or conditions

(2) List examples of hypertrophy, hyperplasia, atrophy, metaplasia and dysplasia

• Hypertrophy

  • Enlarged muscle cells in bodybuilder

• Hyperplasia

  • Breast tissue growth during pregnancy

• Atrophy

  • Muscle wasting in bedridden patients

• Metaplasia

  • Barrett’s esophagus due to acid reflux

• Dysplasia

  • Cervical dysplasia as a precursor to cancer

(3) Compare and contrast apoptosis and necrosis

Apoptosis is programmed cell death, a physiological process eliminating worn-out or damaged cells, while necrosis is cellular death due to injury, causing inflammation and cellular dissolution

Physiological apoptosis is the process that eliminates:

• Worn out cells (RBCs)

• Cells which have been produced in excess WBCs with infectious response/hepatocytes with hepatitis

• Cells which have developed improperly spontaneous abortion

• Cells which have genetic damage cancer

Apoptosis involves cell suicide and controlled breakdown of organelles, leading to cellular fragmentation, whereas necrosis in uncontrolled, causing swelling, membrane rupture, and cellular autodigestion

Apoptosis does not trigger inflammation, as the cell contents are contained and phagocytosed, while necrosis leads to inflammation due to the release of cellular contents

(4) Define dysplasia and discuss its consequences

Dysplasia is a condition characterised by abnormal cell growth leading to cells of varying size, shape, and appearance

It is considered a strong precursor of cancer

Consequences of dysplasia include:

• an increased risk of developing cancer if left untreated

• removing the underlying cause of dysplasia may reverse the condition

Dysplasia is not a truly adaptive process and is often associated with chronic irritation or inflammation

(5) Outline common agents that cause cell injury

Common agents that cause cell injury include:

• ischemia

• hypoxia

• chemical substances

• radiation

• mechanical factors

These agents can lead to mechanisms of injury such as:

• depletion of ATP

• mitochondrial damage

• entry of calcium into the cell

• increase in reactive oxygen species

• membrane damage

• DNA damage

• protein misfolding

Additionally, physical, thermal, and biological factors can also contribute to cell injury

Hepatobiliary

(1) List the risk factors for acute pancreatitis and acute cholecystitis

(2) List the clinical manifestations of acute pancreatitis and acute cholecystitis

(3) Discuss the pathophysiology of acute pancreatitis and acute cholecystitis and how they are related to treatment strategies

(4) Discuss the impact of acute pancreatitis and acute cholecystitis for individuals, family and the society

(1) List the risk factors for acute pancreatitis and acute cholecystitis

The risk factors for acute cholecystitis include:

• obesity

• middle age

• being female

• drastic weight loss or acute illness

• sickle cell disease

• hereditary factors

• pregnancy

• trauma

On the other hand, the risk factors for acute pancreatitis include:

• gallstones

• alcohol consumption

• infections like Hepatitis B and mumps

• certain drugs

• endoscopic procedures

• trauma

• hereditary factors

These risk factors contribute to the development of these conditions

(2) List the clinical manifestations of acute pancreatitis and acute cholecystitis

The clinical manifestations of acute pancreatitis include:

• sudden upper abdominal pain that may radiate to the back

• Nausea

• Vomiting

• Fever

• Hypotension/Hypovolemia due to increased vascular permeability caused by enzymes

On the other hand, acute cholecystitis typically presents with symptoms such as:

• severe right upper quadrant abdominal pain

• nausea

• vomiting

• fever

These symptoms can help healthcare providers in diagnosing and treating these conditions effectively

(3) Discuss the pathophysiology of acute pancreatitis and acute cholecystitis and how they are related to treatment strategies

Acute pancreatitis is characterised by inflammation of the pancreas due to various factors like gallstones or alcohol abuse

• this inflammation can lead to the release of digestive enzymes, causing damage to pancreatic tissue and surrounding organs

• Treatment includes:

  • fluid resuscitation to prevent dehydration

  • antibiotics for infections

  • surgery in cases of gallstones or infected necrosis

Acute cholecystitis, on the other hand, is inflammation of the gallbladder often caused by gallstones blocking the cystic duct

• the treatment involves:

  • antibiotics

  • endoscopy for biliary obstruction

  • surgery to remove gallstones or the gallbladder itself

Both conditions require specific treatments tailored to the underlying causes to manage symptoms and prevent complications

(4) Discuss the impact of acute pancreatitis and acute cholecystitis for individuals, family and the society

Acute pancreatitis and Acute cholecystitis have significant impacts on individuals, families, and society

Individuals may suffer reduced quality of life, weight loss, and potential development of diabetes

Families face pressure and anxiety due to the patient’s recovery period

Societies like NZ have high incidence rates of these conditions, affecting healthcare resources and economic productivity due to hospital stays and loss of income

Acute Abdomen (Peptic/gastric ulcers & Appendicitis)

(1) List the assessment, risk factors and diagnostic tests for peptic ulcer disease and appendicitis

(2) Identify the clinical manifestations of peptic ulcer disease and appendicitis

(3) Discuss the pathophysiology of peptic ulcer disease and appendicitis and how they are related to treatment strategies

(1) List the assessment, risk factors and diagnostic tests for peptic ulcer disease and appendicitis

For peptic ulcer disease, assessment involves endoscopy as the gold standard diagnostic test

Risk factors include:

• H. pylori infection

• NSAID use

• smoking

• alcohol consumption

Diagnostic tests include:

• endoscopy

• testing for H. pylori through stool antigen test

• serology

• histology

• fasting serum gastrin to rule out cancer if multiple or persistent ulcers are present

For appendicitis, assessment includes physical examination checking for rebound tenderness and guarding

Risk factors are unclear but may involve obstruction of the appendix

Diagnostic tests include imaging studies like CT scans or ultrasounds

(2) Identify the clinical manifestations of peptic ulcer disease and appendicitis

The clinical manifestations of peptic ulcer disease include:

• abdominal pain

  • often described as burning or gnawing, that can be relieved by eating or taking antacids

• Other symptoms may include

  • bloating

  • nausea

  • vomiting

  • weight loss

On the other hand, appendicitis typically presents with:

• periumbilical pain that shifts to the right lower quadrant (RLQ) as the appendix becomes more inflamed

  • this pain is accompanied by local tenderness and can progress to peritonitis if the appendix ruptures

(3) Discuss the pathophysiology of peptic ulcer disease and appendicitis and how they are related to treatment strategies

• Peptic ulcer disease is caused by injury to the digestive tract by peptic acid, leading to ulcerations in the gastric mucosa.

  • This can result in ulcerative disorders in the lower esophagus, upper duodenum, and lower stomach

• Appendicitis involves obstruction of the appendix leading to bacterial invasion, inflammation, and swelling

• Treatment strategies for both conditions focus on reducing acid production for peptic ulcers and typically involve surgical removal of the appendix for appendicitis

Delirium

(1) Describe Delirium (also referred to as acute confusional state)

(2) Identify the clinical manifestations of Delirium and recognize the overlap of acute confusional states

(3) Demonstrate knowledge of how to care for patients with Delirium

(1) Describe Delirium (also referred to as acute confusional state)

Delirium, also known as acute confusional state, is characterized by an acute change in level of conciousness and activity over hours to days

It involves a global change in cognition with inattention, a fluctuating course with disturbances in the sleep-wake cycle and motor control

It is important to differentiate between delirium and dementia, as delirium is often not diagnosed or misdiagnosed, sometimes being attributed to medications or dementia

Delirium presents with clinical manifestations such as:

• disordered thinking

• euphoria

• language impairment

• illusions

• delusions

• hallucinations

• reversal of the sleep-wake cycle

• inattention

• inability to focus

• unawareness

• disorientation

• memory deficits

There is no definitive lab test for diagnosing delirium, so observation and ongoing assessment are crucial

The pathophysiology of delirium involves various mechanisms such as:

• depriving the brain of essential substances like oxygen and glucose

• toxic effects from drugs

• peripheral inflammation triggering changes in the brain’s inflammatory and neurotransmitter functions

• physiological and metabolic changes during acute illness

• acute psychological stress like pain, discomfort, fear, and sleep disruption

These factors can disrupt the brain’s complex functions, leading to delirium

3 types of Delirium:

1. Hyperactive delirium is characterized by restlessness, agitation, rapid mood changes, and hallucinations

2. Hypoactive delirium involves inactivity, reduced motor activity, sluggishness, or abnormal drowsiness

3. Mixed delirium displays both hyperactive and hypoactive symptoms, with individuals switching between the two states rapidly

Reticular Activating System (RAS)

Delirium or ACS arises from disruption of a widely distributed neural network involving the RAS o the upper brainstem.

RAS is located within the thalamus, basal nuclei, specific areas of the cortex, limbic regions & brainstem

(2) Identify the clinical manifestations of Delirium and recognize the overlap of acute confusional states

Clinical manifestations of delirium include an:

• acute change in conciousness and activity

• global cognitive changes with inattention

• fluctuating course affecting sleep-wake cycle and motor control

Delirium can be identified through mnemonic DELIRIUM:

• D

  • Disordered thinking

• E

  • Euphoria

• L

  • Language impairment

• I

  • Illusions/Delusions/Hallucinations

• R

  • Reversal of Sleep-wake cycle

• I

  • Inattention, unable to focus

• U

  • Unawareness, disorientated

• M

  • Memory deficits

It is important to differentiate delirium from other conditions like dementia, as delirium is often misdiagnosed or attributed to other factors

The aetiology of delirium includes various factors such as:

• sepsis

  • has been associated with the development of delirium as well

• cerebral hypoperfusion

  • neuroimaging studies have provided evidence that delirium may manifest as a result of widespread brain dysfunction rather than a localised dysfunction.

  • it has been suggested that a disruption to cerebral blood flow affecting a large portion of the brain may play a part in the development of delirium

• sedative/analgesic use

  • There has been lot of proposed mechanism of delirium development surrounding sedative and analgesic use

  • The most common theory involves the use of benzodiazepines which bind GABA receptors in the brain and decrease CNS arousal

  • This can lead to unpredictable neurotransmission and cerebral functioning resulting in neuronal atrophy and long-term cognitive impairment

• neuro-anatomical changes

  • have been noted in different patient populations experiencing delirium

  • One study revealed that 61% of critically ill patients were found to have gross white and gray matter lesions or ventricular enlargements

  • These cellular changes may explain some of the long term cognitive ad behavioural sequelae of delirium

• neurotransmitters and hormone involvement

  • Many different neurotransmitters ad hormones, such as serotonin, catecholamines, cortisol etc. have been suggested to have a part in the development of delirium

  • Their exact mechanism isn’t very clear in the literature, as both increased and decreased levels of these substances appear to be able to cause delirium

Common causes of delirium can be:

• infections (commonly urine or chest)

• trauma

• surgery

• constipation

• drug side-effects (e.g opioids or benzodiazepines)

• sudden drug withdrawals (e.g antidepressants)

Risk factors for developing delirium include:

• advanced age

• high comorbidity burden

• depression

• dementia

• frailty

• alcohol abuse

• benzodiazepine use

(3) Demonstrate knowledge of how to care for patients with Delirium

• To care for patients with delirium, it is important to create a quiet, stable, and well-lit environment

• Use re-orientation techniques like calendars and family photos, provide explanations during procedures, and reinforce orientation

• Avoid physical restraints and ensure correct sensory deficits are addressed

• Encourage support from familiar staff and family members

• In cases of severe delirium, constant supervision may be necessary to prevent non-compliant behaviour

• Additionally, a psych/med review may be needed for managing agitation or aggressive behaviour

Substance Intoxication

(1) Consider the effects of intoxication of substances such as Alcohol, Opioids, and Amphetamines

(2) Outline the processes occurring within the brain during substance intoxication

(3) Identify the harmful effects of overdose and withdrawal from substances

(1) Consider the effects of intoxication of substances such as Alcohol, Opioids, and Amphetamines

• Alcohol intoxication can lead to impaired coordination & judgement, and slurred speech

• Opioid intoxication can cause euphoria, drowsiness, and decreased respiratory rate

• Amphetamine intoxication can result in increased energy, alertness, and decreased appetite

Each substance affects the brain differently, leading to various physical and cognitive effects

Alcohol intoxication:

• Reinforcer:

  • a substance whose pharmacological effects drive the user to continue to use it

  • Positive reinforcing effects:

    • gain pleasure

    • altered conciousness

    • conform to behaviour of peers

  • Negative reinforcing effects

    • relief of stress and negative emotion

    • relief of withdrawal symptoms

• Alcohol (ethanol) absorption

  • Occurs entire length of digestive tract

    • skin, lungs, mucous membranes

    • varies on volume and concentration

    • food/gastric emptying - first pass if gastric emptying slow

    • peak levels reached 30-90 minutes

    • gastric ADH activity

    • genetic variation

    • gender

  • Through body water

    • differences in body composition and total body water

  • Ratios based on blood levels (averages)

    • Blood

      • Serum - 1:1.18

      • Brain - 1:0.75

      • Breath - 2100:1

      • Saliva - 1:1.12

• Metabolism and Excretion

  • Metabolism rate highly variable

  • Metabolised at liver, kidney, muscle, lung, intestine, brain (5% excreted unchanged in urine, feces, breath, sweat)

  • Differences in liver volume, ADH activity

  • 90% ethanol metabolised by ADH

  • Atleast 6 types encoded by 7 genes

    • A fast ADH or slow ALDH leads to elevated acetaldehyde levels thereby reducing alcohol drinking

• Variations in Ethanol Metabolism

  • Heavy vs Occasional drinkers

    • Regular drinkers metabolise alcohol fast than light drinkers as heavy drinkers have more available ADH enzyme

    • Heavy drinkers generally require a much higher blood alcohol levels to achieve a feeling of intoxication

  • Male vs Female

    • Female have proportionally more body fat and less water than males. There Alcohol is dispersed in body water. Women reach intoxication faster than men

  • Genetics

  • Acetylaldehyde (ADLH2*2)

    • is dominant in Chinese, Japanese and Korean descent

    • Responsible for Alcohol flush reaction

    • strongly protective against alcohol dependence

Opioid Intoxication

• Opioids like opiates act on brain receptors, causing the release of dopamine in the ventral tegmental area and nucleus accumbens.

