Lecturer : Dr Abdullah Abdulraham

Summaries by : Christina Welgemoed

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Pathophysiology
Hypersensitivity
Type 1
Anaphylactic reaction/ Reagin reaction/ Atopy

Immediate and strongest type hypersensitivity

Increased histamine

Increased IgE fixation on Mast cells

Leads to:

Generalised skin rash

Decrease in blood pressure

Bronchoconstriction Asthma)

Induced by chemicals

E.g. anaesthetics, antibiotics

Treatment = Adrenaline

Type 2
Antibody dependent

Depends on antibody and antigen interaction

2nd strongest

Associated with blood transfusion

Transfusion shock may occur

Leads to agglutination and a drop in blood pressure

Type 3

Pathophysiology 1
 Immune complex cytotoxicity

Complement system and antibodies are involved

ONLY occurs in Streptococcal tonsillitis

Leads to endocarditis and glomerulonephritis

Type 4
Cellular/ local/ delayed type hypersensitivity

Triggers = chemicals

E.g. drugs, cosmetics

Chemicals touching skin, lips, arm causes sensitivity in a localised area

Rash, reddening, oedema, hotness may occur

Occurs after 24 hrs (delayed type)

Acid- base balance

Normal pH range in the body- 7.35 to 7.45

Less than 7.35 → Acidosis

More than 7.45 → Alkalosis

Alkalosis more dangerous compared to acidosis as it is harder to

compensate against alkalosis

Respiratory Acidosis
Decreased respiratory function leads to an increase in acidosis

Leads to the increased accumulation of CO2

Physiological CO2 accumulation

Physical activity

Break down of carbohydrates, proteins, fats during physical activity

leads to increases in CO2 concentrations

CO2 will accumulate- pH will decrease (acidosis)

Pathological CO2 accumulation

Pathophysiology 2
 Respiratory diseases

Asthma, COPD, pneumonia, emphysema all induce hypoventilation

Hypoventilation increased CO2 in blood

CO2 reacts with water in blood to form H2SO4 H HSO4 acidity
will increase

Metabolic Acidosis
Physiological type

Occurs during exercise

Increased lactic acid formation via glucose metabolism

Increased lactic acid leads to acidosis

Pathological type

Caused by diabetes

Increased blood glucose but lack of glucose in cells

Lack of glucose in cells leads to fat and protein breakdown to

produce energy

BUT ketone bodies form

Leads to increases in acidosis and a decrease in blood pH

27pH will lead to diabetic coma

Occurs due to the low pH denaturing enzymes

Excretory Acidosis
Aka non- gaseous acidosis

Caused by diarrhoea

Diarrhoea

Induces the washing out of the contents of the intestines and colon

pH is basic/ alkaline in colon and intestines

Basic/ alkaline nature of colon/ intestines induced by alkaline

phosphatase

Pathophysiology 3
 Loss of alkaline phosphatase in the colon/ intestines during diarrhoea
= acidosis induced

Respiratory Alkalosis
Decrease in CO2 due to hyperventilation

Decrease in CO2 will decrease H2SO4/ sulfuric acid

pH will increase- alkalosis induced

Excretory Alkalosis
Aka non- gaseous alkalosis

Associated with vomiting

Vomiting- loss of H from the stomach

pH will increase- alkalosis induced

Compensation processes against acidosis and

alkalosis
2 types of compensation organs

Kidney

Lungs

Hyperventilation = overcome metabolic acidosis

Decreases CO2 and decreases pH

Kidney increases excretion of H overcome resp and metabolic acidosis

Acidosis will decrease

Urine will be more acidic

Respiratory acidosis/ alkalosis cannot be compensated by lungs (only by

kidneys)

More dangerous as only 1 organ can induce compensation

Jaundice
Increase in bilirubin levels

Pathophysiology 4
 Caused by increases in direct (conjugated) and indirect (unconjugated)
bilirubin or both

Urobilin
Bilirubin excreted by the kidneys as urobilin

Seen in hepatic jaundice and mechanical jaundice

Stercobilin
Bilirubin present in faeces

Gives faeces brown colour

Hemolytic jaundice
Unconjugated/ indirect bilirubin increase

BOTH stercobilin and urobilin seen- indicates bilirubin in faeces and urine

Mechanical/ Obstructive/ Obturator jaundice

Presence of conjugated/ direct bilirubin

Associated with gallbladder/ bile ducts

Obstruction of the gallbladder leads to cholethiasis- gallbladder stones

ONLY urobilin present

NO stercobilin seen

Faeces will be achromic/ pale as no bilirubin is present

Hepatic jaundice
BOTH indirect (unconjugated) and direct (conjugated) bilirubin increased