• This leads to effects like:

  • analgesia

  • euphoria

  • drowsiness

  • detachment from surroundings

  • relaxation

  • slurred speech

  • impaired judgement

• Side effects can include:

  • nausea

  • vomitting

  • constipation

  • drowsiness

  • constricted pupils

  • decreased respiratory rate

  • reduced sexual and aggressive drives

  • In high doses,

    • opioids can lead to respiratory depression and potentially death, identified by symptoms like pinpoint pupils, unconciousness, and respiratory depression

Amphetamines

• Amphetamine intoxication can lead to various effects on the body

• It can cause

  • euphoria

  • alertness

  • excitation

  • insomnia

  • grandiosity

  • dilated pupils

  • increased heart rate

• Clinically it can manifest as cardiovascular issues like:

  • chest pain

  • palpitations

  • hypertension

  • CNS problems such as:

    • agitation

    • violent behaviour

    • hallucinations

  • Respiratory symptoms like:

    • dyspnea

    • wheezing

  • Integumentary issues including:

    • abscesses

    • lesions

  • GI problems such as:

    • abdominal pain

  • Dental complications like:

    • tooth decay

    • peri-dental abscesses

• These effects can be harmful and may require medical intervention

(2) Outline the processes occurring within the brain during substance intoxication

• Alcohol Intoxication

  • During Alcohol Intoxication. alcohol modifies membranes in the brain, affecting neurotransmitters like dopamine, glutamate, GABA, and serotonin

  • It impacts the reward system by interacting with receptors such as DRD2 and NMDA

  • This alteration in neurotransmitter activity contributes to the pleasurable effects of alcohol consumption

• Opioid Intoxication

  • During substance intoxication, opiates act on opioid receptors in the brain’s ventral tegmental area, leading to the release of dopamine in the nucleus accumbens

  • This dopamine release results in effects like analgesia, euphoria, drowsiness, and impaired judgement

  • The substance also causes side effects such as:

    • nausea

    • vomiting

    • decreased respiratory rate

• Amphetamine intoxication

  • during amphetamine intoxication, the drug promotes the release of neurotransmitters like dopamine, serotonin, and norepinephrine in the CNS and PNS nerve endings

  • It blocks the reuptake of dopamine, leading to euphoric effects in the CNS

  • This excessive release of neurotransmitters can result in:

    • heightened alertness

    • increased energy level

    • insomnia

    • dilated pupils

  • Overtime, tolerance can develop, leading to increased dosages and potential harmful effects on the brain and body

(3) Identify the harmful effects of overdose and withdrawal from substances

• Alcohol poisoning:

  • The most common alcohol poisonings are:

    • Ethanol - mortality 0.1%

    • Methanol - mortality 1.0%

    • Isopropanol - mortality 0.02%

    • Ethylene glycol - mortality 0.3%

  • 10-14 admissions per 1000 people

  • Alcohols are the most common accidental toxic ingestions by children younger than 5 years

  • Treatment:

    • All alcohols

      • Larvage - up to 4 hours post ingestion

      • Activated charcoal

      • Supportive measures - fluid monitoring, oxygen, airway protection

    • Methanol/Ethylene Glycol

      • sodium bicarbonate

      • Ethanol infusion

      • Dialysis

Harmful effects of alcohol overdose can include severe intoxication leading to alcohol poisoning, which can result in symptoms like:

• confusion

• vomiting

• seizures

• slow breathing

• coma or death

Withdrawal from alcohol can lead to symptoms such as:

• sudden extreme high blood pressure

• tremors

• Excite/fear - agitation/irritability

• anxiety

• hallucinations/confusion - delirium

• increased heart rate

• seizures

• in severe cases, delirium tremens (DT)

  • For those with alcohol use disorder suddenly stop drinking - they have a spike in glutamate that causes them symptoms common with DT

  • which is a life-threatening condition characterized by confusion, seizures, and hallucinations and even death as the SNS is in overdrive which can associate to cardiovascular collapse

• Opioid overdose

  • Opioid overdose can lead to:

    • respiratory depression

    • unconciousness

    • pinpoint pupils

  • Withdrawal from opioids can cause symptoms like:

    • nausea

    • vomitting

    • diarrhea

    • muscle pain

    • anxiety

  • Overdose can be reversed with naloxone, while withdrawal may require medical supervision for management

Acute Cardiac Conditions

(1) Identify the risk factors for acute cardiac conditions

(2) Discuss the pathophysiology of angina, MI, pericarditis, endocarditis & valve disorders

(3) Discuss the clinical manifestations, diagnosis and management of pericarditis, endocarditis & valve disorders

(1) Identify the risk factors for acute cardiac conditions

The risk factors for acute cardiac conditions include non-modifiable like:

• advancing age

• being male or female after menopause

• having family history of coronary artery disease

Modifiable risk factors include:

• dyslipidemia

• HTN

• smoking

• diabetes mellitus (DM)

• insulin resistance

• obesity

• sedentary lifestyle

These factors can contribute to conditions like:

• acute coronary syndrome

• angina

• myocardial infarction

• pericarditis

• endocarditis

• valve disorders

(2) Discuss the pathophysiology of angina, MI, pericarditis, endocarditis & valve disorders

• Angina is caused by reduces blood flow to the heart muscle due to narrowed arteries

• Myocardial infarction (MI) occurs when a coronary artery is completely blocked, leading to heart muscle damage

• Pericarditis is inflammation of the pericardium, outer lining of the heart

• Endocarditis is an infection or inflammation of the endocardium, often affecting the heart valves

• Valve disorders can result from various conditions, such as congenital defects or acquired diseases, leading to improper valve function and potential complications

(3) Discuss the clinical manifestations, diagnosis and management of pericarditis, endocarditis & valve disorders

• Pericarditis

  • Clinical manifestations of pericarditis include:

    • chest pain

    • fever

    • pericardial friction rub

  • Diagnosis involves:

    • physical exam

    • ECG changes

    • echocardiography

  • Treatment includes:

    • NSAIDs

    • colchicine

    • corticosteroids

• Endocarditis

  • Endocarditis presents with:

    • fever

    • heart murmur

    • petechiae

  • Diagnosis requires:

    • blood cultures

    • echocardiography

  • Management involves:

    • antibiotics

    • sometimes surgery

• Valve disorders

  • Valve disorders manifest as:

    • heart murmurs

    • chest pain

    • heart failure symptoms

  • Diagnosis includes:

    • echocardiography

  • Treatment may involve:

    • medications

    • valve replacement surgery

Acute respiratory conditions

(1) Provide an overview of the structure and aging of the respiratory system

(2) Discuss the pathophysiology, and clinical manifestations of Asthma and other common acute respiratory conditions

(3) Discuss the risks and potential complications of common acute respiratory conditions

(1) Provide an overview of the structure and aging of the respiratory system

The respiratory system includes structures like:

• nasal cavity

• pharynx

• larynx

• trachea

• bronchi

• bronchioles

• alveoli

• capillaries for gas exchange

Aging can affect:

• immune response

• mucus clearance

• cilia number

• respiratory muscle strength

• ribs

• elastin content

• cough

• chest wall compliance

• risk of infection

• pulmonary function

• gas exchange due to changes in these structures

These changes can lead to:

• decreased lung functions

• reduced vital capacity

• increased risk of respiratory conditions like infections and asthma

(2) Discuss the pathophysiology, and clinical manifestations of Asthma and other common acute respiratory conditions & (3) Discuss the risks and potential complications of common acute respiratory conditions

1. Asthma

   • it is characterised by intermittent or persistent airway obstruction due to factors like:

     • bronchial hyperresponsiveness

     • excess mucus production

     • atopy

     • air trapping

   • this leads to symptoms such as:

     • wheezing

     • SOB

     • chest tightness

     • coughing

     • anxiety

   • Pathophysiological symptoms such as:

     • edema

     • mucus

     • muscle spasms cause resistance to airflow

     • impairing expiration and leading to air trapping and alveolar hyperinflation

   • This results in:

     • uneven ventilation/perfusion

     • decreased pulmonary blood flow

     • impaired gas exchange

     • ultimately, hypoxemia & hypercapnia

   • Clinical manifestations include:

     • respiratory distress

     • increased respiratory rate

     • use of accessory muscles for breathing

     • decreased oxygen saturation levels

   • Asthma diagnosis involves:

     • history

     • physical examination

     • pulmonary function tests

     • laboratory studies

     • chest X-ray

   • Treatment includes:

     • monitoring lung function

     • controlling environmental triggers

     • pharmacologic therapy

     • patient education with an action plan

2. Pulmonary Embolism (PE)

   • occurs when a thrombus dislodges and occludes a pulmonary vessel, leading to decreased blood flow and hypoxia

   • it commonly arises from deep veins due to factors like:

     • venous stasis

     • hypercoagulability

     • vessel injuries

   • Symptoms include:

     • sudden chest pain

     • dyspnea

     • tachypnea

     • tachycardia

     • anxiety

   • The obstruction causes:

     • ventilation-perfusion imbalances

     • decreased PaO2

     • pulmonary infarction

     • HTN

     • decreased cardiac output

     • systemic hypotension

     • shock

   • PE can be life threatening and requires prompt medical intervention to prevent complications

3. Atelectasis

   • is the collapse of lung tissue due to various factors like lack of lung expansion or post-operative complications

   • there are 2 types:

     • Absorption

     • Compression

   • This condition can lead to:

     • decreased pulmonary blood flow

     • impaired gas exchange

     • respiratory failure

   • Clinical manifestations may include:

     • hypoxemia

     • hypercapnia

   • Mechanisms of air trapping in atelectasis involve:

     • issues with air movement during inspiration & expiration

     • mucus

     • bronchial plugs

     • muscle wall collapse

     • alveolar wall issues

   • These factors contribute to uneven ventilation/perfusion and decreased alveolar ventilation, which ca result in impaired gas exchange and respiratory failure

4. Pneumothorax

   

   • occurs when air enters the pleural space due to a rupture in the pleura

   • In traumatic cases, like injury, air enters through the chest wall and parietal pleura

   • This disrupts the pressure balance, leading to lung collapse

   • Clinical manifestations include:

     • sudden chest pain

     • dyspnea

     • tachypnea

     • tachycardia

     • anxiety

   • Treatment involves:

     • removing air from the pleural space to re-expand the lung

5. Pleural effusion

   • is the accumulation of excess fluid in the pleural space

   • it can be caused by various conditions like infections, heart failure, or cancer

   • The pathophysiology involves an imbalance between fluid production and absorption in the pleural space, leading to fluid buildup

   • This can case symptoms such as:

     • chest pain

     • difficulty breathing (dyspnea)

     • rapid breathing (tachypnea)

     • fast heart rate (tachycardia)

   • Diagnosis is usually done through imagine tests like X-rays or ultrasounds

   • Treatment may involve:

     • addressing the underlying cause

     • draining the fluid

     • medication

6. Aspiration

   • occurs when foreign substances are inhale into the respiratory tract

   • it can lead to:

     • inflammation

     • infection

     • respiratory distress

   • Pathophysiology involves the entry of substances like food or liquids into the airways, causing irritation, inflammation, and potential blockage

   • Clinical manifestations include:

     • coughing

     • wheezing

     • chest pain

     • SOB

     • in severe cases, aspiration pneumonia

   • Aspiration can lead to serious complications like lung abscess or respiratory failure if not managed promptly

   • Treatment involves:

     • supportive care

     • antibiotics for infections

     • bronchoscopy to remove the aspirated material

7. Pneumonia

   • is an infection that inflames the air sacs in one or both lungs

   • it can be caused by bacteria, viruses, or fungi

   • The pathophysiology involves the invasion of the lung tissue by the infectious agent, leading to an inflammatory response

   • This response causes the air sacs to fill with pus and other liquid, making it difficult to breathe

   • Types of pneumonia:

     • Community-acquired pneumonia

       • Streptococcus pneumoniae

       • Mycoplasma pneumoniae

       • Influenza, Legionella

     • Hospital-acquired (nosocomial) pneumonia

       • Staphylococcus aureus by fungi, protozoans

   • Clinical manifestations include:

     • cough

     • fever

     • chills

     • difficulty breathing

     • In severe cases, pneumonia can lead to complications such as respiratory failure

   • Risk factors for pneumonia include:

     • age

     • underlying lung disease

     • smoking

     • malnutrition

   • Treatment usually involves:

     • antibiotics for bacterial pneumonia

     • antiviral medications for viral pneumonia

     • supportive care to relieve symptoms

8. Bronchiolitis

   • is a common lower respiratory tract infections, often seen in children under 2 years old

   • it is mainly caused by the respiratory syncytial virus (RSV)

   • Clinical manifestations include symptoms like:

     • runny nose (rhinorrhoea)

     • cough

     • poor feeding

     • labored breathing (dyspnea)

   • Bronchiolitis is highly contagious

   • The pathophysiology involves inflammations and obstruction of the small airways in the lungs, leading to symptoms and potential complications

9. Croup (Acute laryngotracheobronchitis)

   • is an acute condition affecting the upper airway, commonly seen in children aged 6 months to 5 years

   • it is often caused by viruses like:

     • parainfluenza

     • infleunza A

     • RSV

   • The microorganism enters the upper airway, triggering an inflammatory response that leads to swelling and oedema in the upper airway

   • This swelling can cause upper airway obstruction, resulting in symptoms like a seal-like barking cough

   • The inflammation and oedema increase resistance to airflow, leading to increased negative pressure in the chest and potential collapse of the upper airway

   • Clinical manifestations of croup include a:

     • barking cough, which is distinctive, and the condition is usually self-limiting but may require glucocorticoids to reduce inflammation if severe

Review of the Respiratory System

(1) Review the structure and function of the Respiratory system, related to breathing and respiration and perfusion.

(2) Introduce tests relating to measurement of ventilation

(3) Gain an overview of the development of the respiratory system in the unborn.

(4) Consider the effects of aging on the respiratory system

(1) Review the structure and function of the Respiratory system, related to breathing and respiration and perfusion.

The respiratory system consists of the lungs, airways, and muscles involved in breathing

• Air is inhaled through the nose or mouth, travels down the trachea, and enters the lungs through bronchial tubes

• In the lungs, oxygen is exchanged for carbon dioxide in tiny air sacs called alveoli

• This process is known as respiration

Perfusion, the process of oxygenated blood being delivered to tissues, os facilitated by the respiratory system through the exchange of gases in the alveoli

• the diaphragm and intercostal muscles play a crucial role in breathing by expanding and contracting the chest cavity to allow air in and out of the lungs

Overall, the respiratory system ensures the intake of oxygen and removal of carbon dioxide, supporting the body’s metabolic functions

(2) Introduce tests relating to measurement of ventilation

The tests relating to the measurement of ventilation include:

• Tidal Volume (TV)

  • which measures the volume of air breathed in and out during quiet breathing

• Vital Capacity (VC)

  • is the maximum air amount inhaled and exhaled with forced breathing

• Forced Vital Capacity

  • measures the maximum air exhaled forcefully

• Forced Expiratory Volume in 1 second (FEV1)

  • measures the maximum air exhaled in one second

• Residual Volume (RV)

  • is the air volume left in the lungs after forceful exhalation

• Total Lung Capacity (TLC)

  • is the total air amount in maximally expanded lungs, calculated as the sum of RV and VC

These tests provide valuable information about lung function and can help diagnose respiratory conditions

(3) Gain an overview of the development of the respiratory system in the unborn.

The development of the respiratory system in the unborn goes through 5 stages:

1. Embryonic stage (0-7 weeks)

2. Psuedogladular stage (7-16 weeks)

3. Canalicular stage (16-25 weeks)

4. Saccular stage (25-36 weeks)

5. Alveolar stage (36 weeks - 6-8 years)

During these stages, the lungs undergo significant growth and maturation, with the alveolar stage being the final stage where the alveoli, responsible fir gas exchange, continue to develop postnatally.

This process is crucial for the unborn to be able to breathe independently after birth

(4) Consider the effects of aging on the respiratory system

Aging affects the respiratory system in various ways

• With age, there is a reduction in elastic fibers in the lungs, decreased respiratory muscle strength, and reduced cilia activity

  • Additionally, there is a decrease in cough efficiency, making older individuals more vulnerable to respiratory infections

• The ribs can calcify, the vertebrae can develop osteoporosis, and the alveoli can become “baggy”, leading to decreased lung function

• These changes can result in diminished ventilatory response to hypoxia and hypercapnia, making older individuals more susceptible to ventilatory failure or pnuemonia

• Nerves triggering coughing become less sensitive, further compromising the respiratory defense mechanisms

Acid/Base Regulation

(1) Review the basics – acids and bases (alkali)

(2) Discuss the role of hydrogen ion concentration in cellular function and dysfunction

(3) Describe how buffering systems help prevent significant fluctuations in pH

(4) Differentiate between respiratory and metabolic acid-base disorders by causes and mechanisms of compensations

(1) Review the basics – acids and bases (alkali)

1. Acids

   • are substances that donate protons (H+) when dissolved in water

   • they can be identified by their sour taste, ability to turn blue litmus paper red, and their corrosive nature

   • Examples of acids include:

     • hydrochloric acid (HCl) found in the stomach

     • Citric acid in citrus fruits

     • Acetic acid in vinegar

   • Acids plays a crucial role in various chemical reactions and are essential in many biological processes

2. Bases

   • also known as alkalis, are substances that receive protons (H+)

   • they can neutralize acids by accepting hydrogen ions

   • Examples of bases include:

     • metal hydroxides like sodium hydroxide (NaOH) & Potassium hydroxide (KOH)

     • in the context of cellular function, bases help maintain the pH balance by counteracting the acidic effects of hydrogen ions

     • This balance is crucial for various cellular processes to function optimally

(2) Discuss the role of hydrogen ion concentration in cellular function and dysfunction

Hydrogen ion concentration plays a crucial role in cellular function and dysfunction

• In cellular function,

  • hydrogen ions are involved in maintaining the normal pH level within cells, which is vital for various cellular to function optimally

  • for example,

    • enzymes, which are essential for biochemical reactions in cells, have an optimal pH range for their activity, and any significant deviation in hydrogen ion concentration can affect their function

• In cellular dysfunction,

  • an imbalance in hydrogen ion concentration can lead to acid-base disorders, disrupting cellular activities

  • For instance,

    • acidosis, which is characterised by increased hydrogen ion concentration, can interfere with normal cellular functions and lead to serious conditions like hyperkalemia

• Therefore, maintaining the balance of hydrogen ions is crucial for proper cellular function and overall health

(3) Describe how buffering systems help prevent significant fluctuations in pH

• Buffering systems help prevent significant fluctuations in pH by quickly neutralizing excess acids or bases in the body

• The plasma buffer system, respiratory system, and kidneys work together to maintain pH homeostasis

• For example,

  • the respiratory system responds rapidly to pH changes by adjusting CO2 levels

  • the kidneys, although slower to react, can continue buffering for extended periods by excreting H+ ions and regulating bicarbonate levels

• By working in tandem, these systems ensure that pH remains within the normal range, preventing acidosis or alkalosis

(4) Differentiate between respiratory and metabolic acid-base disorders by causes and mechanisms of compensations

Respiratory base disorders are caused by changes in carbon dioxide levels, leading to acidosis (elevated pCO2) alkalosis (low pCO2) due to hypoventilation or hyperventilation, respectively.

Metabolic base disorders result from changes in bicarbonate levels, causing acidosis (reduced HCO3-) or alkalosis elevation of HCO3-) due to non-carbonic acid accumulation or excessive loss of metabolic acids

Compensatory mechanisms involve the kidneys and lungs regulating bicarbonate and carbon dioxide levels to restore pH balance

1. Respiratory acidosis

   • is caused by elevated pCO2 due to alveolar hypoventilation, leading to a decrease in pH

   • The compensation mechanism involves the kidneys retaining bicarbonate (HCO3-) to help normalize pH levels

2. Metabolic acidosis

   • is characterised by reduced HCO3- levels or an increase in non-carbonic acids, lowering pH

   • the compensation mechanism for metabolic acidosis involves the respiratory system increasing ventilation to eliminate carbon dioxide, this raising pH levels

Trauma & Abuse

(1) Understand the impact of adverse childhood events on the individual, whanau and community.

(2) Identify anatomical and pathophysiological changes in child trauma.

(3) Discuss impact of adverse childhood events on adult life

(4) Describe neuroplasticity of the brain

(1) Understand the impact of adverse childhood events on the individual, whanau and community.

Adverse childhood events can have profound impacts on individuals, families (whanau), and communities

• Individuals may exhibit behavioural reactions like:

  • anger

  • avoidance

  • anxiety

  • low confidence

• Families can experience:

  • stress

  • gried

  • feelings of failure

• Communities may see:

  • increased violence

  • aggression

  • lack of trust

These events can lead to a rang of emotional, psychological, and social challenges that affect the overall well-being of individuals, families, and communities

The long-term effects can include relationships, and even societal problems like crime and substance abuse

It is crucial to address these impacts through support systems, therapy, and community interventions to mitigate and lasting consequences of adverse childhood events

(2) Identify anatomical and pathophysiological changes in child trauma.

Childhood trauma can lead to anatomical and pathophysiological changes in the brain

For example, prolonged exposure to stress hormones like cortisol can impact the development of brain regions involved in emotional regulation and memory, such as the amygdala and hippocampus

These changes can result in alterations in brain structure and function, affecting a child’s ability to cope with stress and regulate emotions

Additionally, trauma can disrupt the formation of neural connections and impact neurotransmitter systems, leading to long-term changes in brain circuitry and functioning

These alterations may contribute to symptoms of anxiety, depression, and other mental health issues commonly seen in individuals who have experienced childhood trauma

(3) Discuss impact of adverse childhood events on adult life

Adverse childhood events can have a significant impact on adult life

Individuals who experience ACEs are at a higher risk of mental and physical illnesses, as well as engaging in dysfunctional behaviours in adulthood

These experiences can lead to difficulties in regulating emotions, forming healthy relationships, and coping with stress

The trauma from childhood can manifest in various ways in adulthood, such as:

• increased anxiety

• depression

• substance abuse

• even physical health issues like heart disease or diabetes

Additionally, ACEs can affect cognitive function and decision-making abilities, leading to challenges in work, relationships, and overall well-being

Overall, the impact of adverse childhood events on adult life is profound and can have long-lasting consequences on an individual’s mental, emotional, and physical health

(4) Describe neuroplasticity of the brain

Neuroplasticity refers to the brain’s ability to reorganize itself by forming new neural connections throughout life

• this process allows the brain to adapt to new experiences, learn new information, and recover from injuries

• involves changes in brain structure, such as global volumetric changes, limbic circuitry, frontal regions, cerebellum, and structural connectivity

It is influenced by both genetics and environmental factors, shaping brain development

For example, trauma can impact brain development by affecting the reptillian brain, limbic system, and neocortex, leading to challenges in cognition, emotional regulation, and survival instincts

Overall, neuroplasticity plays a crucial role in how the brain responds to various stimuli and experiences, highlighting its dynamic and adaptive nature

High Risk Behaviours

(1) Describe the neuroscience of high risk behaviours

(2) Discuss possible pathophysiology of suicide and risk factors

(3) Discuss possible pathophysiology of self harm and risk factors

(1) Describe the neuroscience of high risk behaviours

High-risk behaviours involve actions that can lead to harm or negative consequences

In terms of neuroscience, these behaviours are often linked to the brain’s reward system.