Anemia
Reductions in haemoglobin and RBC in blood

Membranopathy
Type of anaemia if a membrane is involved

Pathophysiology 5
 Associated with Minkowski- Chauffard disease

Hereditary disease associated with abnormalities in the Na+ channel

Increased influx of Na+ into the cell- causes water to follow Na+ into the
cell

Erythrocytes become spherical in appearance

Enzymopathy
Glucose- 6 phosphate dehydrogenase deficiency

G6P dehydrogenase deficiency leads to increases in oxidation of

erythrocytes- hemolytic anemia

Hemolytic anemia involves erythrocytes appearing in a Winkowski

spherical form due to Na+ channel abnormalities leading to Na+
accumulation

Haemoglobinopathy
Iron deficiency anemia
Microcytic anemia- decreased size of erythrocytes

Causes haemoglobinopathy

Iron involved in holding O2 in haemoglobin

B12/ folate deficiency anaemia

Leads to a decrease in maturity of erythrocytes

Megaloblastic anaemia increased size of erythrocytes

Haemoglobinopathy induced

Sickle cell anaemia

Deformed shape of erythrocytes (sickle shaped)

Hereditary disease

Glutamate in haemoglobin replaced by valine

Valine causes the cell to change shape

Leads to the RBC appearing in a sickle shape

Pathophysiology 6
 Thalassemia
Loss in one of the 4 globulin units

Mostly affects Palestinian people

Reticulocytes more than 2530% indicates thalassemia

Post- haemorrhagic anaemia

Decrease haemoglobin and erythrocytes

History of haemorrhage in past

Acute cases of haemorrhage

Bleeding after surgery, tooth extraction

Chronic cases of haemorrhage

Blood in faces, vomit

Types of hypoxia
Lack of oxygen in atmosphere

E.g. in mountains- decrease in O2 in atmosphere

Hypoxic hypoxia
Respiratory processes unable to take up oxygen

Respiratory hypoxia
Respiratory hypoxia induced by respiratory diseases

COPD

Bronchitis

Asthma

Hemic/ blood hypoxia

Decrease in erythrocytes and haemoglobin- leads to anemia

Cardiovascular hypoxia

Pathophysiology 7
 Tissue cant use oxygen

Tissue has problems in the e- transport chain in mitochondria

Associated with increases in thyroxine

Krok Questions
Contractures in the heart

Caused by Ca2

Adrenogenital syndrome

Female has male secondary sexual characteristics

E.g. beard, body hair, deep voice

Syndrome caused by increased in androgens

Radiation and lymphopenia

1st 8 hrs of radiation exposure- lose a lot of lymphocytes- lead to

lymphopenia

Radiation and leukocytosis

Increased radiation exposure after 10 hrs leads to neutrophilic

leukocytosis

Dystrophy of the heart

Decrease strength of heart contractions

Heart becomes weaker as it gets bigger- hypertrophy of

cardiomyocytes

Fibres in heart stay the same but cardiomyocytes get bigger- heart
won't be able to fully contract

Myogenic dilation

Dystrophy of the heart

Enlargement of the hearts cavities/ chambers

No change in the outer region of the heart

Tonogenic dilation

Pathophysiology 8
 Dystrophy of the heart

Dilation which causes a change in the outer region of the heart

No change in cavities inside the heart

Transmural MI

Infarction throughout all the layers in the heart

Complications associated with left ventricle insufficiency

Congestion of left atria

Edema in lungs (pulmonary edema)- retrograde effect

Complications associated with right ventricle insufficiency

Lower limb edema

Ascites- increased retention of blood in portal vein

Nutmeg liver

ALWAYS pulmonary hypertension

Congestion

Problem receiving blood

Blood remains in blood vessels

Stenosis of renal artery

Increased secretion of renin lead to increased production of

angiotensin

Lead to increases in hypertension

2nd alteration/ healing

Scar formation is a 2nd alteration/ healing event

Appears as an area of necrosis, edema and hyperemia

1st alteration/ healing

No scar formation

1 Drumstick

Indicates 1 Barr body

XX

Pathophysiology 9
 E.g. in Klinefelter syndrome

Prolonged expiration whilst choking

Indicates expiratory dyspnea

Associated with asphyxia

Prolonged inspiration

Indicates inspiration dyspnoea

Glomerulonephritis

Inflammation of the kidney

Associated with reductions in filtration

Increased erythrocyte, protein, platelet leakage into urine-

proteinuria

Proteinuria will lead to edema formation

Hyperaemia induced during physical activity

Turning of ankle ( jumping and landing awkwardly on outer foot/ ankle

region)