• when engaging in high-risk behaviours, the brain’s reward pathways, particularly the release of dopamine, can be activated

• This activation reinforces the behaviours, making it more likely to be repeated despite the potential negative outcomes

Additionally, factors like genetics, environment, and past experiences can influence an individual’s propensity for engaging in high-risk behaviours by affecting brain function and decision-making processes

These behaviours can become ingrained due to neuroplasticity, where the brain adapts and changes in response to repeated behaviours

(2) Discuss possible pathophysiology of suicide and risk factors

The possible pathophysiology of suicide involves factors like low levels of brain-derived neurotrophic factor (BDNF) and serotonin,

• Low BDNF levels are lined to suicide, major depression, PTSD, schizophrenia, and OCD

Post-mortem studies show reduced BDNF in the hippocampus and prefrontal cortex

Serotonin, a neurotransmitter, is believed to be low in those who die by suicide, with evidence of reduced breakdown product levels in the cerebral spinal fluid

Risk factors for suicide include:

• history of depression

• anxiety

• previous suicide attempts

• PTSD

• family history

• genetic vulnerability

• ethnicity

• age

• poverty

• psychosis

• knowing someone who died by suicide

These factors, along with demographic, distal, proximal factors, and suicidal ideation, contribute to the complex pathophysiology of suicide

(3) Discuss possible pathophysiology of self harm and risk factors

Self-harm, or Non-Suicidal Self-Injury (NSSI), can be influenced by various risk factors

The possible pathophysiology involves a complex interplay of psychological and biological factors

Individuals may engage in self-harm as a maladaptive coping mechanism to deal with emotional distress, trauma, or mental health issues like anxiety and depression

Isolation, being bullied, and adverse childhood experiences (ACEs) can also contribute to self-harm behaviour

The presence of previous NSSI and exposure to NSSI in peers can normalize and reinforce self-harm tendencies

Additionally, underlying mental health conditions can increase the likelihood of engaging in self-harm as a way to regulate emotions or numb psychological pain

Overall, self-harm can be a manifestation of deeper emotional struggles and a cry for help

Pharmacology in Mental Health

(1) Be able to explain one commonly prescribed medication from each major class of mental health medications

1. Anxiolytics (Anti-anxiety, Sedatives, Hypnotics)

   • Alprazolam (Xanax) is benzodiazepine used to treat anxiety disorders

2. Anti-psychotics (Typical and Atypical)

   • Aripiprazole (Abilify) is an atypical antipsychotic used to treat schizophrenia and bipolar disorder

3. Anti-depressants

   • Sertraline (Zoloft) used to treat depression and anxiety disorders

4. Stimulants

   • Methylphenidate (Ritalin) is a common stimulant used to treat attention deficit hyperactivity disorder (ADHD)

(2) Describe the effects on the CNS, indications for use, and Adverse effects and associated risks for:

• Anxiolytics (Anti-anxiety, Sedatives, Hypnotics)

  • Anxiolytics like Benzodiazepine (Diazepam/Valium) act of GABA receptors in the CNS, causing sedation and reducing anxiety by affecting the amygdala in the limbic system

  • They are used for anxiety and panic disorders, and in alcohol withdrawal

  • Adverse effects include:

    • fatigue

    • drowsiness

    • muscle weakness

    • risk of dependence

    • requiring a long withdrawal period

  • They are contraindicated in conditions like COPD and liver disease due to potential complications

  • These medications have CNS depressant effects, are indicated for anxiety-related conditions, and carry risks for side effects and dependency

• Anti-psychotics (Typical and Atypical)

  • Atypical anti-psychotics like Quetiapine (Seroquel) act on CNS receptors for Dopamine and Serotonin, providing a calming effect

    • they are used for acute and chronic psychosis, schizophrenia and bipolar disorder

    • Adverse effects include:

      • increased suicide risk

      • hypotension

      • metabolic syndrome exacerbation

      • dizziness

      • weight gain

  • Typical anti-psychotics like Haloperidol (Serenace) at on multiple CNS neurotransmitter receptors, especially Dopamine, leading to extrapyramidal effects

    • they are indicated for psychosis, schizophrenia, and alcoholic delusions

    • Adverse effects include:

      • extrapyramidal effects (movement disorders)

      • dizziness

      • constipation

      • confusion

      • drowsiness

• Anti-depressants

  • like Fluoxetine (Prozac)

  • the CNS effects involve inhibiting the reuptake of serotonin, leading to increased serotonin levels in the synaptic space, which helps regulate mood

  • Indications for use include treating:

    • depression

    • anxiety

    • bulimia nervosa

    • OCD

    • premenstrual dysphoric disorder

    • panic disorder

    • PTSD

  • Adverse effects and associated risks may include:

    • initial increased risk of suicidal thoughts

    • weight loss

    • nausea

    • vomitting

    • headaches

    • rashes

    • dizziness

• Stimulants

  • like amphetamines and methylphenidate

  • have CNS effects by stimulating neuron activity in excitatory pathways, affecting parts of the brain like the cerebral cortex and limbic region

  • These drugs are indicated for ADHD treatment

  • However, they come with adverse effects and risk such as potential:

    • addiction

    • insomnia

    • headache

    • irritability

    • nausea

  • Prolonged use can lead to:

    • mood changes

    • depression

    • agitation

    • psychosis

  • These drugs act on neurotransmitters like dopamine & norepinephrine, impacting:

    • focus

    • attention

    • impulse control in individuals with ADHD

(3) Be able to describe the difference between a chemical name, generic name and brand name

• The chemical name refers to the exact molecular structure of a drug, providing detailed information about it composition

• The generic name is the official name of the drug, usually derived from its chemical name and recognised by health professionals world wide

• The brand name is the trademarked name given by the pharmaceutical company marketing the drug

• It is unique to that specific company and is used for marketing purposes

For example,

the chemical name for Aspirin is Acetylsalicylic acid, the generic name is Aspirin, and the brand name could be Bayer Aspirin

Acute Diabetic States

(1) The role of the pancreas and hormones insulin and glucagon

(2) Aetiology & cause of diabetes (with a focus on Type 1)

(3) Pathophysiology - the disordered processes and acute complications

(4) The clinical manifestations of acute diabetes states

(1) The role of the pancreas and hormones insulin and glucagon

The pancreas plays a crucial role in regulating blood sugar levels through the secretion of hormones, primarily insulin and glucagon

• These hormones work in tandem to maintain homeostasis in the body, particularly concering glucose metabolism

Insulin:

• is an anabolic hormone produed by the beta cells of the pancreatic islets

• its primary function is to lower blood sugar levels by facilitating the uptake of glucose into cells, especially in the liver, muscle, and adipose tissues

• Insulin promotes several key processes:

  • Glucose uptake, it allows cells to absorb glucose from the bloodstream, which is essential for energy production

  • Protein Synthesis, insulin encourages the synthesis of proteins, which are vital for growth and repair

  • Lipid Storage, it aids in the formation and storage of lipids, helping to regulate fat metabolism

  • Transport of Ions, insulin facilitates the transport of potassium, phosphate, and magnesium across cell membranes, which is important for various cellular functions

In contrast, Glucagon:

• is a catabolic hormone produced by the alpha cells of the pancreatic islets

• Its primary role is to increase blood sugar levels, particularly during periods of low blood sugar (hypoglycaemia)

• Glucagon’s actions include:

  • Glycogenolysis, it stimulates the conversion of glycogen (stored glucose) in the liver into glucose, which is then released into the bloodstream

  • Gluconeogenesis, glucagon may promote the conversion of non-carbohydrate sources, such as amino acids and glycerol, into glucose

  • Lipolysis, it encourages the breakdown of stored fats in adipose tissues, releasing fatty acids into the bloodstream for energy use

  • Response to stress, the sympathetic nervous system can trigger release during stress, ensuring that energy is available when needed

Together, insulin and glucagon maintain blood sugar levels within a narrow range

(2) Aetiology & cause of diabetes (with a focus on Type 1)

The aetiology of Type 1 Diabetes Mellitus (DM) is multifactorial, involving genetic, immunological and environmental components:

• Genetic susceptibility

  • individuals may have a genetic predisposition to Type 1 DM, often linked to specific genes that influence immune system function

  • Monogenic Diabetes, caused by mutations in a single gene, can also occur and requires genetic testing for diagnosis

• Immune response

  • Type 1 DM is primarily characterised by an autoimmune response where the body’s immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas

  • This destruction leads to an absolute or significant deficit of insulin, which is critical for glucose metabolism

• Environmental factors

  • various environmental triggers may initiate or exacerbate the autoimmune process

  • These include:

    • viral infections, certain viruses have been implicated in triggering the autoimmune response that leads to Type 1 DM

    • Dietary Factors, for example, exposure to bovine milk in infancy has been suggested as a potential risk factor

    • Chemical Exposures, certain drugs and chemicals may also play a role in the development of the disease

• Pathophysiological changes

  • the infiltration of lymphocytes and macrophages into the islets of Langerhans in the pancreas results in inflammation and damage to the beta cells

  • This immune-mediated destruction disrupts insulin production, leading to hyperglycaemia and associated symptoms such as glucosuria (glucose in urine) and diabetic ketoacidosis (DKA), a serious acute complication characterised by the hyperketonemia (high levels of ketones in the blood)

In summary, the aetiology of Type 1 DM involves a complex interplay of genetic predisposition, autoimmune destruction of pancreatic beta cells, and environmental factors that together lead to the clinical manifestations of the disease

(3) Pathophysiology - the disordered processes and acute complications

The pathophysiology of diabtes involves complex disordered processes that lead to acute complications, particularly in individuals with Type 1 Diabetes

• Disordered processes

  • Insulin deficiency, in Type 1 diabetes, the pancreas fails to produce insulin due to autoimmune destruction of beta cells

  • Insulin in crucial for glucose uptake by cells, and its absence leads to elevated blood glucose levels (hyperglycaemia)

  • Glucagon overproduction, In response to low insulin levels, glucagon secretion increases. Glucagon promotes gluconeogenesis and glycogenolysis in the liver, exacerbating hyperglycaemia

  • Metabolic imbalance, the lack of insulin and the presence of glucagon lead to a shift from glucose metabolism to fat metabolism, resulting in the production of ketone bodies. This can lead to diabetic ketoacidosis (DKA)

• Acute complications

  • Hypoglycaemia

    • this occurs when blood glucose levels drop too low, often due to excessive insulin administration or inadequate food intake

    • Symptoms include:

      • confusion

      • sweating

      • tremors

      • can lead to seizures or LOC if untreated

  • Diabetic Ketoacidosis (DKA)

    • characterised by high levels of ketones in the blood due to fat breakdown

    • DKA presents with symptoms such as:

      • nausea

      • vomitting

      • abdominal pain

      • rapid breathing

      • fruity-smelling breath

    • It is a medical emergency requiring prompt treatment with insulin and fluids

  • Hyperglycaemic Hyperosmolar State (HHS)

    • This condition is more common in Type 2 diabetes and involves extremely high blood glucose levels without significant ketone production

    • It leads to severe dehydration and hyperosmolarity, causing confusion, lethargy and can progress to coma

  • Metformin Associated Lactic Acidosis (MALA)

    • While primarily associated with Type 2 Diabetes, MALA can occur in patients taking metformin, especially in cases of renal impairment

    • MALA is characterised by blood lactate levels exceeding 5 mmol/L, indicating significant lactic acidosis

    • This conditions is a medical emergency due to the potential for severe metabolic disturbances

    • In summary, MALA results from the interplay of metformin’s pharmacological effects, impaired lactate clearance due to to renal dysfunction, and conditions that promote lactate production, leading to a dangerous accumulation of lactate in the bloodstream

(4) The clinical manifestations of acute diabetes states

The clinical manifestations of acute diabetic states vary depending on the specific condition

Here are the key manifestations for each of the acute complications mentioned:

• Hypoglycaemia

  • this condition occurs when blood glucose levels drop below normal

  • Clinical manifestations include:

    • sweating

    • shakiness or tremors

    • confusion or irritability

    • palpitations

    • hunger

    • dizziness or lightheadedness

    • in severe cases, it can lead to seizures or LOC

• Diabetic Ketoacidosis

  • DKA is characterised by the accumulation of ketones due to insufficient insulin

  • Clinical manifestations include:

    • Polyuria (increased urination)

    • Polydipsia (increased thirst)

    • Nausea & vomitting

    • Abdominal pain

    • Fruity-scented breath (due to acetone)

    • Rapid breathing (Kussmaul respirations)

    • confusion or altered mental status

• Hyperglycaemia Hyperosmolar State (HHS)

  • this condition is marked by extremely high blood sugar levels without significant ketone production

  • Clinical manifestations include:

    • Severe dehydration

    • polyuria

    • Polydipsia

    • confusion or altered consciousness

    • weakness

    • visual disturbances

• Metformin Associated Lactic Acidosis (MALA)

  • this rare but serious condition can occur in patients taking metformin, especially in cases of renal impairment

  • Clinical manifestations include:

    • lactic acidosis symptoms such as muscle pain or weakness

    • abdominal discomfort

    • Rapid breathing

    • confusion or lethargy

    • Hypotension (low blood pressure

Each of these acute states presents distinct clinical signs and symptoms that require prompt recognition and management to prevent serious complications

Pathophysiology of wound healing

(1) Review basic anatomy of skin

(2) Describe the 4 phases of wound healing

(3) Identify what is classified as an acute wound

(4) Describe primary and secondary wound healing

(5) Describe factors that affect wound healing & how they impact the individual

(1) Review basic anatomy of skin

The basic anatomy of the skin consists of 3 primary layers: the epidermis, dermis, and subcutaneous tissue (hypodermis)

• Epidermis

  • this is the outermost layer of the skin, primarily composed of keratinized stratified squamous epithelium

  • It provides a protective barrier against environmental hazards and is responsible for the skin’s pigmentation due to melanocytes

  • The epidermis is avascular, meaning it does not contain blood vessels, and relies on the dermis for nutrient supply

• Dermis

  • located beneath the epidermis, the dermis is much thicker and contains connective tissue, blood vessels, hair follicles, and various glands (such as sweat and sebaceous glands)

  • It provides structural support and elasticity to the skin due to the presence of collagen and elastin fibres

  • The dermis also houses sensory receptors that detect touch, pressure, and temperate

• Subcutaneous Tissue (Hypodermis)

  • this is the deepest later of the skin, consisting of loose connective tissue and fat cells

  • it act as an insulator, helps regulate body temperature, and serves as an energy reserve

  • the hypodermis also anchors structures like muscles and bones

Overall, the skin serves multiple serves multiple functions, including protection, temperature regulation, sensation, immune defense, a biochemical processes such as Vitamin D absorption

(2) Describe the 4 phases of wound healing

The wound healing process consists of 4 main phases: Haemostatis Inflammation, Proliferation, and Maturation/Remodelling

Each phase plays a crucial role in the overall healing of damaged tissue

• Haemostasis

  • this is the initial phase that occurs immediately after injury

  • the primary goal is to stop the bleeding

  • Blood vessels constrict (vasoconstriction) to reduce blood flow, and platelets aggregate at the site of injury, forming a clot

  • This clot not only prevents further blood loss but also serves as a temporary barrier against pathogens

• Inflammation

  • following haemostasis, the inflammatory phase begins, lasting for several days

  • This phase is characterised by the body’s immune response to the injury

  • White blood cells, particularly neutrophils and macrophages, migrate to the wound site to clear debris and pathogens

  • This process results in redness, heat, swelling, and pain

  • The inflammatory response is crucial for preventing infection and setting the stage for tissue repair

• Proliferation

  • this phase typically starts a few days after the injury and can last for weeks

  • It involves the formation of new tissue

  • Key processes include angiogenesis (formation of new blood vessels), collagen deposition, and epithelization (regrowth of skin cells

  • Fibroblasts play a significant role in producing collagen, which provides structural support to new tissue

  • The wound gradually contract's as myofibroblasts pull the edges together

• Maturation/Remodelling

  • The final phase can last for months to years after the injury

  • Duing this phase, the newly formed tissue is strengthened and reorganised

  • Collagen fibers are remodeled, and the wound gains tensile and strength

  • The scar tissue formed during this phase is usually less vascular and has a fewer cells that the original tissue

  • The goal is to restore the tissue to its normal function as much a possible

  • Successful wound healing requires that all 4 phases occur in a coordinated matter

(3) Identify what is classified as an acute wound

An acute wound is classified as a type of injury that generally follows the normal healing trajectory and typically shows signs of healing within a month

Acute wounds are characterised by their ability to progress through the 4 phases of wound healing - haemostasis, inflammation, proliferation, and remodelling - without significant complications

Acute wounds can arise from various cases, including:

• Traumatic Wounds

  • these result from external forces, such as cuts, laceration, or abrasions

  • For example, a deep cut from a sharp object would be considered an acute wound

• Surgical Incisions

  • wounds created intentionally during surgical procedures are also classified as acute

  • These incisions are designed to heal in a controlled manner, typically by primary intentions, where the edges of the wound are brought together

• Burns

  • depending on their severity, burns can be acute wounds

  • First-degree burns may heal quickly, while deeper burns may take longer but still follow the acute healing process

  • Acute wounds are generally expected heal by primary intention, meaning that the wound edges are approximated and heal with minimal scarring

  • Factors that can influence the healing of acute wounds include the patient’s overall health, age, nutritional status, and the presence of any underlying conditions

In summary, acute wounds are defined by their timely healing process, typically resolving within one month and progressing though the normal phases of healing, contrasting with chronic wounds that fail to heal in a timely manner

(4) Describe primary and secondary wound healing

Primary and secondary wound healing are two distinct modes of wound healing that differ primarily in the extent of tissue loss and the method by which the wound heals

• Primary Intention Healing

  • this type occurs when there is minimal tissue loss, typically seen in clean, surgical incisions that can be easily sutured

  • The dermal edges of the wound are closely approximated, allowing for a more straightforward healing process

  • The benefits of primary intention include reduced scarring and a quicker recovery time

  • The healing process involves 4 stages:

    • haemostasis (stopping the bleeding)

    • inflammation (the body’s response to injury

    • proliferation (new tissue formation)

    • maturation/remodeling (strengthening and refining the new tissue)

  • Because the edges are close together, the healing is efficient, and the risk of infection is lower

• Secondary Intention Healing

  • This method is utilised when there is extensive tissue loss, such as in severe lacerations or large pressure injuries that cannot be sutured

  • In this case, the wound edges are not approximated, and healing must occur from the base of the wound upward

  • This process is more prolonged and complex, as it involves the formation of granulation tissue and the eventual contraction of the wound

  • Secondary intention healing often results in increased scarring due to the larger area of tissue that must regenerate and the longer healing time

  • The 4 stages of healing still apply, but the process may be less predictable, and wounds can progress backward or forward based on various internal and external factors affecting the patient

In summary, primary intention is characterised by minimal tissue loss and quick healing with less scarring, while secondary intention involves significant tissue loss, longer healing times, and typically more pronounced scarring

(5) Describe factors that affect wound healing & how they impact the individual

Wound healing is influenced by a variety of factors that can either promote or hinder the healing process

Understanding these factors is crucial for effective patient care

Here are some key factors affecting wound healing:

• Bacterial Infection

  • the presence of bacteria can lead to infection, which prolongs the inflammatory phase and can result in delayed healing or chronic wounds

  • Infections can cause increased inflammation, tissue damage, and can lead to systemic complications

• Wound Dehiscence

  • this refers to the reopening of a wound, often due to inadequate healing or excessive tension on the wound edges

  • Dehiscence can lead to further complications, including infection and prolonged recovery time

• Necrosis

  • the presence of dead tissue (necrotic tissue) in a wound can impede healing by providing a medium for bacterial growth and delaying the formation of new tissue

  • Debriding may be necessary to remove necrotic tissue and promote healing

• Elevated Blood Glucose Levels (BGL)

  • high BGL, commonly seen in diabetic patients, can impair the immune response and reduce the efficiency of the healing process

  • It can lead to poor circulation and neuropathy, which further complicates wound healing

• Nosocomial Infections

  • These are infections acquired in a healthcare setting

  • They can significantly impact wound healing by introducing resistant bacteria, leading to complications that can delay recovery and increase healthcare costs

• Other factors

  • Additional factors include age, nutritional status, oxygenation, underlying health conditions 9like diabetes or vascular diseases), medications (such as corticosteroids) and lifestyle choices (like smoking)

  • for instance, older adults may experience slower healing due to reduced cellular regeneration, while adequate nutrition (especially protein and vitamins) is essential for tissue repair

In summary, the interplay of these factors can significantly affect the wound healing process, influencing the individual’s recovery time, risk of infections, and overall health

Acute Kidney Injury

(1) Review the anatomy and physiology of the Urinary and Renal Systems

(2) Differentiate between Pre-Renal, Intra-Renal &Post-Renal causes of acute kidney injury.

(3) Identify exemplars of Acute Kidney Injury including Tubular Necrosis and Nephrotoxicity

(4) Recognise the impact of AKI on the individual and the community

(1) Review the anatomy and physiology of the Urinary and Renal Systems

The urinary and renal systems are crucial for maintaining homeostasis, regulating fluid balance, and excreting waste products from the body

• Anatomy

  • kidneys

    • there are two kidneys, located on either side of the spine, with the left kidney typically positioned slightly higher than the right

    • Each kidney contains:

      • renal cortex : the outer layer where filtration occurs

      • renal medulla : the inner layer, consisting of renal pyramids and collecting ducts

      • renal pelvis : the funnel-shapes structure that collects urine before it moves to the ureter

      • renal columns and papillae : structurs that separate the renal pyramids and direct urine into the calyx

  • Nephron

    • the functional unit of the kidney, approximately one million per kidney, consists of:

      • Bowman’s Capsule : encloses the glomerulus, where filtration begins

      • Glomerulus : a network of capillaries that filter blood

      • Proximal Convoluted tubule : reabsorbs water, ions, and nutrients

      • Loop of Henle : creates a concentration gradient for urine concentration

      • Distal Convoluted tubule : further adjusts the composition of urine

      • Collecting duct : collects urine from multiple nephrons and transports it to the renal pelvis

  • Ureters

    • two tubes that transport urine from the kidneys to the bladder

  • Bladder

    • a muscular sac that stores urine until excretion

    • Urethra

      • the tube through which urine is expelled from the body

    • Adrenal glands

      • located top each kidney, these glands produce hormones that regulate metabolism, immune response, and blood pressure

Physiology

• the physiology of the urinary and renal systems is centred around the kidneys, which are vital organs responsible for filtering blood, regulating fluid balance and excreting waste products through urine

• Kidney structure:

  • each kidney contains approximately one million functional nephrons

  • A nephron consists of several key components:

    • glomerulus

    • bowman’s capsule

    • proximal convoluted tubule

    • Loop of Henle

    • distal convoluted tubule

    • collecting duct

  • The renal cortex contains the glomeruli an proximal tubules, while the renal medulla houses the Loop of Henle and collecting ducts

• Filtration

  • blood enters the kidneys through the renal arteries, which branch into smaller arterioles leading to the glomeruli

  • Here, blood is filtered under pressure, allowing water, electrolytes, and small molecules to pass into Bowman’s capsule while retaining larger molecules like proteins and blood cells

• Reabsorption

  • as the filtrate moves through the proximal convoluted tubule, essential substances such as glucose, amino acids, and ions are reabsorbed back into the bloodstream

  • The Loop of Henle further concentrates urine by reabsorbing water and sodium, creating a concentration gradient in the medulla

• Secretion

  • in the distal convoluted tubule, additional waste products and excess ions are secreted into the filtrate from the blood, helping to maintain electrolyte balance and pH levels

• Excretion

  • the final urine, which contains waste products, excess water, and electrolytes, is collected in the renal pelvis and transported to the bladder via the ureters

  • The bladder stores urine until it is excreted through the urethra

• Regulation

  • the kidneys also play a crucial role in homeostasis by regulating blood pressure through the renin-angiotensin-aldosterone system, maintaining acid-base balance, and controlling electrolyte levels

  • Hormones such as erythropoietin and renin, produced by the kidneys, further contribute to these regulatory functions, with EPO stimulating red blood cell production and renin playing a key role in blood pressure regulation through the RAS system

(2) Differentiate between Pre-Renal, Intra-Renal &Post-Renal causes of acute kidney injury.

Acute Kidney Injury (AKI) can be categorised into 3 main types based on the underlying causes: Pre-Renal, Intra-renal, and Post-renal

• Pre-Renal AKI

  • this type occurs due to factors that reduce blood flow to the kidneys, leading to ischemia

  • common causes include:

    • dehydration

    • heart failure

    • severe blood loss

  • the kidneys are structurally normal, but their function is impaired due to inadequate perfusion

• Intra-Renal AKI

  • this type involves direct damage to the kidney tissue itself

  • the most common cause is Acute Tubular Necrosis (ATN)

    • which can result from ischemia or exposure to nephrotoxins such as certain antibiotics and contrast media used in imaging studies

    • Intra-Renal AKI reflects structural damage, often seen in hospitalised patients

  • Post-Renal AKI

    • this type arises from obstruction in the urinary tract that impedes urine flow, leading to increased pressure in the kidneys

    • Causes can include:

      • kidney stones

      • tumors

      • enlarged prostate

    • The obstruction can occur at any point in the urinary system, from the kidneys to the urethra

In summary, Pre-Renal AKI is due to reduced blood flow, Intra-Renal AKI is due to direct kidney damage, and Post-Renal AKI is due to obstruction in the urinary tract

(3) Identify exemplars of Acute Kidney Injury including Tubular Necrosis and Nephrotoxicity

Acute Kidney Injury (AKI) can be exemplified by conditions such Acute Tubular Necrosis (ATN) and Nephrotoxicity

• Acute Tubular Necrosis (ATN)

  • is the most common cause of intrarenal AKI, characterised by damage to the kidney’s tubular cells

  • this damage can occur due to two primary factors:

    • Ischaemia, refers to reduced blood flow to the kidneys which can happen in situations like severe dehydrations or shock

    • Nephrotoxins, are substances that can harm the kidney tissue, including certain medications (like some antibiotics) and contrast media used in imaging studies

  • The significance of ATN lies in its prevalence, especially among hospitalised patients, indicating a critical area for monitoring and intervention

• Nephrotoxicity

  • refers to the toxic effects on the kidneys caused by various substances

  • this can include drugs (e.g non-steroidal anti-inflammatory drugs, certain antibiotics, and chemotherapy agents) and environmental toxins

  • Nephrotoxic agents can lead to cellular injury and death in the renal tubules, contributing to the development of AKI

  • The recognition of nephrotoxicity is crucial for preventing AKI, especially in patient’s with pre-existing kidney conditions or those receiving high-risk medications

Both ATN and nephrotoxicity highlight the importance of early detection and management of AKI, as they can significantly impact an individual’s health and the broader community by increasing healthcare costs and the burden on medical resources

Early intervention can improve outcomes and reduce the long-term effects of kidney damage

(4) Recognise the impact of AKI on the individual and the community

Acute Kidney Injury (AKI) has significant impacts on both individuals and communities, affecting health outcomes, healthcare systems, and economic stability

• Impact on the individual

  • Health consequences

    • AKI is associated with a rapid decline in renal function, leading to the retention of metabolic wastes, which can cause symptoms like:

      • fatigue

      • confusion

      • fluid overload

    • The mortality rate exceed 30%, indicating a severe risk to life

  • Quality of life

    • individuals may experience complications such as chronic kidney injury disease (CKD) or require dialysis, leading to a diminished quality of life

    • Symptoms of AKI can lead to hospitalisation, which disrupts daily activities and responsibilities

  • Psychosocial Effects

    • the stress of dealing with a serious health condition can lead to anxiety and depression

    • Patients may also face stigma or fear regarding their health status, impacting their social interactions and mental well-being

• Impact on the community

  • Healthcare system Burden

    • AKI contributes to increased healthcare costs due to hospital admissions, prolonged stays, and the need for specialised treatment like dialysis

    • This can strain healthcare resources, particularly in regions with limited medical facilities

  • Economic impact

    • the economic burden extends beyond healthcare costs, as individuals may be unable to work during recovery, leading to lost wages and decreased productivity

    • this can have a ripple effect on local economies

  • Public health concerns

    • high rates of AKI can indicate broader public health issues, such as inadequate access to healthcare, environmental factors, or prevalent diseases

    • Addressing these underlying causes is essential for community health improvement

In summary, AKI poses serious health risks for individuals, leading to potential long-term complications and psychological distress

For communities, it represents a significant burden on healthcare systems and economic stability, necessitating comprehensive strategies for prevention, early detection, and management

Infectious Diseases

(1) Refresh your knowledge of common pathogens and how the immune system works against infectious diseases.