Inflammation, hyperemia, warmth increased

Arterial hyperemia disturbances observed

Obstructive alveolar ventilation disturbance

Asthma

COPD

Restrictive alveolar ventilation disturbance

Fibrosis

Neuromuscular/ Dysregulatory alveolar ventilation disturbance

Paralysis of muscles in respiration

Problem with muscles and CNS

Protopathic pain

Acute and dull pain at the same time

E.g. during tooth extraction

Pathophysiology 10
 Left ventricle failure

Aka acute heart failure

Essential hypertension ALWAYS linked to LEFT ventricle

Breathlessness, cyanosis of lips, skin and face are symptoms of left

ventricle failure

Right ventricle failure

ALWAYS associated with pulmonary hypertension

Lower limb edema and ascites

Nutmeg liver

Congestion problems, blood remains in blood vessels

Cyanotic induration of the kidneys and spleen

Neuroparalytic

WPW syndrome

Interleukin- 1

Associated with increases in body temperature

Interleukin- 2

Activates B cells and T cells

Interleukin- 3 and 4

Activates immunoglobulins

Colour index range

85 to 1.15

Colour index less than 0.85

Indicates iron deficiency anemia

Microcytic anemia

Colour index more than 1.15

Indicates B12 deficiency anemia

Megalocytic anemia

Hyperfunction of medulla region of adrenal gland

Pathophysiology 11
 Increased adrenaline activity

Adrenaline associated with increases in hypertension,

hyperglycemia

Excessive adrenaline secretion associated with hyperfunction of

the medulla region of the adrenal gland

Diastole in heart caused by

Heart fully relaxed

Increased K

Hyperkalemia

Indicates heart is in a repolarised state

Systole on heart caused by

Heart CONTRACTION

Caused by increased influx of Ca2 into the heart

Na+ ONLY induces an increase in heart rate

Hydrodynamic oedema

Edema associated with heart failure

Proteinuria associated with glomerulonephritis

Associated with a decrease in oncotic pressure

High concentrations of proteins will be found in urine

Karyotype

Confirm a genetic disorder by carrying out Karyotyping/ Cytogenetic

test

Restriction surface of the lungs

Indicated by fibrosis in the lungs

AVN block arrhythmia

P-wave is greater than QRS indicates that the impulse from the atria
isn't reaching the ventricles

P Q prolongation

Thyroid hormone and hypoxia

Pathophysiology 12
 Thyroid hormone acts in the mitochondria in the e- transport chain

Thyroxine increases oxidation and phosphorylation in mitochondria

which leads to hypoxia (increased need for oxygen)

Extrasystole

Premature contraction in the heart

Lack of a P-wave and QRS deformities indicates extrasystole occuring

in the ventricles

Psychoemotional state and coronary artery spasm

Leads to increases in the secretion of adrenaline

Increased adrenaline leads to increases in the spasm/ constriction of

the coronary artery

Hypokinetic hypertension

Increases in Cardiac Output

No changes in the blood vessel resistance

Hyperkinetic hypertension

Increases in peripheral resistance (general peripheral resistance)

No change to Cardiac Output

Eukinetic hypertension

Increases in Cardiac Output

Increases in peripheral resistance (general peripheral resistance)

Narrowing of blood vessel and increased blood flow

Acquired hemolytic

Free haemoglobin indicates hemolytic anemia

Age determines whether acquired or hereditary hemolytic anemia

Acquired hemolytic anemia- Onset occurs later in life

Hereditary hemolytic anemia- Observed in early stages of life

Leading cause of hypertension

Stress is a leading cause of essential hypertension

Pathophysiology 13
 Stress caused by neurogenetic mechanism

Renal insufficiency

Decrease in renal function

Presence of urea in blood- indicated by convulsions

Decreases in diuresis- indicator for acute renal failure

Pathophysiology 14