(2) Understand the complex interactions between humans and microorganisms

(3) Describe types of infectious organisms and the types of diseases they cause

(4) Identify who is at risk for infectious diseases

(5) Discuss how infectious agents cause damage to the body

(1) Refresh your knowledge of common pathogens and how the immune system works against infectious diseases.

Common pathogens include bacteria, viruses, fungi, and parasites, each capable of causing various infectious diseases

• Bacteria

  • these are sing-celled organisms that can reproduce independently

  • some bacteria are beneficial, but pathogenic bacteria can cause diseases such as strep throat, tuberculosis, and urinary tract infections

  • The immune system combats bacterial infections primarily through the action of antibodies and phagocytic cells, which engulf and destroy bacteria

• Viruses

  • are much smaller than bacteria and require a host cell to replicate

  • they can cause diseases such as influenza, HIV/AIDS, and COVID-19

  • The immune response against viruses involves both humoral immunity (antibody production) and cell-mediated immunity, where cytotoxic T cells recognise and destroy infected cells

• Fungi

  • these can be unicellular (like yeast) or multicellular (like molds)

  • Fungal infections, such as athlete’s foot and candidiasis, often affect individuals with weakened immune systems

  • the immune system responds to fungi through the activation of T cells and the production of specific antibodies

• Parasites

  • these organisms live on or in a host and can cause diseases such as malaria and giardiasis

  • the immune response to parasites is complex and often involves both innate and adaptive immunity, including the production of antibodies and the activation of eosinophils

The immune system works against these pathogens through various mechanisms:

• Innate immunity

  • this is the first line of defense and includes physical barriers (like skin), chemical barriers (like stomach acid), and immune cells (like macrophages and neutrophils) that respond quickly to infections

• Adaptive immunity

  • this is a more specific response that develops over time

  • it involves the activation of lymphocytes (B & T cells)

    • B cells produce antibodies that specifically target antigens (substances from pathogens)

    • T cells can directly kill infected cells or help coordinate the immune response

In summary, common pathogens include bacteria, viruses, fungi, protozoa, and prions, each capable of causing various diseases upon invading the body and multiplying. The immune system defends against these infectious agents through a complex network of cells and mechanisms. It identifies and targets pathogens using innate immunity, which provides immediate but non-specific responses, and adaptive immunity, which develop specific responses tailored to particular pathogens. This dual approach enables the immune system to recognise, attack, and eliminate invading microorganisms while also remembering past infections to mount faster responses in future encounter

(2) Understand the complex interactions between humans and microorganisms

The complex interactions between humans and microorganisms encompass a dynamic relationships that can lead to both beneficial and harmful outcomes

These interactions are influenced by various factors, including the type of microorganisms, the host’s immune response, and environmental factors

• pathogen invasion

  • microorganisms such as bacteria, viruses, fungi, protozoa, and prions can invade the human body

  • infection occurs when these pathogens multiply and produce disease, often causing harm to the host

  • for instance, bacteria can cause localised infections like strep throat or systemic infections such as sepsis

• Immune response

  • the human immune system plays a crucial role in defending against these pathogens

  • it recognises and responds to foreign invaders through innate and adaptive immunity

  • Innate immunity provides immediate defense through barriers (like skin) and immune cells, while adaptive immunity develops a targeted response to specific pathogens, creating memory cells for faster responses in future encounters

• Microbiome Interactions

  • not all microorganism are harmful; many are beneficial and form part of the human microbiome

  • these beneficial microbes help in digestions, synthesize vitamins, and protect against pathogenic organisms by competing for resources and space

  • The balance between beneficial and harmful microorganisms is critical for maintaining health

• Environmental factors

  • the interactions are also influenced by environmental factors such as sanitation, nutrition, and healthcare access

  • Poor sanitation can facilitate the spread of infectious diseases, while good nutritions can enhance immune function

• Evolving pathogens

  • pathogens can evolve rapidly, developing resistance to treatments and vaccines

  • this evolution can lead to the emergence of new diseases or the resurgence of previously controlled infections, a complicating the human-microbe relationship

• Risk factors

  • certain populations are at higher risk for infectious diseases, including the immunocompromised, elderly, and those with chronic conditions

  • Understanding these risk factors in essential for public health strategies to prevent and control infections

In summary the complex interactions between humans and microorganism involve a dynamic and evolving relationship where pathogens - such as bacteria, viruses, fungi, protozoa, and prions - invade the human body, multiply and potentially cause disease

This interaction is not merely adversarial; it encompasses a range of responses from the human immune system, which works to combat these infections can vary, leading to localised infections, disseminated infection, or systemic diseases that can harm the host.

Understanding these interactions is crucial for identifying at-risk populations and developing effective strategies to maintain to manage an

(3) Describe types of infectious organisms and the types of diseases they cause

Infectious organisms, also known as pathogens can be categorised into several types, each associated with specific diseases

• Bacteria

  • these are single-celled organism that can cause a variety of diseases

  • Three major types of bacteria are:

    • Cocci, spherical bacteria, which can lead to infections such as strep throat (caused by Streptococcus) and toxic shock syndrome (associated with Staphylococcus)

    • Bacilli, rod-shaped bacteria, responsible for diseases like tuberculosis (Myobacterium tuberculosis) and pnuemonia (various bacterial strains)

    • Spirilla, spiral-shaped bacteria, which can cause diseases such as syphillis (Treponema pallidum)

• Viruses

  • these are much smaller than bacteria and require a host cell to repicate

  • Viral infections can lead to diseases such as infleuenza, HIV/AIDS, and COVID-19

• Fungi

  • these organisms can be single-celled (like yeast) or multicellular (like molds)

  • Fungal infections can cause conditions such as athlete’s foot, ring worm, and systemic infections in immunocompromised individuals

• Protozoa

  • These are singe-celled organisms that can cause diseases such as malaria (caused by Plasmodium species) and giardiasis (caused by giardia lamblia)

• Prions

  • these are infectious proteins that ccan lead to neurodegenerative diseases such as Creutzfeldt-Jakob disease and mad cow disease (BSE)

Each of type of pathogen interacts with the host’s immune system differently, leading to various disease manifestations

For instance, bacterial infections often involve the production of toxins that damage tissues, while viral infections may hijack host cells for replications, leading to cell death

Understanding these interactions is crucial for developing effective treatments and preventive measures against infectious diseases

(4) Identify who is at risk for infectious diseases

Individuals at risk for infectious diseases can be categorised based on several factors, including age, health status, lifestyle, and environmental conditions

Here are some key groups:

• Young children and infants

  • their immune systems are still developing, making them more susceptible to infections

  • Vaccination schedules are critical for protecting this group

• Elderly Individuals

  • older adults often have weakened immune systems due to age-related decline in immune function, chronic illnesses, or medications that suppress immunity

• Individuals with Chronic diseases

  • people with conditions such as diabetes, heart disease, or HIV/AIDS are at higher risk because their immune systems may be compromised or less effective at fighting infections

• Immunocompromised individuals

  • this includes those undergoing chemotherapy, organ transplant recipients, or individuals on immunosuppressive medications

  • their bodies are less capable of defending against pathogens

• Pregnant women

  • pregnancy can alter immune responses, making women more vulnerable to certain infections that can also affect fetal health

• Healthcare workers

  • they are frequently exposed to infectious agents due to their work environment, increasing their risk of contracting diseases

• Travelers

  • individuals who travel to areas with endemic diseases or poor sanitation may be at risk of infectious not common in their home countries

• Individuals with poor nutrition

  • malnutrition can impair immune function, making individuals more susceptible to infections

• People living in overcrowded for unsanitary conditions

  • high population density and inadequate sanitation can facilitate the spread of infectious diseases

• Substance abusers

  • those who use intravenous drugs or engage in risky sexual behaviours may be at increased risk for infections like HIV or hepatitis

Understanding these risk factors is crucial for implementing preventive measures and targeting innterventions effectively

As highlighted in the objectives, recognising who is at risk helps in managing and controlling the spread of infectious diseases

(5) Discuss how infectious agents cause damage to the body

Infectious agents cause damage to the body through various mechanisms, which can be broadly categorised based on the type of pathogen involved - bacteria, viruses, fungi, protozoa, and prions

Each type of pathogen has unique methods of causing harm:

• Bacteria

  • can cause damage tissues directly by invading cells and multiplying, leading to cell lysis (bursting) and inflammation

  • they may also produce toxins that disrupt normal cellular functions

  • for example, some bacteria release exotoxins that can interfere with nerve function or enterotoxins that can affect the GI tract, causing symptoms like diarrhea

• Viruses

  • invade host cells and hijack their machinery to replicate

  • this often results in cell death, either through direct lysis of the cell or by triggering apoptosis (programmed cell death)

  • The immune response to viral infections can also cause tissue damage, as the body attempts to eliminate the infected cells

• Fungi

  • Fungal infections can cause damage through the release of enzymes that break down host tissues, leading to inflammation and necrosis

  • some fungi can also produce mycotoxins, which can have systemic effects on the body, impacting organs and causing severe illness

• Protozoa

  • Protozoan parasites can invade and destroy host cells, leading to tissue damage

  • they often evade the immune system and can cause chronic infections, leading to ongoing inflammation and damage to organs, as seen in diseases like malaria

• Prions

  • are misfolded proteins that induce abnormal folding of normal proteins in the brain, leading to neurodegenerative diseases

  • this results in progressive damage to neural tissue, causing severe neurological symptoms and ultimately death

Overall, the damage caused by infectious agents can manifest as localised symptoms (like redness and swelling), systemic effects (such as fever and malaise), and long-term complications (like organ failure or chronic disease). The immune system’s response to these pathogens is crucial in determining the extent of damage caused by infectious agents. When a pathogen invades the body, the immune system activates various mechanisms to counteract the infection.

This response can lead to localised symptoms, such as redness and swelling, which are often signs of inflammation as the body directs immune cells to the site of infection

In addition to localised responses, the immune system can trigger systemic effects, including fever and malaise

These symptoms are part of the body’s broader response to infection, often aimed at creating an environment less favorable for pathogens and signaling the need for rest and recovery

Furthermore, if the immune response is inadequate or if the infection is particularly severe, long-term complications may arise. These can include organ failure or the development of chronic diseases, as the body may suffer lasting damage from the infection or from an overactive immune response that attacks healthy tissues.

Overall, the immune system plays a pivotal role in managing infections, balancing the need to eliminate pathogens while minimizing harm to the host

Understanding these interactions is essential for recognising who is at risk for infectious diseases and for developing effective treatment strategies

Traumatic Brain Injury

(1) Revise relevant neuroanatomy and physiology

(2) Outline general mechanisms of neuronal injury

(3) Discuss the aetiology, pathophysiology, clinical manifestations, diagnosis and treatment methods for decreased level of consciousness and brain injury

(1) Revise relevant neuroanatomy and physiology

Relevant neuroanatomy and physiology encompass the structure and function of the nervous system, which is divided into the Central Nervous system (CNS) and the Peripheral Nervous system (PNS):

• Central Nervous system (CNS)

  • this includes the brain and spinal cord

  • the brain is responsible for processing sensory information, controlling motor functions, and facilitating cognitive processes

  • It consists of various regions such as the cerebrum, cerebellum, and brainstem, each with distinct functions

  • The spinal cord serves as a conduit for signals between the brain and the rest of the body, and it also mediates reflex actions

• Peripheral Nervous System (PNS)

  • this system comprises cranial and spinal nerves that extend from the CNS to the rest of the body.

  • it is further divided into the autonomic nervous system (ANS) and the somatic nervous system

  • The ANS regulates involuntary bodily functions and is subdivided into the sympathetic and parasympathetic systems, which control the body’s fight-or-flight response and rest-and-digest activities, respectively

  • The somatic nervous system controls voluntary movements by innervating skeletal muscles

• Neuronal physiology

  • neurons are the fundamental units of the nervous system, responsible for transmitting information through electrical impulses

  • They consist of a cell body, dendrites (which receive signals), and an axon (which sends signals)

  • Neurotransmitters facilitate communications between neurons at synapses. The physiology of neurons involves mechanisms such as action potentials, synaptic transmission, and plasticity, which are crucial for learning and memory

Understanding these components is essential for discussing neuronal injury, as damage to any part of this system can lead to various clinical manifestations, including decreased levels of consciousness and brain injury

(2) Outline general mechanisms of neuronal injury

General mechanisms of neuronal injury caa

(3) Discuss the aetiology, pathophysiology, clinical manifestations,

Diagnosis and treatment methods for decreased level of consciousness and brain injury can be categorised into several key types:

• Traumatic Injury

  • this includes physical damage to neurons caused by external forces, such as in concussions or to her head injuries

• Ischaemic injury

  • this occur when there is a reduction in blood flow to the brain, leading to a lack of oxygen (hypoxia) and nutrients necessary for neuronal survival

• Excitation

  • excessive stimulation of neurons can lead to excitotoxicity, where neurons become damages due to overactivation, often seen in conditions like seizures

• Pressure

  • increased intracranial pressure can compress brain tissue, disrupting normal neuronal function and potentially leading to cell death

• Environmental alterations

  • various factors that disrupt the stable environment of neurons can cause injury

  • This includes:

    • Hypoxia - lack of oxygen

    • Electrolyte imbalance - disruption in ion concentrations can affect neuronal excitability

    • Hypoglycaemia - insufficient glucose supply impairs energy metabolism in neurons

    • Acidosis/Alkalosis - pH imbalances can adversely affect neuronal function

    • High temperature - elevated body temperature can lead to cellular stress and damage

    • Sepsis - systemic infections can lead to inflammatory responses that harm neuronal tissue

• These mechanisms can lead to primary injuries, which may include complications like raised intracranial pressure and decreased cerebral blood flow, ultimately resulting in further neuronal damage and dysfunction

Transmission of pain

(1) Define and consider the role of pain

(2) Review the different types of pain

(3) Explore the physiology of pain and pain pathways

(4) Define pain perception & methods of modulation of pain

(1) Define and consider the role of pain

Pain serves a crucial role in the human nervous system, functioning as an essential mechanism for survival.

It acts as a warning system that alerts us to actual or potential injury, prompting immediate attention and action to prevent further harm.

This protective aspect of pain is vital; without it, individuals might not recognise dangerous situations or injuries, leading to more severe damage

According to the International Association for the Study of Pain (IASP), pain is defined as “an unpleasant and emotional experience with actual or potential tissue damage.”

This definition highlights the complexity of pain, which is not merely a physical sensation but also involves emotional and psychological components

Pain can vary widely in its experience, being highly subjective and influenced by individual factors such as past experiences, cultural background, and psychological state

The role of pain extends beyond mere detection of harm; it also motivates behavioural changes

For instance, if someone touches a hot surface an feels pain, the immediate rection is to withdraw the hand thereby preventing further injury

This immediate response underscores pain’s function as a protective mechanism, ensuring that the body can respond quickly to threats. Moreover, pain perception can be modulated through various methods, including pharmacological interventions, psychological therapies, and physical treatments

Understanding the physiology of pain and its pathways is essential for developing effective pain management strategies, which can enhance quality of life for individuals suffering from chronic pain conditions

In summary, pain is a fundamental aspect of human experience, serving as a critical alert system that protects us from harm, motivates us to take action, and is influenced by a myriad of physiological and psychological factors

(2) Review the different types of pain

• Nociceptive pain

  • this type of pain arises from actual or potential tissue damage and is typically a response to noxious stimuli

  • it is characterised by the activation of inflammatory processes and is considered a normal biological response

  • Nociceptive pain is generally acute and resolves once the underlying tissue heals

  • It responds well to typical analgesics

• Somatic pain

  • this is a subtype of nociceptive pain that is well-localised and can be felt in the skin, tissues, and muscles

  • it is often described as sharp, aching, or throbbing

  • for example, a cut on the skin or muscle strain would produce somatic pain, which is easily identifiable and localised to the affected area

• Visceral pain

  • in contrast, visceral pain is poorly localised and originates from internal organs

  • It is often described as dull, cramping, or colicky and may be associated with additional symptoms such as nausea or sweating

  • An example of visceral pain could be the discomfort felt during a gallbladder attack, which may be referred to other areas of the body, making it harder to pinpoint

Understanding these classifications is crucial for effective pain management and treatment strategies, as different types of pain may require different approaches for relief

(3) Explore the physiology of pain and pain pathways

The physiology of pain involves a complex interplay of various components within the nervous system, primarily through specialised nerve endings known as nociceptors

These nociceptors are the first-order neurons that detect harmful stimuli, such as thermal, mechanical, or chemical insults, and convert these signals into electrical impulses

Once activated, nociceptors transmit pain signals via their axons to the spinal cord, specifically through the dorsal horn

Here, they synapse with second-order neurons, which are part of the spinothalamic tract. This tract carries the pain signals upward to the brain. The spinothalamic neurons ascend through the spinal cord and brainstem, ultimately reaching the thalamus, where they synapse with third-order neurons

The thalamus acts as a relay station, processing and forwarding the pain information to the cerebral cortex, where pain is consciously perceived and interpreted

In the cerebral cortex, different areas are involved in the perception of pain, including the somatosensory cortex, which helps localise the pain, and the anterior cingulate cortex and insula, which are associated with the emotional aspects of pain

Pain modulation can occur at various levels of this pathway. For instance, descending pathways from the brain can influence the transmission of pain signals at the spinal cord level, either enhancing or inhibiting the perception of pain

This modulation can involve neurotransmitters such as endorphins, which can reduce the perception of pain, or other chemicals that may amplify it.

In summary, the pain pathway involves a series of neurons from nociceptors to the cerebral cortex, where pain is processed and perceived

Understanding this pathway is crucial for developing effective pain management strategies

(4) Define pain perception & methods of modulation of pain

Pain perception is the process by which the nervous system interprets pain signals

It involves the activation of pain pathways in the nervous system, which can be influenced by various factors, including tissue injury and inflammation

When tissue is damaged, excitatory neuromodulators such as substance P, glutamate, and somatostatin are released, enhancing the sensation of pain

Conversely, inhibitory neuromodulators like GABA, glycine, serotonin, norepinephrine, and endorphins work to dampen the pain signals, providing a balance in pain perception

Methods of modulation of pain can be categorised into pharmacological and non-pharmacological approaches

Pharmacologically, medications can target the excitatory or inhibitory pathways. For instance, opioids like beta-endorphins and enkephalins bind to opioid receptors, providing significant pain relief by enhancing inhibitory neuromodulation

Other medications may include non-steroidal anti-inflammatory drugs (NSAIDs) that reduce inflammation and thus decrease the release of excitatory neuromodulators

Non-pharmacological methods can include physical therapy, cognitive-behavioral therapy, acupuncture, and mindfulness can also modulate pain perception by addressing the psychological and physical aspects of pain

In summary, pain perception is a complex interplay of physiological processes and subjective experiences, with various methods available for modulation, ranging from medications to

Musculoskeletal & Spinal Cord Injury

(1) Provide a review of muscle fibres and the types of muscle tissue.

(2) Introduce types of muscle damage.

(3) Provide an overview and definitions for types of fractures.

(4) Review the process of fracture healing and consider complications that can occur.

(5) Review types of spinal injury and how damage at varying levels impact on functioning

(1) Provide a review of muscle fibres and the types of muscle tissue.

Muscle fibers, also known as myocytes, are specialised contractile cells that play a crucial role in movement by generating force through contraction

These cells are rich in mitochondria, which provide the necessary ATP for energy during muscle activity.

There are 3 primary types of muscle tissue:

• Skeletal muscle

  • this the of under voluntary control and is responsible for the movement of bones and the body

  • skeletal muscle fibres are striated and can contract rapidly but tire easily

  • they are typically attached to the skeleton and are involved in activities such as walking, running, and lifting

• Cardiac muscle

  • found exclusively in the heart, cardiac muscle is involuntary and striated, similar to skeletal muscle

  • however, cardiac muscle fibres are interconnected, allowing for synchronised contractions that pump blood throughout the body

  • this type of muscle is highly resistant to fatigue due to its continuous activity

• Smooth muscle

  • this type is also involuntary and non-striated

  • Smooth muscle fibres are found in the walls of hollow organs such as the intestines, blood vessels, and bladder

  • They contract more slowly than skeletal muscle and can sustain contractions for longer periods, facilitating functions like digestion and blood flow regulation

In summary, muscle fibers are essential for movement, and the three types of muscle tissue - skeletal, cardiac, and smooth - each serve distinct functions in the body, contributing to overall mobility and physiological processes

(2) Introduce types of muscle damage.

muscle damage can occur in various forms, primarily categorised into strains, sprains, and avulsions

• Strain

  • this refers to a tear or injury to a muscle or tendon

  • strains typically occur when a muscle is stretched beyond its limits or forced to contract too strongly

  • the severity of a strain can vary from mild overstretching to complete tears, which can significantly impact muscle function and strength

• Sprain

  • a sprain involves a tear or injury to a ligament, which is the tissue that connects bones at a joint

  • Sprains can affect the stability of joints and range of motion, leading to pain, swelling, and difficulty in movement

  • like strains, sprains can range from mild (slight stretching) to severe (complete tears)

• Avulsion

  • an avulsion is a more severe form of injury where a tendon or ligament completely separates from its bony attachment site

  • This type of injury often requires surgical intervention for repair and can lead to significant functional impairment if not treated properly

  • In addition to these types of damage, the repair process for skeletal muscle involves unique mechanisms

  • Skeletal muscle fibers cannot divide like other cells but can undergo hypertrophy, where they enlarge by laying down new protein

  • The process of satellite cells, which are mononucleated quiescent cells located beneath the basal lamina, plays a crucial role in muscle repair

  • when muscle damage occurs, these satellite cells can divide slowly and, after division, fuse with existing muscle fibers to help regenerate and repair the damaged tissue

  • However, their capacity to repair is limited, particularly in cases of severe damage

Understanding these types of muscle damage is essential for effective treatment and rehabilitation strategies, as each type may require different approaches to healing and recovery

(3) Provide an overview and definitions for types of fractures.

Fractures are classified based on their characteristics and the nature o the break in the bone

Here’s an overview of the main types of fractures:

• Complete vs Incomplete

  • Complete fracture

    • the bone is broken all the way through, resulting in two separate pieces

  • Incomplete fracture

    • the bone is partially broken meaning it may be cracked but not fully separated

• Closed vs Open

  • Closed (simple) fracture

    • the fracture does not penetrate the skin, meaning there is no external wound

  • Open (compound) fracture

    • the broken bone breaks through the skin, creating an open wound and increasing the risk of infection

• Comminuted fracture

  • this type involves the bone being shattered into three or more pieces, often resulting from high-impact trauma

• Linear fracture

  • a fracture that runs parallel to the long axis of the bone, typically seen in long bones

• Oblique fracture

  • this fracture occurs at an angle across the bone, often resulting from a twisting or bending force

• Spiral fracture

  • similar to an oblique fracture but caused by a twisting force, resulting in a spiral-shaped break

• Transverse fracture

  • a straight break across the bone, which is typically caused by a direct blow or stress

Understanding these classifications is crucial for diagnosis and treatment as the type of fracture can influence the healing process and the approach to management

Treatment often involves reduction (realigning of the bone) and immobilization (using casts or splints) to allow proper healing

(4) Review the process of fracture healing and consider complications that can occur.

The process of fracture healing involves several stages, beginning immediately after the fracture occurs.

Initially, a haematoma forms at the fracture site due to blood vessel damage, creating a blood-filled swelling. This haematoma serves as a foundation for the healing process

Next, fibrocartilage is laid down to form a soft callus, which splints the broken bone. Phagocytes play a crucial role in this phase by removing cellular debris, while fibroblasts deposit collagen to stabilise the fracture. This soft callus is eventually replaced by a bony callus made of spongy bone through a process called endochondral ossification

The bony callus is then remodeled over time. The spongy bone is gradually replaced by compact bone, resulting in a permanent patch that restores the bone’s strength and structure

However, complications can arise during this healing process. Improper reduction or immobilization of the fracture can lead to several issues:

• Nonunion

  • this occurs when the bone ends do not heal together, resulting in a persistent fracture

• Delayed union

  • the healing process takes longer than expected, which can be due to factors like inadequate blood supply, infection, or poor nutrition

• Malunion

  • this happens when the bone heals in an incorrect position, leading to deformity or functional impairment

In summary, fracture healing is a complex process involving stages of haematoma formation, callus development, and remodeling

Proper treatment and monitoring are essential to ensure effective healing and minimize complications

(5) Review types of spinal injury and how damage at varying levels impact on functioning

Spinal injuries can be categorised based on the nature of the injury and the level of the spinal cord affected

The types of spinal injuries include:

• Cord concussion

  • a temporary disruption of spinal cord function without structural damage

  • symptoms may resolve completely

• Cord contusion

  • bruising of the spinal cord, which can lead to varying degrees of neurological deficits depending on the severity

• Cord compression

  • pressure on the spinal cord, often due to vertebral injuries or herniated discs, which van impair function below the injury site

• Cord laceration

  • a cut or tear in the spinal cord, leading to significant loss of function and potential permanent damage

• Cord Transection

  • complete severing of the spinal cord, resulting in total loss of function below the injury level

The impact of spinal cord damage varies significantly depending on the level of the injury:

• Cervical Injuries (C1-C8)

  • these injuries can lead to quadriplegia, affecting all our limbs and potentially impairing respiratory function if the injury is high (C1-C3)

• Thoracic Injuries (T1-T12)

  • these typically result in paraplegia, affecting the legs and lower body

  • Individuals may retain arm function but lose control over bowel, bladder, and sexual functions

• Lumbar Injuries (L1-L5)

  • these can also result in paraplegia, with varying degees of leg function

  • individuals may retain some hip and knee movement but may have difficulty with walking

• Sacral injuries (S1-S5)

  • these injuries usually affect the pelvic organs and lower limbs, leading to issues with bowel and bladder control, but may allow for some leg movement

In summary, the level and type of spinal injury directly correlate with the extent of functional loss, impacting mobility, autonomic functions, and overall quality of life

Allergy & Anaphylaxis

(1) Revise the 5 classes of antibodies

The 5 classes of antibodies, also known as immunoglobins, are distinguished by their structure, function, and the type of immune response they mediate:

• IgM, this is the first antibody produced during the primary immune response to an antigen

  • it is typically found in the bloodstream and is effective in formula complexes with antigens, leading to their destruction

• IgA, predominantly found in mucosal areas, such as saliva, tears, and secretions, IgA plays a crucial role in mucosal immunity

  • it helps protect body surfaces that are exposed to foreign substances

• IgD, this class functions primarily as a receptor on B cells, helping to initiate the B cell’s activation and the subsequent immune response

  • its exact role in serum is less understood compared to other immunoglobulins

• IgG, the most abundant antibody in the bloodstream, constituting about 80-85% of immunoglobulins, IgG is vital for long-term immunity

  • it can cross the placenta, providing passive immunity to the fetus

• IgE, this antibody is primarily involved in allergic reactions and defense against parasitic infections

  • it binds to allergens and triggers histamine release from mast cells and basophilis, leading to allergic symptoms

Each class of antibody has unique characteristics that enable it to perform specific roles in the immune response, contributing to the body’s defense against pathogens and foreign substances

(2) Define the terms allergen and hypersensitivity

• An allergen is a specific type of antigen that triggers and exaggerated immune response, leading to hypersensitivity reactions in susceptible individuals

  • Allergens can be derived from various environmental sources, such as pollens, moulds, foods, animal dander

  • when a person is exposed to an allergen, their immune system may react inappropriately, resulting in inflammation and tissue damage

  • This response can manifest in different ways, including immediate reactions to proteins or complex organic materials, or delayed reactions to simpler inorganic substances like metals

• Hypersensitivity refers to the inappropriate or exaggerated immune response to an allergen

  • it is categorised into different types based on the mechanism of the immune response and the timing of the reaction

  • for example, immediate hypersensitivity occurs rapidly after exposure to the allergen, often within minutes, while delayed hypersensitivity may take hours or even days to develop

  • The immune system’s response can lead to various symptoms, ranging from mild (such as sneezing or skin rashes) to severe (such as anaphylaxis, a life-threatening reaction)

In summary, allergens are specific antigens that provoke hypersensitivity reactions, which are inappropriate immune responses that can cause a range of symptoms and health issues

Understanding these terms is crucial for identifying and managing allergic reactions effectively

(3) Define and describe anaphylaxis

Anaphylaxis is a severe and potentially life-threatening allergic reaction that occurs rapidly, often within minutes of re-exposure to an allergen

It is characterised by a systemic response that can affect multiple body systems simultaneously

The primary features of anaphylaxis include:

• Symptoms

  • the reaction is marked by significant edema (swelling) and bronchoconstriction, which can lead to difficulty breathing

  • In severe cases, swelling of the throat may occur, potentially blocking the airway and resulting in respiratory distress

  • Other symptoms may include hives, swelling of the face or lips, abdominal pain, nausea, and vomiting

• Cardiovascular effects

  • Anaphylaxis can cause a dramatic drop in blood pressure due to widespread vasodilation (the widening of blood vessels) and increased permeability of blood vessels, leading to fluid leakage

  • This can result in shock and collapse if not treated promptly

• Mechanism

  • the underlying mechanism of anaphylaxis involves IgE-mediated hypersensitivity

  • when an individual is exposed to an allergen, IgE antibodies is exposed to an allergen, IgE antibodies bind to mast cells, triggering the release of histamine and other inflammatory mediators

  • this leads to the rapid onset of symptoms

• Treatment

  • the immediate treatment for anaphylaxis is the administration of adrenaline (epinephrine), typically delivered via an EpiPen

  • this medication acts quickly to reverse the symptoms by constricting blood vessels, increasing blood pressure, and dilating airways, thus alleviating respiratory distress

• Prevention and Management

  • individuals with known severe allergies are often advised to carry an EpiPen and to avoid known allergens

  • education on recognizing the early signs of anaphylaxis is crucial for timely intervention

In summary, anaphylaxis is a critical medical emergency that requires immediate recognition and treatment to prevent severe complications or death

(4) Define and describe other types of hypersensitivity reactions

Hypersensitivity reactions are exaggerated or inappropriate immune responses to antigens that can lead to disease or damage in the host

There are 4 main types of hypersensitivity reactions:

• Type I - IgE mediated

  • this reaction is characterised by the production of Immunoglobulin E (IgE) antibodies in response to an allergen

  • Upon re-exposure to the allergen, IgE binds to mast cells and basophils, leading to the release of histamines and other mediators

  • This can cause immediate allergic reactions such as hay fever, asthma, and anaphylaxis, which is a severe systemic response that can occur when allergens enter the bloodstream

• Type II - Tissue-specific Reactions

  • in this type, antibodies (usually IgG or IgM) bind to antigens on the surface of specific cells, leading to cell destruction through mechanisms such as complement activation or phagocytosis

  • Clinical examples include autoimmune hemolytic anemia and Goodpasture syndrome, where the immune system mistakenly targets its own tissues

• Type III - Immune Complex Mediated

  • this reaction occurs when immune complexes (antigen-antibody complexes) are formed and deposited in tissues, leading to inflammation and tissue damage

  • this can activate the complement system and recruit inflammatory cells

  • Conditions such as systemic lupus erythematosus and rheumatoid arthritis are examples of type III hypersensitivity

• Type IV - Cell Mediated

  • as mentioned in the excerpt, this type involves T lymphocytes and macrophages

  • it is a delayed response, meaning symptoms may take hours or days to manifest

  • T cells recognise specific antigens and initiate an immune response, which can result in inflammation and tissue damage

  • Clinical examples include contact dermatitis (e.g., poison ivy), tuberculosis skin test reactions, and graft rejection.

Each type of hypersensitivity has distinct mechanisms and clinical manifestations, highlighting the complexity of the immune system’s response to perceived threats

Shock States

(1) Identify the various types of shock leading to impaired perfusion

There are several types of shock that lead to impaired perfusion each with distinct causes and mechanisms

• Cardiogenic Shock

  • this type occurs due to ineffective cardiac pumping, often resulting from conditions like myocardial infarction or severe heart failure

  • The heart’s inability to pump blood effectively leads to decreased cardiac output and inadequate tissue perfusion

• Hypovolaemic shock

  • this is caused by a significant decrease in blood volume, which can be further categorised into:

    • Hemorrhagic shock

      • resulting from severe blood loss, such as from trauma or surgery

    • Non-hemorrhagic shock

      • caused by fluid loss from other sources, such as severe dehydration, burns, or gastrointestinal losses

• Septic shock

  • this type arises from massive systemic vasodilation due to severe infections, leading to a drop in blood pressure and inadequate perfusion to organs

  • the body’s inflammatory response to infection causes blood vessels to dilate excessively

• Neurogenic shock

  • this occurs due to a loss of sympathetic tone, often following spinal cord injuries

  • it results in vasodilation and decreased vascular resistance, leading to hypotension and impaired perfusion

• Anaphylactic shock

  • this is a severe allergic reaction that causes widespread vasodilation and increased vascular permeability, leading to a rapid drop in blood pressure and impaired organ perfusion

Understanding these types of shock is crucial for identifying risk factors, recognising clinical manifestations, and developing appropriate treatment strategies.

Each type has unique pathophysiological mechanisms that can lead to severe consequences if not promptly addressed, including organ damage and systemic inflammation

(2) List the risk factors for types of shock

The risk factors for types of shock, particularly hypovolemic shock, include:

• Severe bleeding

  • this can be either internal or external and leads to significant fluid loss

• Major or multiple fractures or major trauma

  • these conditions can result in substantial blood loss

• Severe burns or scalds

  • such injuries can cause fluid loss from the body

• Severe diarrhoea and vomiting

  • both can lead to dehydration and a decrease in blood volume

• Severe sweating and dehydration

  • excessive fluid loss through sweat can contribute to hypovolemic shock

These factors highlight the critical nature of maintaining fluid volume in preventing hypovolemic shock and its associated complications

(3) Discuss pathophysiology of shock states and how they are related to treatment strategies

The pathophysiology of shock states involves a complex interplay of physiological responses aimed at maintaining tissue perfusion and oxygenation when faced with a critical reduction in blood flow

Shock can be categorised into several types, including hypovolaemic, cardiogenic, distributive, and obstructive shock, each with distinct underlying mechanisms

In hypovolaemic shock, which is charaterised by a significant decrease in intravascular volume (typically over 15%), the body initiates compensatory mechanisms to restore perfusion

These include sympathetic nervous system activation, which increases heart rate and contractility, and the renin-angiotensin-aldosterone system (RAAS), which promotes fluid retention and vasoconstriction

Antidiuretic hormone (ADH) is also released to conserve water.

However, if the shock state persists, these compensatory mechanisms can fail, leading to decreased blood pressure, vascular fluid shifts, and impaired organ perfusion, ultimately resulting in acidosis and systemic inflammation

The treatment strategies for shock states are closely related to their pathophysiology For hypovolemic shock, the primary treatment involves fluid resuscitation to restore intravascular volume and improve cardiac output

This can include crystalloids or colloids, depending on the severity and cause of the shock. In cases of cardiogenic shock, where the heart’s ability to pump is compromised, treatment may involve medications to improve cardiac contractility or mechanical support devices

Distributive shock, such as septic shock, often requires vasopressors to counteract vasodilation and restore systemic vascular resistance

Understanding the pathophysiology of shock is crucial for developing effective treatment strategies. For instance, recognising that hypovolaemic shock results from volume loss informs the need for rapid fluid replacement

Similarly, understanding the role of systemic inflammation in septic shock can guide the use of antibiotics and other supportive therapies

Overall, timely and appropriate interventions based on the underlying mechanisms of shock can significantly improve patient outcomes

(4) Discuss the impact of shock states for individuals, family, and the society

Shock states have profound impacts on individuals, families, and society, stemming from their physiological, psychological, and economic consequences

• Impact on Individuals

  • for individuals, experiencing shock can lead to severe health complications, including organ failure, prolonged hospitalisation, and even death

  • the immediate effects of shock, such as hypotension and impaired organ perfusion, can result in acute symptoms like confusion, lethargy, and respiratory distress

  • Long-term consequences may include chronic health issues, reduced quality of life, and mental health challenges such as anxiety or depression due to the trauma of the experience and potential loss of independence

• Impact on families

  • Families of individuals in shock states often face emotional and financial strain

  • The stress of a loved one’s critical condition can lead to anxiety and emotional distress among family members

  • Additionally, the need for caregiving and support during recovery can disrupt family dynamics and responsibilities

  • Financially, families may incur high medical costs, especially if prolonged treatment or rehabilitation is necessary, which can lead to economic hardship or debt

• Impact on Society

  • On a societal level, shock states contribute to a significant burden on healthcare systems

  • increased hospital admissions, extended lengths of stay, and the need for specialised care can strain resources and lead to higher healthcare costs

  • This can affect insurance premiums and public health funding

  • Furthermore, the loss o productivity due to illness or disability can impact the workforce, leading to economic losses

  • Public health initiatives aimed at preventing shock states, such as education on risk factors and early intervention strategies, become essential to mitigate these impacts

In summary, the effects of shock states extend beyond the individual, affecting families emotionally and financially, while also placing a considerable burden on societal resources and healthcare systems

Addressing these impacts requires a comprehensive approach that includes medical treatment, psychological support, and community resources